COLUMBIA  LIBRARIES  OFFSITE 

HEALTH  SCIENCES  STANDARD 


HX641 32668 
RC681  .H61  1918   Diseases  of  the  hear 


(}C&61 


Left  common  carotid  artery 
.    Innominate  artery     ,  _^— Left  subclavian  artery 

Right  innominate  vein 


Left  innominate  vein 
Superior  vena  cava 
Vena  azygos 
Pulmonary  vein 


Left  internal  jugular  vein 


Stump  of  sup.  cava 
R.  auricular  append. 

Aorta 

Left  coronary  artery 

Right  coronary  vessels 

Right  marginal  artery 


Right  ventricle 


Left  pulmonary  artery 


Superior  pulmO' 
nary  vein 


Inferior  pul  mo 
nary  vein 


Left  auricular 
appendage 
Conus  anteriorsus 
Interventricular  branches 
of  left  coronary  vessels 
Leftventricle 


Fig.  1A. — The  heart  and  great  vessels,  viewed  from  the  front.     (After  Piersol.) 


Left  pulmonary  artery" 


Superior  left  pulmonary  vein, 

Inferior  left  pulmonary  vein 
Termination  of  left  coronary 
vein 
Transverse  branch  of  left 
coronary  artery 


Left  ventricle 


Supeiior  vena  cava 

Superior  right  pulmonary  vein 
Right  pulmonary  artery 

— --—Inferior  right  pulmonary  vein 


Inferior  vena  cava 


Coronary  sinus 

Right  coronary  vein 
Transverse  branch  of  right 

coronary  artery 
'Posterior  descending  branch  of 

right  coronary  artery 

Middle  cardiac  vein 


Right  ventricle 


Fig.  IB. — Same,  from  behind.     (After  Piersol.) 


DISEASES 

of  the 

HEART  AND  AORTA 


BY 

ARTHUR  DOUGLASS  HIRSCHFELDER,  M.D. 

PROFESSOR   OF   PHARMACOLOGY,    UNIVERSITY  OF    MINNESOTA;    CONSULTING    PHARMACOLOGIST   TO   THE 
UNIVERSITY    HOSPITAL;   FORMERLY   ASSOCIATE    IN    MEDICINE,   JGH      >    HOPKINS   UNIVERSITY 


WITH   AN  INTRODUCTORY  NOTE 
BY 

LEWELLYS    F.    BARKER,    M.D.,    LL.D. 

PROFESSOR    OF    CLINICAL   MEDICINE,   JOHNS    HOPKINS    UNIVERSITY 


TWENTY  PLATES  AND 
325  ILLUSTRATIONS  BY  THE  AUTHOR 


THIRD  EDITION  REVISED 


PHILADELPHIA  fcf  LONDON 

J.   B.    LIPPINCOTT    COMPANY 


Copyright,  1910,  By  J.  B.  Lippincott  Company 


Copyright,  1913,  By  J.  B.  Lippincott  Company 


Copyright,  1918,  By  J.  B.  Lippincott  Company 


1  CCSl 
VAGI 


Eleclrotyped  and  Printed  by  J.  B.  Lippincott  Company 
The  Washington  Square  Press,  Philadelphia,  U.S.A. 


TO 
MY    FATHER 


Emeritus  Professor  of  Clinical  Medicine,  Leland  Stanford  Junior  University 


Clinical  Professor  of  Medicine,  Johns  Hopkins  University 

CHIEFS    OF    THE    CLINICS    IN   WHICH   THE    WORK   WAS   DONE  J    WHO 

HAVE   TAUGHT   ME    BY   PRECEPT   AND   EXAMPLE    HOW 

SCIENCE,  ART,  AND  HUMANITY  SHOULD  BE 

WOVEN   INTO  THE   PRACTICE 

OF   MEDICINE 

THIS  BOOK  IS  AFFECTIONATELY  DEDICATED 


INTRODUCTORY    NOTE 


The  researches  in  the  great  field  of  inner  medicine  have  so  multiplied 
in  recent  years  that  it  has  become  highly  desirable  that  we  should  have  from 
time  to  time,  in  addition  to  the  summaries  of  progress  contained  in  the  gen- 
eral text-books  on  practice,  monographs  which  picture  more  completely 
the  status  of  our  knowledge  in  the  several  special  divisions  of  the  subject. 
In  diseases  of  the  circulatory  system  new  methods  of  study  have  led  to  the 
discovery  of  many  new  facts,  and  a  great  many  workers  have  been  attracted 
during  the  last  twenty  years  to  this  domain  of  cardiovascular  inquiry. 

In  the  medical  clinic  at  the  Johns  Hopkins  Hospital,  Dr.  Hirschfelder 
has  during  the  past  few  years  occupied  himself  especially  with  such  studies. 
The  present  volume  is  an  attempt  to  epitomize  the  actual  condition  of  the 
subject  at  the  present  time,  as  viewed  from  the  standpoint  of  an  active  in- 
vestigator of  extensive  first-hand  experience  who  has  also  a  wide  acquaint- 
ance with  the  literature  of  the  physiology  and  pathology  of  the  circulatory 
apparatus. 

The  clearness  and  brevity  of  the  presentation  and  the  excellent  arrange- 
ment of  the  material  will,  I  am  sure,  appeal  to  students  and  practitioners 
of  medicine.  It  is  no  easy  matter  adequately  to  combine  the  most  recent 
results  of  anatomical,  physiological,  pathological,  and  clinical  studies  in  a 
form  which  will  satisfy  the  critical  demands  of  the  scientific  investigator 
and  at  the  same  time  be  useful  as  a  guide  to  the  every-day  practitioner. 
Especial  attention  has  been  paid  in  the  volume  to  the  practical  facts  of  diag- 
nosis and  treatment;  in  the  more  theoretical  portions  there  will  be  found 
evidence  of  careful,  critical  sifting,  and  an  appreciation  of  the  distinction 
between  what  is  essential  and  what  non-essential  for  the  more  general  reader. 

The  bibliographic  references  make  no  attempt  at  completeness,  but 
have  been  chosen  with  the  idea  in  mind  of  permitting  those  who  desire  to  do 
so  to  consult  the  most  important,  and  especially  the  more  recent,  treatises, 
monographs,  and  original  articles  which  deal  with  the  various  matters 
discussed. 

A  notable  feature  of  Dr.  Hirschfelder's  book  is  the  liberality  of  illustra- 
tions; the  majority  of  the  figures  are  made  from  original  drawings  and  tracings 
and  are  in  pleasing  contrast  with  the  time-worn  figures  which  pass  from 
compilation  to  compilation. 

Lewellys  F.  Barker. 
Baltimore,  May  12,  1910. 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diseasesofheartaOOhirs 


PREFACE   TO  THE   THIRD   EDITION 

The  changes  in  the  subject  which  have  arisen  since  the  appearance  of 
the  second  edition  have  been  in  the  main  changes  of  evolution  rather  than 
revolution.  Graphic  methods  with  phlebogram  and  electrocardiogram  have 
become  routine,  and  the  use  of  the  Frank  mirror  and  tambour  as  a  recording 
device  almost  free  from  fling  has,  in  the  hands  of  Wiggers  and  Hewlett,  added 
more  accurate  records  of  both  nervous  and  arterial  pulsations.  Hewlett's 
studies  with  the  volume  pulse  have  demonstrated  the  importance  of  back- 
flow  in  the  peripheral  arteries  and  have  given  a  new  meaning  to  the  normal 
pulse  curve,  as  well  as  to  those  obtained  in  fevers,  after  the  administration 
of  drugs,  and  in  aortic  insufficiency.  The  larger  number  of  cases  which  have 
been  collected  and  reported  have  manifested  additional  evidence  for  the  con- 
tention made  by  the  author  in  1908  and  by  Thomas  Lewis  in  1909  that 
extrasystoles,  auricular  tachycardia  and  auricular  fibrillation  are  closely  re- 
lated phenomena  which  represent  an  ascending  scale  of  increased  irritability 
of  the  heart  muscle.  The  great  war  has  brought  a  terribly  rich  harvest  of 
cardiac  overstrains  among  soldiers,  the  manifestations  of  which  have  stood 
as  a  brilliant  memorial  to  the  completeness  of  the  great  work  done  by  Da 
Costa  during  the  American  Civil  War. 

The  studies  of  Barcroft  and  his  collaborators  and  of  Peabody  have  cast 
much  fight  upon  the  C02  metabolism,  alveolar  air  content  and  the  mechanism 
of  cardiac  dyspnoea,  confirming  and  enlarging  upon  the  work  of  Grey  and  the 
writer  mentioned  in  the  second  edition  of  this  book. 

The  studies  of  Rowntree  and  Levy  have  introduced  a  new  method  for 
the  accurate  study  of  the  total  volume  of  the  blood  in  cardiac  disease,  which 
promises  to  lead  to  a  more  accurate  understanding  of  the  role  of  plethora  and 
the  importance  of  relieving  it. 

A  bolder  method  for  the  use  of  digitalis  in  larger  doses  than  has  been 
used  heretofore  has  been  introduced  by  Eggleston,  and  has  led  in  many  cases 
to  more  rapid  and  certain  relief  from  the  symptoms  of  decompensation.  Real 
light  has  been  thrown  into  the  indefinite  border-line  between  the  normal 
dyspnoea  and  true  cardiac  overstrain  in  pregnancy  by  the  studies  of  Litzen- 
berg  upon  liver  function  in  this  disease,  by  means  of  the  urobilin  excretion 
in  the  urine. 

The  isolation  of  the  active  principle  of  the  thyroid  gland  from  both  nor- 
mal thyroids  and  those  of  exophthalmic  goitre  has  furnished  chemical  proof 
that  the  latter  condition  is  a  true  hyperthyroidism,  while  the  pathological 


viii  PREFACE  TO   THE   THTRD   EDITION. 

and  clinical  studies  of  Wilson  and  Plummer  throw  much  light  upon  the  re- 
lation of  the  pathology  of  the  gland  to  its  clinical  manifestations.  Conve- 
nience of  arrangement  has  dictated  that  the  group  of  paroxysmal  tachycardia, 
now  recognized  as  a  transition  form  between  extrasystolic  arrhythmia  and 
auricular  flutter  and  auricular  fibrillation,  be  placed  in  the  chapter  upon  car- 
diac arrhythmias,  as  in  Part  I,  instead  of  remaining  as  a  separate  chapter  in 
Part  III,  as  in  the  first  and  second  editions.  A  number  of  new  figures,  new 
sets  of  curves  illustrating  the  action  of  various  drugs  upon  the  cardiac  func- 
tion, have  been  added  and  several  new  sets  of  venous  tracings  and  electrocar- 
diograms from  the  Medical  Service  of  the  University  of  Minnesota  have  been 
furnished  by  Dr.  Ralph  E.  Morris  of  that  department,  to  whom  the  writer 
takes  pleasure  in  expressing  his  sincere  thanks. 

University  of  Minnesota,  Minneapolis 
June  15,  1918. 


PREFACE   TO    THE   SECOND    EDITION 


Since  the  appearance  of  the  first  edition  numerous  advances  have  been 
made  in  the  subject  of  cardiac  disease  of  such  importance  that,  in  order  to 
embody  them  in  the  text,  several  chapters  have  had  to  be  rewritten  and 
enlarged. 

The  electrocardiograph,  which  has  now  assumed  a  role  of  primary  im- 
portance in  physiology,  pharmacology,  and  clinical  observation,  has  been 
discussed  in  detail  as  to  theory,  construction,  and  application.  The  study  of 
the  mechanism  of  the  normal  and  pathological  heart-beat  by  this  method 
has  thrown  so  much  light  upon  the  site  of  origin  of  the  normal  and  abnormal 
heart-beat,  the  action  of  the  cardiac  nerves,  and  the  paroxysmal  tachycardias 
and  the  permanent  irregularity  that  it  has  become  a  procedure  of  routine 
examination  of  heart  cases  in  many  medical  clinics,  and  in  the  hands  of 
Mackenzie,  Cushny  and  Lewis  has  led  the  way  to  more  exact  methods  for 
the  use  of  digitalis.  Other  drugs  which  have  merited  consideration  have 
come  into  use,  and  the  chapters  and  sections  upon  treatment  have  been  con- 
siderably enlarged.  The  studies  of  Haldane,  Pembrey  and  Yandell  Hender- 
son upon  acapnia,  and  of  Sir  William  Ewart  upon  C02  inhalations,  have 
given  a  clinical  importance  to  the  investigation  of  C02  in  the  alveolar  air  of 
the  lungs.  The  recent  investigations  upon  syphilitic  arterial  disease  and  its 
frequency  have  made  possible  a  more  clear-cut  classification  of  arterioscle- 
rotic conditions,  and  in  the  light  of  these  the  section  upon  the  pathology  of 
arteriosclerosis  has  been  rewritten. 

It  is  a  pleasant  duty  to  the  author  to  express  his  grateful  appreciation 
of  the  cordial  reception  which  the  book  has  received  at  the  hands  of  his  medi- 
cal colleagues,  to  many  of  whom  he  owes  his  thanks  for  suggestions  that  have 
been  helpful  in  the  revision.  To  Dr.  George  S.  Bond  he  is  particularly  in- 
debted for  the  preparation  of  the  electrocardiograms  used  throughout  the 
book,  as  well  as  to  Dr.  Milton  C.  Winternitz  for  many  helpful  suggestions 
and  for  the  preparation  of  a  number  of  photomicrographs. 


2245  Linden  Avenue, 
January  10,  1913. 


IX 


PREFACE   TO   THE   FIRST   EDITION 


In  the  preparation  of  this  book  it  has  been  the  writer's  aim  to  present 
side  by  side  the  phenomena  observed  at  the  bedside  and  the  facts  learned 
in  the  laboratory  in  order  to  show  how  each  supplements  the  other  in 
teaching  us  how  to  observe  the  patient  and  to  direct  the  treatment.  Many 
of  the  results  obtained  in  the  laboratory  have  not  yet  attained  practical 
importance  because  they  have  been  scattered  through  the  literature  and 
have  not  reached  the  eye  of  the  clinician;  but  wherever  the  clinicians  have 
looked  to  the  laboratory  or  laboratory  workers  have  looked  to  the  clinic 
for  verification  or  application  of  their  theories  the  great  pillars  of  progress 
have  been  raised.  In  accordance  with  this  idea  the  clinical  presentation 
in  each  chapter  is  preceded  by  an  introductory  section  dealing  with  the 
experimental  pathology  and  more  fundamental  principles  of  the  subject, 
which  has  been  used  as  a  basis  for  frequent  reference  in  the  clinical  dis- 
cussions. 

The  trend  of  clinical  observation  during  the  past  two  decades  has  been 
toward  more  accurate  study  of  disturbances  of  function  and  toward  the 
introduction  of  mechanical  methods  for  their  observation,  methods  of 
precision  which  tend  to  supplement  or  supplant  the  older  and  simpler 
methods  of  physical  diagnosis.  Chief  among  these  may  be  mentioned  the 
study  of  blood-pressure,  the  graphic  studies  upon  alterations  in  cardiac 
rhythm  by  means  of  the  venous  pulse,  the  outlining  of  the  heart  and  vessels 
by  means  of  the  X-ray,  and  the  phonographic  recording  of  the  heart  sounds. 
Each  of  these  subjects  has  been  reviewed  with  special  reference  to  the 
general  principles  upon  which  the  method  is  based,  in  order  to  point  out 
its  applicability,  it's  limitations,  the  character  of  information  which  it  has 
yielded  in  clinical  conditions,  the  conditions  under  which  the  same  informa- 
tion may  be  gained  by  simpler  methods,  the  conditions  under  which  its 
employment  is  essential  and  those  under  which  it  is  superfluous. 

The  failure  of  the  heart  has  been  traced  through  its  varying  stages 
from  the  simple  fatigue  of  the  normal  heart  in  exercise,  through  the  stage 
of  primary  overstrain,  to  that  of  broken  compensation,  especial  attention 
being  devoted  to  the  states  of  broken  pulmonary  compensation  arising 
from  failure  of  the  left  ventricle  and  of  broken  systemic  compensation 
from  failure  of  the  right. 

xi 


xii  PREFACE  TO  THE  FIRST  EDITION. 

The  pathogenesis  of  cardiac  symptoms  is  fully  discussed,  with  their 
pathological  physiology,  occurrence,  and  the  symptomatic  treatment  for 
their  relief. 

The  general  methods  of  treatment  in  cardiac  diseases,  dietetic,  phar- 
macological, gymnastic,  hydrotherapeutic,  and  electrical,  have  been  treated 
both  as  empirical  procedures  and  as  experimental  methods  to  correct 
definite  disturbances  in  the  physiology  of  the  circulation,  especially  changes 
in  cardiac  force,  cardiac  tonicity,  and  peripheral  resistance. 

The  chapters  upon  the  individual  organic  lesions  include  discussions 
of  pathological  anatomy,  pathogenesis,  pathological  physiology,  as  well 
as  of  symptomatology,  course,  notes  of  typical  cases,  diagnosis,  treatment, 
and  prognosis.  Considerable  attention  is  also  paid  to  functional  disturb- 
ances (valvular  insufficiencies,  etc.)  which  may  bring  about  conditions 
similar  to  those  resulting  from  organic  changes  or  may  accompany  the 
latter.  The  Adams-Stokes  syndrome  seems  so  definitely  associated  with 
lesions  of  the  auriculo ventricular  muscle  bundles  as  to  justify  its  classifi- 
cation among  conditions  due  to  organic  lesions. 

The  congenital  heart  lesions  are  viewed  as  disturbances  in  embryologic 
development  in  which  primary  malformations  or  states  in  fetal  life  have 
diverted  the  blood  current,  modifying  the  further  course  of  development 
and  producing  concomitant  secondary  malformations.  The  effect  of  these 
lesions  upon  the  adult  circulation  and  their  relation  to  cardiac  overstrain 
in  producing  the  syndrome  of  the  morbus  cceruleus  are  discussed,  as  well 
as  the  signs,  diagnosis,  prognosis,  and  treatment. 

Short  chapters  are  devoted  to  the  subjects  of  pregnancy  in  heart 
disease  and  the  effects  of  trauma  and  wounds  of  the  heart. 

Considerable  space  is  given  to  the  purely  functional  disturbances  of 
cardiac  action,  especially  to  the  physiological  mechanisms  by  which  many 
of  them  result  from  disturbances  in  distant  organs  as  well  as  to  the  improve- 
ments resulting  when  these  disturbances  are  corrected. 

A  great  deal  of  care  has  been  bestowed  by  the  writer  in  the  prepara- 
tion of  the  illustrations,  especially  upon  the  cardiosphygmographic  trac- 
ings, the  diagrammatic  representations  of  clinical  conditions  and  of  effects 
upon  the  blood  flow  in  different  parts  of  the  circulation  as  well  as  in  differ- 
ent stages  of  the  disease.  When  necessary,  figures  have  been  borrowed 
from  other  sources,  to  whom  due  credit  has  been  given. 

Since  the  aim  of  the  book  is  not  only  to  present  the  principal  facts. 
but  to  aid  the  reader  in  following  out  lines  in  which  he  is  especially  inter- 
ested, an  adequate  bibliography  has  been  added  to  each  chapter,  embrac- 
ing the  articles  referred  to  in  the  text. 

It  is  a  pleasant  duty  for  the  writer,  in  conclusion,  to  express  his  thanks 
to   Professors  Barker  and  Thayer  for  the  privilege  of  using  the  clinical 


PREFACE  TO  THE  FIRST  EDITION.  xiii 

material  and  records  of  the  Johns  Hopkins  Hospital,  to  Professor  T.  B. 
Futcher  for  that  of  the  Johns  Hopkins  Dispensary,  and  to  his  father,  Pro- 
fessor J.  0.  Hirschf elder,  for  the  cases  at  the  City  and  County  Hospital 
of  San  Francisco;  to  Professor  F.  P.  Mall  and  Drs.  Knower,  Retzer,  and 
Evans  in  matters  of  anatomy  and  embryology;  to  Professors  W.  H.  Howell, 
J.  Loeb,  and  Dr.  D.  R.  Hooker  in  physiology;  to  Professors  W.  S.  Hal- 
sted,  T.  S.  Cullen,  and  J.  M.  Slemons  in  matters  of  surgery,  gynaecology, 
and  obstetrics;  to  Professors  W.  G.  MacCallum  and  W.  Ophiils,  as  well 
as  to  Major  F.  F.  Russell,  Dr.  Lamb,  and  Dr.  Gray,  of  the  Army  Medical 
Museum,  for  the  use  of  pathological  material;  to  Professor  C.  M.  Cooper 
for  the  collection  of  radiographs;  to  Dr.  Chas.  S.  Bond  for  his  untiring 
labors  in  the  preparation  of  photomicrographs;  to  Professor  W.  Einthoven 
of  Ley  den  for  the  use  of  electrocardiograms;  to  Professor  Max  Broedel 
for  his  kind  instruction  and  suggestions  in  matters  of  illustration;  to  Dr. 
Caroline  B.  Towles  for  her  assistance  in  reading  of  proof  as  well  as  for 
many  helpful  suggestions;  and  to  Miss  Alberta  E.  Bush  for  her  care  in  the 
technical  matters  pertaining  to  the  manuscript  and  index. 


CONTENTS 


PART  I. 
GENERAL  CONSIDERATIONS  AND  METHODS  OF  DIAGNOSIS. 

PAGE 

I.  Physiological  Considerations 1 

II.  Blood-pressure  and  Blood  Viscosity 25 

III.  The  Arterial  Pulse 63 

IV.  The  Venous  Pulse  and  Electrocardiogram  in  Health  and  Disease  ...  71 
V.  Alterations  in  Cardiac  Rhythm 98 

VI.  X-ray  Examination 144 

VII.  Physical  Examination 152 


PART  II. 

I.  Primary  Cardiac  Overstrain 189 

II.  Pathological    Physiology    of    Exercise,    Cardiac    Overstrain,    Heart 

Failure,  and  Compensation 197 

III.  Symptoms  op  Cardiac  Disease 215 

IV.  General  Principles  of  Treatment  of  Failure  of  the  Heart 231 

V.  The  Effects  of  Drugs  in  Cardiac  Disease 245 

VI.  Gymnastics  and  Hydrotherapy 279 

VII.  Hypertrophy  and  Atrophy 291 

VIII.  Fatty  Deposits  in  and  about  the  Heart %  304 

IX.  Affections  of  the  Myocardium 314 

X.  Arteriosclerosis 339 

XL  Vasomotor  Crises  and  the  Angioneurotic  Lesions 388 

XII.  Sclerosis  of  the  Coronary  Arteries,  >nd  Angina  Pectoris 378 


PART  III. 

I.  Endocarditis 398 

II.  Mitral  Insufficiency 420 

III.  Mitral  Stenosis 440 

IV.  Aortic  Insufficiency 462 

V.  Aortic  Stenosis 483 

VI.  Pulmonary  Insufficiency 492 

xv 


xvi  CONTENTS 

VII.  Tricuspid  Insufficiency 498 

VIII.  Tricuspid  Stenosis 508 

IX.  Marriage,  Pregnancy  and  Labor  in  Cases  of  Heart  Disease 515 

X.  Congenital  Heart  Disease 525 

XL  Heart-Block  and  the  Adams-Stokes  Syndrome 565 

XII.  Pericarditis 590 

XIII.  Wounds  of  the  Heart  and  Cardiac   Trauma 623 

XIV.  Aneurism 631 


PART  IV. 

I.  Thyroid  Heart 674 

II.  Miscellaneous    Disturbances    of    Cardiac    Function — The    So-called 

"Cardiac   Neuroses"  and  "Cardiac   Neurasthenia" 694 


LIST  OF  ILLUSTRATIONS 


FIG.  PAGE 

1.  The  heart  and  great  vessels Frontispiece 

2.  Relations  of  the  heart  and  great  vessels,  viewed  from  the  front xxviii 

3.  The  heart  and  thoracic  viscera,  viewed  from  behind xxviii 

4.  Sagittal  section  of  the  thorax,  viewed  from  the  right xxviii 

5.  Heart  muscle-fibres 1 

6.  Section  through  the  endocardium,  showing  cross-section  of  the  muscle- fibres . ...  2 

7.  Curve  showing  the  catalysis  of  hydrogen  peroxide  by  mercury 2 

8.  Apparatus  for  perfusing  the  mammalian  heart  4 

9.  The  auricular  end  of  the  human  heart,  viewed  from  the  right 6 

10.  The  sinus  region  of  the  heart  and  the  auriculoventricular  bundle 7 

11.  Diagram  showing  the  arrangement  of  the  strands  of  muscle-fibres  in  the  ventricle  9 

12.  Apparatus  for  registering  the  volume  of  the  ventricles 11 

13.  Diagram  showing  the  events  of  a  single  cardiac  cycle •• .  .  12 

14.  Methods  for  demonstrating  the  movements  of  the  heart  valves 13 

15.  Volume  curves  of  the  ventricles  at  increasing  pulse  rates 14 

16.  Diagram  showing  the  effect  of  varying  venous  pressures  upon  the  volume  of  the 

heart,  upon  the  rapidity  of  filling  of  the  ventricles,  and  upon  the  position  as- 
sumed by  the  mitral  and  tricuspid  valves  at  the  end  of  the  first  inflow  into 

the  ventricles 15 

17.  Diagram  showing  the  condition  of  the  heart  with  varying  degrees  of  tonicity 

but  with  systolic  output  normal 16 

18.  Origin  and  course  of  the  cardiac  nerves,  and  cutaneous  distribution  of  the  corre- 

sponding branches 18 

19.  Curve  of  intraventricular  and  aortic  pressures 25 

20.  Diagram  showing  the  effect  of  compression  upon  various  types  of  arteries 27 

21.  Types  of  manometer  used  for  determining  blood- pressure 27 

22.  Erlanger  blood-pressure  apparatus  with  Hirschfelder  polygraph  attachment 27 

23.  Auscultatory  method  of  determining  blood-pressure,  as  used  with  the  Oliver 

apparatus 29 

24a.  Diagram  showing  arrangement  of  Erlanger  apparatus 29 

24b.  Curve  taken  with  the  Erlanger  blood-pressure  apparatus,  showing  the  points  of 

maximal  and  minimal  pressure 29 

25.  Diagram  showing  the  effect  of  varying  degrees  of  compression  upon  the  excursion 

of  the  arterial  wall 30 

26.  Diagram  showing  the  maximal  and  minimal  pressures  in  various  parts  of  the 

circulatory  system 35 

27.  Diagram  showing  effects  of  vasoconstriction,  vasodilation,  increased  and  decreased 

force  of  ventricular  contraction  upon  the  maximal  and  minimal  blood-pressures 

and  upon  the  form  of  the  pulse 35 

28.  Diagram  of  apparatus  for  determining  the  rate  of  blood-flow  through  the  human 

arm 37 

29.  Diagram  showing  the  curve  of  blood-pressure  during  asphyxia 39 

30.  Diagram  showing  typical  blood-pressures  in  various  diseases 41 

31.  Hooker  and  Eyster's  modification  of  v.  Recklinghausen's  method  of  determining 

the  venous  pressure  in  man 51 

32.  Determann's  apparatus  for  determining  the  viscosity  of  the  blood 59 

xvii 


xviii  LIST  OF  ILLUSTRATIONS 

33a.  Diagram  showing  principle  of  apparatus 64 

33b.  Mounting  of  capsules 64 

34.  Absolute  sphygmograms,  all  of  which  correspond  to  the  radial  tracing  above ....  65 

35.  Significance  of  the  pulse-curve 66 

36.  Diagram  showing  the  time  relations  of  ventricular  volume  and  pressure  curves  to 

pulse  tracings  from  the  aorta,  carotid  and  radial  arteries 66 

37.  Three  types  of  arterial  pulse-curve  corresponding  to  the  same  pulse-pressure  and 

same  pulse-rate 67 

38.  Effect  of  inhalation  of  amyl  nitrite  upon  the  pulse-form 67 

39.  Mercury  manometer  tracing  from  the  carotid  artery  of  a  dog,  showing  rhythmic 

variations  in  blood-pressure  and  rhythmic  increase  in  dicrotism 68 

40.  Diagram  showing  various  forms  of  pulse-curve  encountered  clinically 68 

41.  Sites  for  recording  the  jugular  and  carotid  pulsations 73 

42.  Apparatus  for  recording  the  respiration 74 

43.  V.  Jaquet's  cardiosphygmograph 74 

44.  Normal  venous  tracings 75 

45.  Diagram  representing  the  various  events  in  a  cardiac  cycle 75 

46.  Venous  tracing  showing  absence  of  the  c  wave  in  a  case  of  heart  failure 77 

47.  Venous  tracing  showing  auricular  paralysis  (absence  of  a  wave)  with  large  (x) 

depression 77 

48.  Venous  tracing  from  a  very  slow  heart,  with  loud  third  heart  sound,  showing  the 

presence  of  the  h  wave 78 

49.  Tracing  from  the  same  person  one  hour  later,  after  giving  atropine  and  quickening 

the  pulse 78 

50.  Showing  a  wave  w  occurring  shortly  before  the  a  wave       79 

51.  Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insufficiency,  showing 

absence  of  the  a  wave 80 

52.  Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insufficiency,  showing 

absence  of  the  a  wave 80 

53.  Method  of  taking  tracing  from  the  oesophagus  to  show  the  contractions  of  the  left 

auricle 81 

54.  (Esophageal  and  carotid  tracings  from  a  normal  man 81 

55.  Photograph  of  the  electrocardiograph  laboratory  or  "heart  station"  of  the  Johns 

Hopkins  Hospital 82 

56.  Cambridge  modification  of  Einthoven's  string  galvanometer 83 

57.  Edelmann's  convenient  switchboard  and  short-circuiting  keys 84 

58.  Diagram  showing  main  connections  for  the  electrocardiograph 85 

59.  Diagram  showing  the  relation  between  the  compensated  and  uncompensated 

currents 87 

60.  Distribution  of  electromotive  force  in  the  body  in  the  three  principal  leads  or 

derivations 89 

61.  Normal  electrocardiogram  showing  time  relations  to  the  venous  and  carotid  pulse 

wave 92 

62.  Factors  involved  in  the  production  of  the  normal  electrocardiogram 92 

63.  Diagram  representing  various  types  of  irregular  pulse 99 

64a.  Respiratory  arrhythmia 102 

64b.  Diagram  showing  the  relation  of  the  afferent  impulses  in  the  vagus  to  the 

threshold  of  irritability  of  the  medulla 102 

65.  Venous  tracings  in  heart-block.    Partial  heart-block  (3  : 1  rhythm)  during  pres- 

sure on  the  vagus  in  a  case  of  Adams-Stokes  disease 104 

66.  Venous  tracings  in  heart-block.    Complete  heart-block  in  a  case  of  Adams-Stokes 

disease 104 

67.  Occasional  absence  of  apex  impulse  during  inspiration  simulating  interventricular 

heart-block 105 


LIST  OF  ILLUSTRATIONS  xix 

68.  Alternating  pulse  in  a  case  of  paroxysmal  tachycardia 106 

69.  Response  of  frog's  ventricle  to  abnormal  stimuli 107 

70.  Tracing  from  the  right  jugular  vein  and  radial  artery  of  a  patient  showing  ven- 

tricular extrasystoles 109 

71.  Tracings  from  the  jugular  vein  and  brachial  artery  of  a  patient  with  trigeminal 

pulse 112 

72.  Volume  curve  of  the  ventricles,  showing  the  dilation  which  followed  the  entrance 

of  an  air-bubble  into  the  right  auricle 115 

73.  Extrasystoles  with  shortened  conduction  time,  supposed  to  arise  in  the  auriculo- 

ventricular  bundle 115 

74.  Variations  in  conduction  time  in  a  case  of  mitral  stenosis 115 

75.  Tracing  from  right  jugular  vein  and  left  radial  artery  showing  absolute  arrhythmia 

due  to  auricular  fibrillation 116 

76.  Diagram  showing  the  alterations  of  rhythm  which  may  cause  a  pulsus  bigeminus  116 

77.  Perpetual  arrhythmia  of  the  ventricles 119 

78.  Diagram  showing  abnormal  electrocardiograms  and  the  structures  in  which  they 

arise 120 

79.  Effect  of  arrhythmia  on  the  circulation,   blood-pressure,   and  volume  of  the 

ventricles 122 

80a.  Venous  pulse  in  a  case  of  paroxysmal  tachycardia 125 

80b.   Diagram  showing  the  various  types  of  tachycardia 126 

80c.   Slightly  more  intense  stimulation 129 

80d.  Diagram  showing  the  effect  of  a  paroxysm  of  tachycardia  upon  circulation ....  130 

81.  Radiograph  of  a  normal  chest 145 

81a.  X-ray  shadows  in  different  axes  of  the  body 146 

82.  A  simple  form  of  orthodiagraph 147 

83.  Diagram  showing  the  use  of  the  orthodiagraph 147 

84.  Orthodiagraphic  outline  of  normal  heart,  showing  Moritz's  conjugates 147 

85.  Movements  of  the  heart  leading  to  the  protrusions  and  retraction  during  systole  153 

86.  Rubber  funnel  for  cardiographic  tracings 154 

87.  Tracing  from  the  apex  impulse  and  carotid  artery.    Cardiograms  obtained  over  a 

normal  apex  and  over  the  fourth  left  interspace 154 

88.  Various  forms  of  apex  tracings 155 

89.  Areas  of  pulsation  and  retraction 156 

90.  Eddies  producing  thrills  as  illustrated  by  a  stream  of  water 156 

91.  Goldscheider's  orthopercussion 157 

92.  Percussion  with  the  orthoplessimeter 158 

93.  The  heart  as  outlined  by  ordinary  percussion,  by  orthopercussion  perpendicular 

to  the  measuring  tape,  and  by  orthodiagraph 159 

94.  Areas  of  cardiac  dulness  and  flatness  in  a  normal  man 159 

95.  Cardiac  outlines  in  a  child  of  nine  years 160 

96.  Diagrams  illustrating  the  movements  of  the  normal  heart  on  change  of  posture 

from  side  to  side,  and  in  the  various  phases  of  respiration 161 

97.  Graphic  records  of  the  heart  sounds 162 

98.  Diagram  for  representing  the  heart  sounds  in  clinical  notes 165 

99.  Choice  of  stethoscope  bells 167 

100.  The  "valvular  areas " 168 

101.  The  propagation  of  the  heart  sounds  from  valves  to  chest  wall 169 

102.  Graphic  records  of  the  fetal  heart-sounds 170 

103.  Diagram  illustrating  the  split  sounds  and  gallop  rhythms  and  their  phonetic 

equivalents 171 

104.  Graphic  records  of  presystolic  gallop  rhythm  and  split  pulmonic  second  sound.  .    172 

105.  Graphic  record  of  the  third  heart  sound 173 

106.  Jugular  and  carotid  tracings  from  a  normal  individual  with  a  well-marked  third 

heart  sound 174 


xx  LIST  OF  ILLUSTRATIONS 

107.  Forces  supposed  to  be  at  work  in  the  production  of  the  third  heart  sound 174 

108.  Similarity  between  the  production  of  voice  sounds  and  the  production  of  murmurs  176 

109.  Distribution  of  the  accidental  murmur 181 

110.  Graphic  record  of  an  accidental  murmur 182 

111.  Diagram  showing  the  relation  of  the  more  common  simple  murmurs  to  events  of 

the  cardiac  cycle 183 

112.  Cardiac  dulness  in  v.  Leyden's  case  upon  his  three  successive  admissions 193 

113.  Alterations  of  blood- pressure  due  to  rapid  lifting  of  light  weights  with  the  feet.  .  198 

114.  Effect  of  walking  on  a  level  on  patient  with  badly  broken  compensation 199 

115.  Effect  of  prolonged  exercise  upon  the  blood-pressure  of  men  in  various  degrees  of 

muscular  strength 199 

116.  Rise  of  blood-pressure  during  Valsalva's  experiment  and  during  exercise 200 

117.  Semi-schematic  drawing  showing  variations  in  size  of  the  heart  of  a  long-distance 

bicycle  rider,  as  the  result  of  a  very  long  race 201 

118.  Effect  of  strain  upon  the  dog's  heart  whose  tonicity  is  good 203 

119.  Volume  curve  of  a  dog  whose  cardiac  tonicity  is  low 204 

120.  Effect  upon  the  volume  of  the  dog's  heart  produced  by  clamping  the  descending 

thoracic  aorta 205 

121.  Diagram  showing  changes  in  the  circulation:    I,  normal;  II,  broken  pulmonary 

compensation;  III,  broken  systemic  compensation;  IV,  both  compensations 
fail;  stases  in  lungs  and  veins '. 207 

122.  The  two  types  of  Cheyne-Stokes  respiration  in  their  relations  to  the  blood-pressure 

curves 220 

123.  Legs  of  a  patient  with  extreme  cedema  and  tremendous  ulcers 222 

124.  Curschmann's  modification  of  the  Southey  tubes  for  draining  cedema  of  the  legs  223 

125.  Electrical  record  of  afferent  impulses  travelling  up  the  vagi 225 

126.  Insertion  of  the  knife  in  venesection 234 

127.  Effect  of  venesection  on  the  cardiac  outline,  showing  diminution  in  size  of  right 

heart 235 

128.  Typical  effect  of  venesection  upon  the  circulation 235 

129.  Effect  of  inhalation  of  carbon  dioxide  on  the  ventilation  of  the  lungs 242 

130.  Tracings  showing  the  action  of  digitalis  upon  the  dog's  blood-pressure 251 

131.  Variations  in  blood-pressure  in  a  patient  under  the  influence  of  digitalis  and 

nitroglycerin 252 

132.  Effect  of  digitalis  on  cardiac  tonicity  in  the  dog 253 

133.  Chart  showing  effects  of  strychnine  and  digitalis  in  a  case  of  continuous  irregularity  263 

134.  Effects  of  drugs  of  the  nitrite  series  upon  the  blood- pressure  in  man 269 

135.  Schott  resisted  movements 282 

136.  Hypertrophic,  normal,  and  atrophic  hearts 291 

137.  Photomicrographs  of  atrophic  and  hypertrophic  heart  muscle 292 

138.  Heart  of  normal  dog  and  of  dog  which  has  run  for  three  months  on  a  tread-mill.  .  294 

139.  Areas  of  pulsation  and  reaction  hypertrophy  of  the  right  and  left  ventricles 297 

140.  Diagram  showing  power  of  normal  and  hypertrophied  (athlete's)  heart  at  rest  and 

during  exercise,  also  that  of  a  diseased  heart 301 

141.  Distribution  of  fat  in  and  about  the  heart 304 

142.  Photomicrographs  of  fat  deposits  in  the  heart 305 

143.  An  excessive  deposit  of  epicardial  fat 306 

144.  Infiltration  along  the  course  of  the  blood-vessels  in  subacute  myocarditis;  blood- 

vessels injected 315 

145.  Septic  myocarditis  with  multiple  abscesses  in  the  heart  wall 316 

146.  Photomicrograph  showing  an  abscess  in  the  heart  muscle 317 

147.  Orthodiagraphic  outlines  of  the  heart  of  a  child  during  the  course  of  a  severe 

diphtheria 320 

148.  Specimen  showing  a  cardiac  aneurism  covered  with  pericardial  adhesions 324 


LIST  OF  ILLUSTRATIONS  xxi 

149.  Chronic  myocarditis  (cardiosclerosis) 324 

150.  Specimens  showing  chronic  myocarditis 325 

151.  Hypertrophy  of  some  muscle  bundles  in  the  auricle  with  atrophy  (transparency) 

of  other  areas 326 

152.  Curve  of  blood-pressure  in  a  case  of  chronic  myocarditis,  showing  the  high  blood- 

pressure  persisting  until  shortly  before  death 327 

153.  Various  types  of  arteriosclerotic  lesions.     (Schematic) 342 

154.  Types  of  aortic  lesions 342 

155.  Syphilitic  aortitis  (atherosclerosis)  with  deposition  of  calcified  plaques  just  above 

and  upon  the  aortic  valves 344 

156.  Arteriosclerosis  of  the  descending  aorta,  showing  atheromatous  plaques 352 

157.  Tortuous  radial  artery 358 

158.  Retinal  changes  in  arteriosclerosis  (colored  plate) 358 

159.  Effect  of  arteriosclerosis  upon  the  circulation 359 

160.  Blood-pressure  chart  of  case  of  typical  vasomotor  crisis 369 

161.  Blood-pressure  chart  showing  a  vascular  crisis  of  the  cerebral  type 370 

162.  Diagram  to  illustrate  the  elimination  of  CO  by  the  blood  in  normal  and  sclerotic 

arteries 371 

163.  Thromboangitis  obliterans  and  endarteritis  obliterans 374 

164.  Hands  and  feet  of  a  patient  with  thromboangitis  obliterans,  showing  gangrenous 

ulcers  and  the  stumps  of  amputated  toes 375 

165.  Effect  of  ligation  of  a  large  coronary  artery  upon  the  blood-pressure 378 

166.  Sclerosis  of  a  coronary  artery,  producing  an  area  of  infarction  near  the  apex ....   380 

167.  Distribution  of  pain  in  attacks  of  angina  pectoris 384 

168.  Distribution  of  attacks  of  pain  and  sensory  disturbances  in  a  case  of  angina 

pectoris 385 

169.  Blood-pressure  curve  showing  crises  of  hypertension  during  attacks  of  angina 

pectoris 386 

170.  Fibrinous  deposit  upon  an  aortic  cusp  one  hour  after  mechanically  injuring  the 

valve 398 

171.  Mitral  endocarditis  showing  large  vegetations 399 

172.  Injection  of  chronically  inflamed  valves 399 

173.  Structure  of  the  normal  auriculoventricular  valve .   400 

174.  Photomicrograph  of  a  specimen  showing  acute  and  subacute  endocarditic  lesions 

upon  the  mitral  valve 401 

175.  Ulcerative  and  healed  endocarditis 402 

176.  Temperature  curve  from  a  case  of  malignant  endocarditis 404 

177.  Temperature  curve  from  a  case  of  simple  acute  endocarditis 404 

178.  Diagram  showing  relative  frequency  of  the  most  important  valvular  lesions  at 

various  ages 411 

179.  Diagram  showing  the  relative  frequency  of  the  various  valvular  lesions  in  cases 

of  valvular  heart  disease 411 

180.  Regurgitant  streams  in  organic  and  functional  mitral  insufficiencies 421 

181.  Diagram  showing  the  volume  and  pressure  curves  under  these  conditions 423 

182.  Curve  of  intraventricular  pressure  in  mitral  insufficiency  produced  on  a  mechanical 

model 424 

183.  Diagram  showing  the  effects  of  mitral  insufficiency  upon  the  circulation 425 

184.  Distribution  of  the  murmur  in  mitral  insufficiency 428 

185.  Cross  section  of  the  body  showing  how  the  thrill  and  murmur  reach  the  chest  wall  429 

186.  Radiograph  of  a  patient  with  mitral  insufficiency,  showing  horizontal  enlarge- 

ment of  the  heart  to  the  left 429 

187.  Diagram  of  Fig.  186,  showing  the  directions  in  which  cardiac  enlargement  has 

taken  place 430 


xxii  LIST  OF  ILLUSTRATIONS 

188.  Graphic  records  of  the  heart  sounds,  showing  the  systolic  murmur 430 

189.  Human  heart,  showing  mitral  and  tricuspid  stenosis.    Viewed  from  above.     The 

auricles  have  been  cut  through 440 

190.  Diagram  showing  the  changes  in  the  circulation  due  to  mitral  stenosis 442 

191.  Volume  of  the  ventricles  in  experimental  mitral  stenosis 443 

192.  Diagram  illustrating  the  variations  in  the  volume  curve  of  the  ventricles  in 

increasing  degrees  of  mitral  stenosis 443 

193.  Diagram  showing  the  direction  of  the  stream  entering  the  left  ventricle  through 

the  stenotic  mitral  orifice 445 

194.  Cardiac  outline  and  distribution  of  the  presystolic  rumble  in  mitral  stenosis 446 

195.  Radiograph  from  a  case  of  mitral  stenosis,  showing  increase  of  the  shadow  due  to 

the  dilated  left  auricle 447 

196.  Diagram  representing  the  shadows  shown  in  Fig.  195 447 

197.  Graphic  record  of  carotid  pulse  and  heart  sounds  in  mitral  stenosis 447 

198.  Diagram  showing  the  relations  of  the  various  sounds  heard  in  uncomplicated 

mitral  stenosis  to  events  in  the  filling  and  emptying  of  the  ventricle 448 

199.  Venous  pulse  of  a  patient  with  mitral  stenosis  during  an  attack  of  acute  heart 

failure 449 

200.  Permanent  arrhythmia  in  a  case  of  mitral  stenosis,  showing  persistence  of  the 

auricular  contractions  (a  wave)  upon  the  venous  pulse 451 

201.  Specimen  showing  vegetations  upon  the  aortic  valves 462 

202.  Schematic,  showing  the  various  forms  of  lesions  producing  aortic  insufficiency .  .   463 

203.  Effect  of  aortic  insufficiency  in  the  mechanical  model 464 

204.  Diagram  of  the  circulation  in  aortic  insufficiency 465 

205.  Diagram  showing  how  the  high  cardiac  tonicity  hastens  the  equilibrium  between 

aortic  pressure,  intraventricular  pressure,  and  tonicity,  and  thus  diminishes  the 
amount  of  blood  regurgitating 466 

206.  Effect  of  rupturing  an  aortic  valve  in  a  dog,  showing  a  transitory  dilatation 

followed  by  a  permanent  diminution  in  size 466 

207.  Area  of  cardiac  dulness  and  distribution  of  the  cardiac  sounds  and  murmurs  in 

aortic  insufficiency 470 

208.  Radiograph  of  a  case  of  aortic  insufficiency,  showing  elongation  of  the  long  axis  of 

the  heart 470 

209.  Diagram  of  Fig.  208,  showing  the  hypertrophy  of  the  left  ventricle 470 

210.  Direction  of  the  primary  regurgitant  streams  in  aortic  insufficiency 472 

211.  Relation  of  murmurs  in  aortic  insufficiency  to  the  cardiac  cycle 473 

212.  Functional  mitral  stenosis  in  aortic  insufficiency  as  demonstrated  on  the  excised 

heart  by  Baumgarten's  method 473 

213.  Variations  in  the  form  of  the  pulse-wave  encountered  clinically  in  aortic  insuffi- 

ciency    474 

214.  Tracings  from  a  dog  with  experimental  aortic  insufficiency,  showing  the  con- 

version of  a  collapsing  into  an  anacrotic  pulse  by  clamping  the  descending 

aorta 475 

215.  Radial  pulse  tracings  showing  extrasystoles,  probably  of  ventricular  origin 476 

216.  Specimen  showing  aortic  stenosis.    Viewed  from  above 483 

217.  Forms  of  stenotic  aortic  orifices 483 

218.  Carotid  pulse  and  intraventricular  pressure  in  experimental  aortic  stenosis 484 

219.  Diagram  of  the  circulation  showing  the  effect  of  aortic  stenosis 485 

220.  Diagram  showing  the  cardiac  outline  and  distribution  of  the  murmur  in  aortic 

stenosis 486 

221.  Murmur  of  aortic  stenosis 487 

222.  Diagram  showing  the  pulsus  tardus  and  the  anacrotic  type 488 

223.  Pulse  tracings  from  cases  of  aortic  stenosis 488 

224.  Diagram  of  the  circulation  in  pulmonary  insufficiency 493 


LIST  OF  ILLUSTRATIONS  xxiii 

225.  Distribution  of  the  murmur  in  pulmonary  insufficiency 494 

226.  The  outline  of  a  normal  heart  superposed  upon  that  of  a  dilated  heart,  showing 

the  enlargement  of  the  tricuspid  orifice 499 

227.  Diagram  showing  the  changes  in  the  circulation  in  tricuspid  insufficiency 500 

228.  Venous  pulse  of  patients  with  tricuspid  insufficiency  (positive  venous  pulse) ....   501 

229.  Venous  pulse  of  another  patient 501 

230.  Distribution  of  the  murmur  and  cardiac  outline  in  tricuspid  insufficiency 503 

231.  Cross  section  of  the  body,  showing  the  paths  of  propagation  of  the  murmur  of 

tricuspid  insufficiency 503 

232.  Tracings  of  liver  pulsation 504 

233.  Systolic  pulsation  of  the  liver  of  patient  W.  H 505 

234.  Diagram  showing  the  changes  in  the  circulation  in  tricuspid  stenosis 510 

235.  Cardiac  outline  and  distribution  of  the  presystolic  rumble  and  snapping  first 

sound  in  tricuspid  stenosis 511 

236.  Very  early  stage  in  the  development  of  the  human  circulatory  system 525 

237.  Human  embryo  4  mm.  long  (about  the  fourth  week  after  fertilization),  showing 

the  further  development  of  the  heart  and  of  the  branchial  or  aortic  arches ....   526 

238.  Heart  of  an  embryo,  slightly  older  than  that  shown  in  Fig.  237,  showing  the 

earliest  stages  in  the  formation  of  two  auricular  and  two  ventricular  pouches .   527 

239.  A  diagram  showing  the  interior  of  this  heart 527 

240.  Schema  to  show  the  development  of  the  arterial  system  from  out  of  the  primitive 

aortic  arches 527 

241.  Heart  of  slightly  older  embryo,  showing  separation  of  aortic  and  pulmonary 

channels  in  truncus  arteriosus 528 

242.  Still  later  stage,  showing  the  complete  division  of  the  truncus  arteriosus  into 

pulmonary  artery  and  aorta 529 

243.  Auricular  end  of  the  same  heart .  .  . 529 

244.  Development  of  the  pericardial  cavity 530 

245.  The  circulation  in  the  foetus  just  before  birth 532 

246.  Pulmonary  stenosis  due  to  fusion  of  the  cusps 535 

247.  Pulmonary  stenosis  due  to  a  lesion  of  the  inf undibulum 535 

248.  Complete  pulmonary  atresia 535 

249.  Schema  illustrating  the  genesis  of  pulmonary  stenosis 536 

250.  Currents  and  lines  of  force  in  the  embryonic  heart  which  result  from  pulmonary 

stenosis  and  tend  to  produce  patency  of  the  septa  and  of  the  ductus  arteriosus  538 

251.  Three-chambered  heart  (cor  biatriatum  triloculare)  produced  by  complete  atresia 

of  the  pulmonary  and  tricuspid  orifices 539 

252.  Diagram  of  the  circulation  in  pulmonary  stenosis  and  atresia 540 

253.  Dilatation  and  irregularity  of  the  retinal  vessels 543 

254.  Clubbed  fingers 543 

255.  Distribution  of  the  pulmonary  systolic  murmur  of  pulmonary  stenosis 544 

256.  Direction  of  blood-streams — and  propagation  of  murmurs  accompanying  defect  in 

the  interventricular  septum,  pulmonary  stenosis,  and  open  ductus  arteriosus .  .  544 

257.  Distribution  and  character  of  the  murmur  due  to  a  patent  interventricular  septum 

(Roger's  murmur) 548 

258.  Open  foramen  ovale 550 

259.  Diagram  showing  a  cross-section  of  the  same 550 

260.  Openings  between  strands  of  muscle  in  the  interauricular  septum 551 

261.  Radiograph  of  a  thirteen-year-old  boy  with  patent  ductus  arteriosus  and  aneuris- 

mal  dilatation  of  the  ductus  and  pulmonary  artery 555 

262.  Stenosis  of  the  isthmus  of  the  aorta  above  the  ductus  arteriosus — type  of  the 

new-born 557 

263.  Stenosis  below  the  ductus  arteriosus — adult  type 558 

264.  Transposition  of  the  viscera  in  embryo  and  adult 560 


xxiv  LIST  OF  ILLUSTRATIONS 

265.  Transposition  of  the  valves 562 

266.  Pulmonary  artery  with  four  cusps 562 

267.  Tracing  of  the  apex  beat  in  a  case  of  Adams-Stokes  disease 566 

268.  Partial  heart-block  (3 : 1  rhythm)  produced  by  pressure  upon  the  vagus  in  a 

patient  with  disturbed  conductivity  who  was  also  subject  to  attacks  of  the 
Adams-Stokes  syndrome 567 

269.  The  right  branch  of  the  auriculoventricular  bundle  in  the  dog's  heart 568 

270.  Tracings  from  the  carotid  artery  and  the  jugular  vein  of  a  patient  with  Adams- 

Stokes  disease,  showing  stoppage  of  the  ventricles  and  continuance  of  the 
auricular  contractions  during  the  attack 569 

271.  The  Erlanger  heart-block  clamp  compressing  the  auriculoventricular  bundle.  . . .  570 

272.  Effect  of  gradually  tightening  the  clamp 570 

273.  Tracing  from  jugular  vein  and  carotid  artery  in  a  case  of  complete  heart-block 

after  the  syncopal  attacks  had  subsided 573 

274.  Diagram  representing  the  conditions  found  in  the  tracing  Fig.  273 574 

275.  Pleart  of  a  patient  showing  calcifications  which  produced  Adams-Stokes  disease  575 

276.  Diagram  showing  the  two  types  of  ventricular  stoppage  producing  the  Adams- 

Stokes  syndrome 576 

277.  Section  of  a  luetic  infiltration  of  the  auriculoventricular  bundle 576 

278.  Acute  fibrinous  pericarditis 592 

279.  Tuberculous  pericarditis  (cor  villosum) 592 

280.  Diagram  showing  the  relations  of  the  pericardial  and  pleural  frictions  to  the 

cardiac  and  respiratory  movements 594 

281.  The  circulation  in  cases  with  pericardial  effusion 598 

282.  Area  of  cardiac  dulness  from  pericardial  effusion 599 

283.  Positions  of  the  heart  in  pericarditis  with  effusion 601 

284.  Radiograph  of  a  patient  with  pericardial  effusion 602 

285.  Sites  for  paracentesis  pericardii  and  pericardiotomy 606 

286.  Specimen  showing  the  two  layers  of  pericardium  united  in  some  parts  by  long 

strands  and  in  others  by  short  bands  of  dense  adhesions 610 

287.  Sections  showing  adherent  pericardium 611 

288.  Anterior  and  posterior  pericardial  adhesions.    (Semi- schematic) 612 

289.  Cardiac  outline  in  adherent  pericardium 615 

290.  Inspiratory  and  expiratory  dropping  of  beats  (Riegel's  pulse  and  the  pulsus 

paradoxus)  in  adherent  pericardium,  showing  the  position  of  the  adhesions 

which  bring  the  condition  about 616 

291.  Radiograph  of  a  case  of  adherent  pericardium 617 

292.  Case  of  pericarditic  pseudocirrhosis 619 

293.  Wounds  of  the  left  ventricle 624 

294.  Exposure  of  the  heart  for  suturing  a  wound 626 

295.  Specimen  of  a  large  aneurism 631 

296.  Aneurism  arising  just  above  a  sinus  of  Valsalva 634 

297.  Aneurism  of  the  ascending  arch  and  innominate  artery 634 

298.  Aneurism  of  the  transverse  portion  of  the  aortic  arch  penetrating  through  the 

sternum 634 

299.  Aneurism  of  the  descending  aorta  eroding  the  vertebra? 634 

300.  Sections  through  the  wall  of  an  aneurism 635 

301.  Composite  figure  showing  the  relations  of  various  aneurisms  to  surrounding 

structures 638 

302.  Tracings  of  the  outlines  of  an  aneurism  of  the  innominate  artery,  showing  its 

growth  and  the  formation  of  secondary  prominences  upon  its  surface 639 

303.  Method  of  inspecting  for  pulsations 642 

304.  Effect  upon  the  circulation  of  interposing  an  inelastic  and  an  elastic  bulb  along 

the  course  of  an  artery  in  a  model  of  the  circulation 644 


LIST  OF  ILLUSTRATIONS  xxv 

305.  Effect  of  aneurisms  at  various  sites  upon  the  blood-pressure,  rate  of  transmission, 

and  the  form  of  the  pulse-wave . .   645 

306.  Radial  pulse  tracings  from  the  right  and  left  radial  arteries  of  a  patient  with 

aneurism  of  the  first  part  of  the  arch  of  the  aorta 645 

307.  Radiograph  of  a  patient  with  a  large  aneurism  of  the  ascending  aorta  and  the 

arch,  viewed  from  behind 646 

308.  Radiograph  of  a  patient  with  diffuse  dilatation  of  the  arch  of  the  aorta 647 

309.  Diagram  of  the  radiograph  shown  in  Fig.  308 647 

310.  Cardiac  dulness  in  cases  of  aneurism 650 

311.  Area  of  cardiac  dulness  in  a  patient  with  dilated  arch  of  the  aorta 653 

312.  Tumor  and  pulsation  in  a  case  of  patient  with  aneurism  of  the  abdominal  aorta.  655 

313.  Tortuous  subclavian  artery,  simulating  a  small  aneurism 656 

314.  Dissecting  aneurisms 657 

315.  Diagrams  showing  the  various  methods  for  the  operative  treatment  of  aneurism.  663 

316.  Specimen  of  wired  abdominal  aneurism,  showing  an  island  of  clot  within  the  coils 

of  wire  surrounded  by  a  free  blood-channel 668 

317.  Photograph  of  a  patient  with  Basedow's  disease 676 

318.  Photograph  of  a  portion  of  the  thyroid  gland  removed  from  the  patient  shown 

in  Fig.  317 677 

319.  Drawing  of  a  histological  specimen  from  the  same  thyroid 679 

320.  Diagram  showing  the  relation  of  the  various  anatomical  structures  concerned  in 

the  production  of  the  ocular  and  cardiac  manifestations  of  Basedow's  disease .  .   685 

321.  Respiratory  arrhythmia  in  a  young  cigarette  smoker 695 

322.  Cross  section  of  the  thorax  of  a  flat  chested  individual,  showing  the  systolic 

heaving  of  the  chest  wall  and  the  forces  bringing  it  about 697 

323.  Low,  normal,  and  high  hearts.    (Semi-schematic) 699 

324.  Radiograph  of  a  patient  with  dropping  heart  (bathycardia) 700 

325.  Photograph  of  a  patient  with  enteroptosis 703 

PLATES. 

I.  Stanton,  v.  Recklinghausen,  Oliver,  and  Tycos  sphygmomanometers 31 

II.  Fig.  1.  Two  segments  of  radial  and  carotid  pulse 64 

Fig.  2.  Volume  pulse  curve  superposed 64 

III.  Forms  of  clinical  polygraphs:  A.  G.  Gibson's  polygraph,  Mackenzie's  polygraph, 

Uskoff 's  sphygmotonograph 74 

IV.  Electrocardiograms  from  a  normal  man '. 91 

V.  Typical  electrocardiograms 92 

VI.  Electrocardiogram  of  sinus  arrhythmia  (respiratory),  with  diagram  showing  the 
course  of  the  impulses  within  the  heart.  Extrasystole  arising  at  the  node  of 
Keith  and  Flack  (homogenetic),  with  diagram  showing  the  course  of  the 

normal  and  extrasystolic  impulses 100 

VII.  Tracing  showing  auricular  extrasystoles  arising  from  an  abnormal  site  (hetero- 
genetic),  with  diagram  showing  the  course  of  the  extrasystolic  impulse.  Trac- 
ing showing  an  extrasystole  arising  in  the  right  ventricle,  with  diagram 110 

VIII.  Tracing  showing  an  extrasystole  arising  in  the  left  ventricle,  with  diagram. 
Tracing  showing  one  extrasystole  arising  in  the  right  ventricle  and  one  arising 
in  the  left  ventricle Ill 

IX.  Absolute  arrhythmia  due  to  auricular  fibrillation  of  the  coarse  type,  with  diagram 
showing  the  origin  and  transmission  of  the  impulses.  Absolute  arrhythmia 
due  to  auricular  fibrillation  of  the  fine  type,  with  diagram  showing  the  origin 

and  transmission  of  the  impulses 121 

X.  Electrocardiograms  from  a  patient  with  a  lesion  of  the  right  branch  of  the  His 

bundle,  verified  at  autopsy 126 

XL  Electrocardiograms  showing  auricular  and  ventricular  tachycardia 128 


xxvi  LIST  OF  ILLUSTRATIONS 

XII.  Electrocardiogram  showing  partial  heart  block  after  digitalis  with  sudden  onset 

of  auricular  nutter  and  auricular  fibrillation  and  return  to  normal 129 

XIII.  Fig.  1.  Card  held  against  the  skin  over  the  jugular  vein — vein  full,  shadow 
between  the  skin  and  card  is  narrow  at  the  instant  of  the  A  and  V  waves  on  the 
venous  pulse 138 

Fig.  2.  Same  with  vein  collapsed,  shadow  wide,  as  at  the  instant  of  the  x  and  y 
depressions 138 

Fig.  3.  Normal  double  venous  pulse.  The  black  bands  indicate  the  correspond- 
ing waves  on  the  pulsations 138 

Fig.  4.  Venous  pulse  and  waves  of  an  auricular  extrasystole  (AE)  showing 
"double "  venous  pulse 138 

Fig.  5.  Venous  pulse  with  ventricular  extrasystole  (VE)  showing  the  large 
"single"  venous  pulse,  accompanying  the  extrasystole. 138 

Fig.  6.  Positive  "single"  venous  pulse  with  absolute  arrhythmia,  accompanying 
ventricular  fibrillation 139 

Fig.  7.  Similar  "single"  venous  pulse  with  small  wavelets  due  to  auricular 
flutter 139 

Fig.  8.  Venous  pulsation  in  partial  heart-block,  a  constant  number  of  small 
auricular  waves,  two  in  each  diastole,  occurring  between  the  larger  ventricular 
waves 139 

Fig.  9.  Venous  pulsation  in  complete  heart-block  showing  a  varying  number  of 
auricular  waves  in  successive  diastoles 139 

Fig.  10.  Tracing  of  heart  sounds  from  a  patient  with  complete  heart-block  and 

ventricular  extrasystoles 139 

XIV.  Diagram  showing  the  connections  for  taking  graphic  records  of  the  heart  sounds 
by  means  of  the  Einthoven  galvanometer.    Record  showing  the  third  heart 

sound  and  its  relation  to  the  venous  pulse 163 

XV.  Heart-block  resulting  from  prolonged  use  of  digitalis  and  removed  by  atropine. 
Blood  pressure  tracing  from  a  dog  showing  absolute  arrhythmia  produced  by 
fibrillation  of  the  auricles  brought  on  by  direct  faradization  of  the  right  auricle  256 

XVI.  Electrocardiograms  showing  hypertrophy  of  the  ventricles.     Tracing  from  a 

patient  with  hypertrophy  of  the  left  ventricle  by  the  first,  second  and  third 
leads  respectively 298,  299 

XVII.  A.  Endarteritis  with  thickening  of  intima  in  a  patient  dying  from  typhoid 

fever  without  complications.  B.  Degeneration  of  the  media  of  a  cerebral 
artery,  showing  destruction  of  the  elastic  fibres.  C.  Radial  artery  showing 
great  hypertrophy  of  tuni  media.  D.  Syphilitic  aortitis  showing  destruction 
of  the  elastic  fibres  in  the  media  and  their  replacement  by  fibrous  tissue. 
E.  Mononuclear  infiltration  along  the  course  of  the  vasa  vasorum  of  adven- 
titia  and  media  in  syphilitic  aortitis.  F.  Endarteritis  productiva  et  obliterans 
in  the  vasa  vasorum  and  periarteritis  of  the  latter  in  a  case  of  syphilitic 
aortitis.    G.  Treponemata  (spirochsetse)  from  the  wall  of  an  aneurism .  .   350,  351 

XVIII.  Typical  electrocardiogram  from  a  case  of  mitral  stenosis  showing  large  P  wave. 

Electrocardiogram  from  a  case  of  mitral  stenosis  with  permanent  arrhythmia 
due  to  auricular  fibrillation,  showing  one  extrasystole  arising  in  the  right 
ventricle 458 

XIX.  Electrocardiogram  from  a  patient  with  complete  inversion  of  the  heart  dextro- 

cardia with  the  other  organs  in  their  normal  positions,  showing  a  curve  of 
normal  form.    Electrocardiogram  from  a  case  of  complete  transposition  of  all 

the  organs  (situs  inversus),  showing  all  the  waves  inverted 561 

XX.  Electrocardiogram  from  a  case  of  complete  heart-block.     Electrocardiogram 

from  a  case  of  auricular  fibrillation  with  complete  heart-block 577 


SYNONYMOUS  ANATOMICAL  TERMS. 


Old  Terminology. 

Basle  Anatomical  Nomenclature 
(BNA)  >. 

Latin. 

Auriculoventricular  groove . .  . 

Coronary  sulcus 

Sulcus  coronarius. 

Septum  of  ventricles 

Septum  ventriculorum. 

Septum  musculare. 
Septum  membranaceum. 
Atrium. 

Auricle 

Forechamber 

Auricular  appendix 

Auricle 

Auricula. 

Interauricular  septum 

Columns;  carnea: 

Septum  of  atria 

Septum  atriorum. 
Trabeculae  carneae. 

Fleshy  cords 

Annulus  ovalis 

Edge  of  oval  fossa 

Limbus  fossae  ovalis  (Vieus- 

senii) . 

Intervenous  tubercle  of  Lower 

Tuberculum  intervenosum 

(Loweri) . 

Eustachian  valve 

Valve  of  inferior  vena  cava.  . 

Valvula  venae  cavae   (infe- 

rioris,  Eustachii). 

Valve  of  Thebesius;  coronary 
valve 

Value  of  coronary  sinus 

Valvula  sinus  coronarii  (The- 
besii) . 

Foramina  Thebesii 

Foramina  of  the  smallest 
veins 

Foramina  venarum  minim- 

arum  (Thebesii). 

Tricuspid  valve    (right   auri- 
culoventricular valve) 

Tricuspid  valve 

Valvula  tricuspidalis. 

Infundibular  cusp' 

Anterior  cusp 

Cuspis  anterior. 

Cuspis  posterior. 

Cuspis  medialis. 

Valvula   bicuspidalis   (mi- 
tralis). 

Marginal  cusp 

Posterior  cusp 

Septal  cusp 

Medial  cusp 

Left  auriculoventricular  valve 

Bicuspid  or  mitral  valve  .... 

Corpora  Arantii 

Nodules  of  the  semilunar 
valves 

Noduli  valvularum   semilu- 

narium. 

Ductus  arteriosus  (Botalli) . .  . 

Arterial  duct 

Ductus  arteriosus  (Botalli). 

Fasciculus    atrioventricu- 
laris. 

Auriculoventricular    bundle 
(Kent,  His) 

Atrioventricular  bundle  (His) 

1  Quoted  from  Barker,  L.  F.,  Anatomical  Terminology,  with  special  reference  to  the 
BNA,  Phila.,  1907. 

The  Basle  Anatomical  Nomenclature  (BNA)  is  the  terminology  adopted  by  an  inter- 
national convention  of  anatomists  at  Basle  in  1895,  for  the  purpose  of  securing  uniformity 
of  terminology.  As  it  has  hot  yet  supplanted  the  old  terminology  in  clinical  usage, 
the  latter  is  adhered  to  in  this  book,  though  the  BNA  terms  are  frequently  given  in 
parentheses. 


Fig.  2. — Relations  of  the  heart  and  great  vessels,  viewed  from  the  front.  SVC,  superior  vena 
cava ;  R  A,  right  auricle  (atrium)  ;  L  V,  left  ventricle;  R  V,  right  ventricle ;  P  A,  pulmonary  artery; 
PL,  pleura. 


Ftg.  3. — The  heart  and  thoracic  viscera  viewed 
from  behind.  The  lungs  have  been  cut  away.  L  A, 
left  auricle ;  L  V,  left  ventricle. 


Fig.  4. — Sagittal  section  of  the  thorax  viewed 
from  the  right.  AZ.,  great  azygos  vein ;  POST. 
MEDIAST.,  posterior  mediastinum;  ANTER. 
M  EDI  AST.,  anterior  mediastinum;  R  A,  right 
auricle  ;  PHREN,  right  phrenic  nerve. 


DISEASES 

OF  THE 

HEART  AND  AORTA 


PART   I.    ■ 

GENERAL  CONSIDERATIONS  AND  METHODS  OF  DIAGNOSIS, 


PHYSIOLOGICAL  CONSIDERATIONS. 

PROPERTIES   OF   HEART  MUSCLE. 

The  heart  is  composed  of  striated  muscle-fibres  which  differ  anatomi- 
cally from  the  skeletal  muscles  in  being  almost  devoid  of  connective-tissue 
sheaths  and  from  most  of  the  skeletal  muscles1  in  the  fact  that  they  anas- 
tomose freely  with  one  another,  forming  a  continuous  mesh  work  of  muscle 


Fig.  5. — Heart  muscle-fibres,  X  375.     (After  Piersol.) 

tissue  (Figs.  5  and  6).  Physiologically  heart  muscle  differs  from  skeletal 
muscle,  for  (1)  it  is  continually  undergoing  rhythmic  contractions,  and  (2), 
as  Bowditch  has  shown,  every  contraction  is  maximal. 

Rhythmicity  in  Physico=chemical  Phenomena. — Reactions  which  proceed  rhythmi- 
cally are  not  purely  vital  phenomena,  but  are  well  known  to  physical  chemists.  One  of 
the  most  striking  is  shown  in  the  catalysis  of  hydrogen  peroxide  by  metallic  mercury, 
which  has  been  studied  recently  by  Bredig  and  Wilke.  When  hydrogen  peroxide  acts 
upon  mercury,  a  yellow  or  brownish  film  of  an  oxide  of  mercury  forms  upon  the  surface 

1  The  tongue  of  the  frog  and  some  other  forms  of  muscle  somewhat  resemble  heart 
muscle  in  structure. 

1 


2  DISEASES  OF  THE  HEART  AND  AORTA. 

of  the  latter.  This  film  remains  for  a  moment,  after  which  it  goes  into  solution,  leaving 
the  surface  of  the  mercury  bright;  and  the  reaction  is  repeated.  As  Kastle  and  Loevenhart 
have  shown,  the  splitting  of  hydrogen  peroxide  is  inhibited  whenever  an  insoluble  film  is 
formed  over  the  surface  of  the  catalyzer;  so  that  the  splitting  of  the  hydrogen  peroxide 
is  not  a  continuous  but  an  interrupted  process.  Bredig  and  Wilke  recorded 
the  liberation  of  oxygen  bubbles  by  means  of  a  tambour, 
and  found  that  such  tracings  closely  resembled  tracings 
from  the  heart.  They  were  rhythmic;  the  rate  could  be  much  accelerated  by  the 
passage  of  an  electric  current ;  and  under  certain  circumstances  even  irregularities 
resembling   extr asy stolic   arrhythmias   could  be  produced. 

A  great  deal  of  perspicuity  has  been  added,  especially  to  the  clinical 
study  of  the  cardiac  function,  by  discriminating  between  influences  which 


Endothelium 


Subendothelial 
stratum 


Layer  rich  in 
elastica 


Deepest  layer 


Heart  muscle 

Blood-vessel  :     :^\5&£3 

Fig.  6. — Section  through  the  endocardium  showing  cross-section  of  the  muscle-fibres.     (After  Piersol.) 

affect  the  cardinal  properties  of  the  cardiac  muscle  (Engelmann).  One 
recognizes  those  which  affect  (1)  rhythmicity  (chronotropic 
influences);  (2)  irritability  (bathmotropic);  (3)  con- 


Fig.  7. — Curve  showing  the  catalysis  of  hydrogen  peroxide  by  mercury  under  the  influence  of  galvanic 
currents  of  increasing  strengths.      (After  Bredig  and  Wilke,  Biochem.  Ztschr.,  1908,  xi,  67.) 

ductivity    (dromotropic);    (4)    contractility   (inotro- 
pic),  as   well   as    (5)    tonicity   (Mackenzie). 

Influences  improving  these  properties  are  designated  as  positive,  those 
which  depress  them  as  negative. 


ORIGIN   OF   THE   HEART-BEAT. 

Role  of  the  Salts. — Merunowicz,  under  Ludwig's  direction,  demon- 
strated that  the  rhythmicity  of  the  heart  depended  not  only  upon  its  intrin- 
sic characteristics  but  particularly  upon  the  action  of  the  inorganic  salts 
present  in  the  blood-serum.  Ringer  (1882),  and  later  Howell,  showed  that 
the  antagonistic  actions  of  potassium  and  calcium  salts  were  the  factors 


PHYSIOLOGICAL  CONSIDERATIONS.  3 

chiefly  concerned  in  determining  the  rhythm  of  the  heart,  while  Loeb  and  his 
pupil,  Lingle,  showed  that  without  the  sodium  salts  it  would  not  beat  at  all. 
Accordingly,  as  Loeb  and  Howell  agree,  the  heart-beat  can  be  maintained 
only  when  these  three  salts  or  their  ions  are  present  in  certain  definite  pro- 
portions, or  in  what  Loeb  has  termed  "a  balanced  solution." 
However,  while  Ringer  and  Howell  believe  that  the  cal- 
cium liberates  the  motive  power  of  the  cardiac 
contraction,  Loeb  and  his  pupils  believe  that  this 
is  done  by  the  sodium  and  that  the  calcium  and  potassium  merely 
keep  the  sodium  from  liberating  too  much. 

Their  mode  of  action  has  been  explained  by  Loeb  in  1899  in  the  follow- 
ing words : 

"The  salt  or  electrolytes  in  general  do  not  exist  in  living  tissues  as  such  exclusively, 
but  are  partly  in  combination  with  proteids  (or  fatty  acids).  The  salt  or  electrolytes  do 
not  enter  into  this  combination  as  a  whole,  but  through  their  ions.  The  great  importance 
of  these  ion-proteid  combinations  (or  soaps)  lies  in  the  fact  that  by  substitution  of  one  ion 
for  another,  the  physical  properties  of  the  proteid  change  (e.g.,  their  surface  tension,  their 
power  to  absorb  water  or  their  viscosity  or  state  of  matter).  We  thus  possess  in  these 
ion-proteid  or  soap  compounds  essential  constituents  of  living  matter,  which  can  be  modi- 
fied at  desire,  and  hence  enable  us  to  vary  and  control  the  life  phenomena  themselves. 

''Life  phenomena,  and  especially  irritability,  depend 
upon  the  presence  in  the  tissues  of  a  number  of  the  various 
metal  proteids,  or  soaps  (Na,  Ca,  K,  and  Mg)  in  definite 
proportions.  .  .  .  Solutions  of  Na-salts  produce  rhythmical  contractions  only 
if  the  muscle  cells  contain  Ca-ions  in  sufficient  numbers.  As  soon  as  there  is  a  lack  of  Ca- 
ions  in  the  tissue  the  Na-ions  are  no  longer  able  to  cause  rhythmical  contractions.  On 
the  other  hand,  if  we  add  Ca-salts  in  sufficient  quantity  to  the  NaCl  solution,  it  will  no 
longer  cause  rhythmical  contractions  in  the  fresh  muscle  of  the  frog.  .  .  .  It  is  hardly 
necessary  to  mention  that  this  suggested  the  possibility  that  muscular  contraction  in  gen- 
eral is  due  to  a  substitution  of  Na  for  Ca,  or  vice  versa,  in  certain  compounds  (proteins  or 
soaps)  in  the  muscle." 

The  hypothesis  that  the  main  physiological  antagonism  lies  between 
K  and  Ca  is  stated  by  Howell  in  the  following  words: 

"The  well-nourished  heart  contains  a  large  supply  of  energy-yielding  material  which 
is  in  a  stable  form,  so  that  it  neither  dissociates  spontaneously  nor  can  be  made  to  do  so 
by  the  action  of  external  stimuli.  It  is  possible  that  this  stable,  non-dissociable  form  con- 
sists of  a  combination  between  it  and  the  potassium  or  the  potassium  salts,  and  that  therein 
lies  the  functional  importance  of  the  potassium  contained  in  the  tissue.  This  compound 
reacts  with  the  calcium  or  with  the  calcium  and  sodium  salts  and  a  portion  of  the  potas- 
sium is  replaced;  and  a  compound  is  formed  which  is  unstable.  At  the  end  of  the  diastolic 
period  this  compound  reaches  a  condition  of  instability  such  that  it  dissociates  spontane- 
ously, giving  rise  to  the  chain  of  events  that  culminates  in  the  normal  systole.  Before 
spontaneous  dissociation  occurs  it  may  be  hastened  by  an  external  stimulus,  as  we  know 
is  the  case  when  a  mechanical  or  electrical  shock  is  applied  to  the  heart  at  any  time  after 
diastole  begins." 

Erlandsen  has  found  in  heart  muscle  a  lipoid  substance  (cuorin)  which  is 
allied  to  lecithin  but  contains  two  phosphate  group  radicals  (diphosphatid) 
instead  of  one.  Cuorin  is  not  present  in  any  other  tissue  nor  in  skeletal 
muscle.  It  is  capable  of  forming  compounds  with  Na,  K,  Ca,  and  other 
metals,  which  differ  greatly  in  their  physical  and  chemical  properties  and 
especially  in  their  solubilities.  It  is  possible  that  this  substance  may  play 
an  intermediary  role  in  the  process  assumed  by  Howell. 


DISEASES  OF  THE  HEART  AND  AORTA. 


In  this  connection  it  is  interesting  to  note  that  Harden  and  Young  have 
found  that  the  phosphate  radical  plays  a  very  essential  role  in  the  process  of 
yeast  fermentation  of  glucose.  It  is  quite  possible  also  that  in  the  glycolysis 
which  accompanies  the  liberation  of  energy  in  the  cardiac  contraction  this 
radical  may  play  a  similar  role. 

Any  single  ion  or  salt  is  poisonous  by  itself,  but  in  the  presence  of  cer- 
tain others  may  be  beneficial.  This  very  interesting  question  of  "balanced 
ion  solutions"  has  been  extensively  investigated  by  Loeb  and  his 
pupils,  not  only  upon  heart  but  upon  skeletal  muscle  and  upon  lower  medusae, 
molluscs,  and  fishes. 

G.  R.  Mines  (Jour.  Physiol.,  1913,  xlvi,  p.  xxiii)  has  shown  that  by  de- 
creasing alkalinity  the  conduction  time  can  be  prolonged  and  the  duration  of 

systole  shortened,  and  increasing 
the  alkalinity  produces  the  opposite 
effect.  Moreover,  Dorothy  Dale  has 
shown  that  increasing  the  alkalinity 
may  cause  the  ventricle  to  beat  be- 
fore the  auricle. 

Even  the  mammalian  heart  can 
be  readily  revived  and  kept  beating 
outside  the  body  if  perfused  with  a 
solution  containing  these  substances 
together  with  sodium  bicarbonate 
(Howell)  and  saturated  with  oxygen 
(Locke's  solution — NaCl,  0.9  per 
cent. , + CaCl2, 0.024  percent. ,  +  KC1, 
0. 042  +  NaHC03, 0.01  to  0. 03 , + dextrose  ,0.1  per  cent.) .  It  is  necessary  to  main- 
tain the  blood-pressure  at  50-100  mm.  Hg,  and  the  temperature  36°  to  37°. 
Kuliabko  and  others  have  revived  excised  human  hearts  many  hours  after  death. 
The  study  of  the  excised  heart  has  been  very  useful  both  in  testing  the 
effect  of  drugs  and  in  simulating  conditions  of  disease;  but  the  conditions  of 
circulation  are  not  exactly  comparable  to  those  within  the  animal,  and  the 
results  should  always  be  carefully  checked  upon  the  intact  animal  before 
assuming  them  to  be  normal  or  drawing  any  conclusions  as  to  pharmaco- 
logical action. 

Myogenic  and  Neurogenic  Theories. — Whether  the  salts  or  ions  which 
maintain  the  rhythmicity  of  the  heart-beat  do  so  by  acting  directly  upon 
the  muscle  tissue  (myogenic),  or  whether  the  stimuli  are  first  generated 
in  nerve  tissue  (neurogenic)  and  then  transmitted  to  the  muscle,  is  a 
question  which  has  been  disputed  for  centuries.  And  though  the  pendulum 
has  repeatedly  swung  from  one  opinion  to  the  other,  this  question  cannot 
at  present  be  answered.  It  is  quite  certain  that  all  the  extrinsic  cardiac 
nerves  can  be  removed  without  stopping  the  rhythmic  contractions,  and 
that  the  ganglion  cells  may  be  stimulated  without  materially  affecting  the 
rhythm  (Gaskell).  But  the  meshwork  of  muscle-fibres  in  the  heart  is  so 
permeated  by  a  meshwork  of  fine  nerve-fibres  that  it  has  been  impossible 
to  determine  whether  the  impulse  arises  in  the  muscle-cells  or  in  the  nerve 
endings  upon  their  surfaces.  Wm.  His,  Jr.,  has  indeed  shown  that  the  heart 
of  the  chick  embryo  beats  before  nerve-fibres  have  entered  it  at  all,  but  the 


Fig.  8. — Apparatus  for  perfusing  the  mamma- 
lian heart.  A,  auricle;  V,  ventricle;  TAMB., 
tambour;  TH.,  thermometer;  MAN.,  manometer; 
GASCH,  gas  check;    O2,  tank  of  oxygen. 


PHYSIOLOGICAL  CONSIDERATIONS.  5 

possibility  still  remains  that  after  once  entering  the  heart  the  nerves  may- 
take  the  initiation  of  contraction  away  from  the  adult  heart-muscle.  More- 
over, the  recent  experiments  of  Carlson  and  of  Magnus  in  allied  fields  give 
considerable  evidence  that  such  may  be  the  case;  so  that,  in  spite  of  its  im- 
portance for  both  the  physiology  and  the  pathology  of  the  heart,  neither  the 
myogenic  nor  the  neurogenic  theory  of  the  heart-beat  has  been  finally  proved. 
Maximal  Contractions  and  Irritability. — As  Bowditch  has  shown — the 
heart  liberates  all  its  available  energy  at  each  contraction,  which  resembles 
in  this  way  the  explosion  of  gunpowder  or  the  liberation  of  a  spring  by  a 
trigger.1  Like  the  power  of  the  spring,  the  strength  of  the  cardiac  contrac- 
tion depends  upon  the  energy  stored  up.  This  energy  seems  to  depend  upon 
the  regeneration  of  the  contractile  substance  mentioned  above  by  Howell. 
When  the  next  contraction,  normal  or  abnormal  (extrasystole),  occurs 
soon  after  the  last  (early  in  diastole),  the  contraction  is  weaker  than  the 
preceding,  since  it  liberates  less  energy,  but  the  contractile  substance  is  again 
completely  destroyed  and  requires  another  pause  (compensatory 
pause,  see  page  109)  to  regenerate  it.  When  it  occurs  late,  the  contrac- 
tion is  of  almost  or  quite  original  strength,  and  the  stored-up  energy  is  again 
liberated  completely.  Moreover,  Erlanger  has  shown  that  the  irritability  of 
the  heart  increases  progressively  as  diastole  is  prolonged  and  as  the  muscle 
becomes  overloaded  with  the  energy-producing  substance. 

ORIGIN   AND    COURSE    OF   THE    CARDIAC    IMPULSE. 

The  Sinus  as  "  Pace=maker  "  of  the  Heart. — In  the  frog,  where  the  car- 
diac impulse  travels  slowly,  it  is  very  easy  to  see  that  it  arises  at  the  sinus 
venosus,  which  executes  a  contraction.  This  is  followed  by  contraction  of 
the  auricle,  the  latter  after  an  appreciable  interval  by  a  visible  contraction 
of  the  small  ring  of  muscle  about  the  auriculoventricular  ring  (Bond),  and 
this  in  turn  by  contraction  of  the  ventricles. 

It  is  probable  that  the  sinus  initiates  the  cardiac  rhythm,  because  it  is 
the  chamber  which,  when  isolated,  beats  at  the  fastest  rhythm  in  the  blood- 
serum,  and  herce  it  becomes  what  Erlanger  terms  "the  pace-maker  of  the 
heart."  2  Indeed,  if  the  impulse  from  the  sinus  is  blocked  by  crushing  or  by 
cooling  the  sino-auricular  border,  the  impulses  no  longer  reach  the  auricles, 
which  must  then  contract  by  their  own  slower  rhythm  or  not  beat  at  all 
(sino-auricular  heart-block). 

Anatomy  of  the  Sinus  Region  in  Mammals. — In  the  mammalian  embryo 
the  sinus  venosus  or  sinus  reuniens  exists  as  a  separate  chamber  bounded  by 
the  mouths  of  the  vense  cavse,  the  interauricular  septum,  and  the  Eustachian 
valve,  which  at  this  stage  of  development  is  relatively  large  and  almost  com- 
pletely partitions  it  from  the  cavity  of  the  auricle.  As  the  heart  grows,  how- 
ever, the  region  about  the  Eustachian  valves  grows  very  little,  and  the  sinus 
reuniens  becomes  incorporated  in  the  cavity  of  the  right  auricle,  so  that  in 
the  adult  it  is  represented  by  only  a  few  bundles  of  smooth  muscle-fibres 
lying  indefinitely  between  the  vense  cavse  and  the  auricle  proper.     In  1906 

1  Burridge  (Jour.  Physiol.,  1914,  xlvii,  p.  xxxi)  has  shown  recently  that  frog's  ventricle 
poisoned  with  calcium  salts,  chloral  hydrate,  or  alcohol  may  carry  on  submaximal  stimuli 
and  may  be  tetanized  like  skeletal  muscle. 

2  Under  pathological  conditions,  and  expecially  in  the  excised  heart,  the  ventricle  may 
become  more  irritable  and  may  become  the  pace-maker  (reversed  rhythm). 


6 


DISEASES  OF  THE  HEART  AND  AORTA. 


Wenckebach  described  one  of  these  bands  which  crossed  the  veno-auricular 
junction  from  the  superior  vena  cava  to  the  upper  surface  of  the  right  auricle 
and  penetrated  downward  toward  the  coronary  sinus.  This  was  soon  con- 
firmed by  Keith  and  Flack,  who  stated: 

"Our  search  for  a  well-differentiated  system  of  fibres  within  the  sinus,  which  might 
serve  as  a  basis  for  the  inception  of  the  cardiac  rhythm,  has  led  U3  to  attach  import- 
ance to  this  peculiar  musculature  surrounding  the  artery  at  the  sino-auricular  junction. 
In  the  human  heart  the  fibres  are  striated,  fusiform,  with  well-marked  elongated  nuclei, 
plexiform  in  arrangement,  and  embedded  in  densely  packed  connective  tissue — in  fact, 
of  closely  similar  structure  to  the  Knoten.  The  amount  of  this  musculature  varies, 
depending  upon  how  much  of  the  sinus  has  remained  of  the  primitive  type;  but  in  the 
neighborhood  of  the  taenia  terminahs  there  is  always  some  of  this  primitive  tissue  found. 
Macroscopically  the  fibres  resemble  those  of  the  a.-v.  bundle  in  being  paler  than  the  sur- 


Systemic  aorta 
Pulmonary  aorta  or  artery 


Right  auricular  appendage 

■Right  ventricle,  conus 
arteriosus 


Sup.  pulm 
vein 


Inf.  pulm. 
vein 

Fossaovalis 
surrounded 
by  annulus 
Inferior 
vena  cava 


Orifice  of  coronary  sinus,  guarded  by  Thebesian  valve 
Eustachian  valve  Depression  receiving  Thebesian  veins 

Fig.  9. — The  auricular  end  of  the  human  heart  viewed  from  the  right.     (After  Piersol.) 


rounding  musculature, — i.e.,  in  being  of  the  white  variety.  They  can  be  dissected  out 
on  the  superior  vena  cava  in  the  region  corresponding  to  the  right  venous  valve  and  at 
the  coronary  sinus  in  the  interval  between  it  and  the  inferior  vena  cava  and  left  auricle. 
Another  remarkable  point  in  connection  with  these  fibres  is  the  special  arterial  supply 
with  which  they  are  provided.  These  arterial  branches,  as  noticed  by  Wenckebach,  em- 
brace the  sino-auricular  junction.  It  will  be  seen  that  they  come  from  both  right  and  left 
coronary  arteries  and  form  what  may  be  termed  the  'sino-auricular  arterial  circle.'  We 
might  mention  also  that,  in  some  of  the  pathological  hearts  cut  by  us,  sections  of  this 
region  appeared  to  show  a  definite  increase  in  the  amount  of  fibrous  tissue  present — a  fact 
of  considerable  importance,  since  we  have  found  that  the  fibrous  tissue  of  the  Knoten  and 
a.-v.  bundle  is  sometimes  increased  in  pathological  hearts." 

These  observations  have  been  confirmed  by  Schonberg,  W.  Koch,  de 
Witt,  Cohn,  Lewis  and  Oppenheimer,  and  a  host  of  others. 


PHYSIOLOGICAL  CONSIDERATIONS.  7 

The  Veno=auricular  Junction. — Schonberg  studied  the  veno-auricular  junction  in  a 
large  number  of  normal  and  abnormal  human  hearts  by  means  of  serial  sections,  each  series 
being  composed  of  300  to  800  sections.  At  a  level  10  to  15  mm.  above  the  entrance  of  the 
superior  vena  cava  into  the  auricle  (atrium)  he  found  the  usual  structure  of  vein  wall. 
Below  this  level  the  media  is  found  to  contain  groups  of  striated  muscle-fibres  separated 
from  one  another  by  fat  and  connective  tissue.  These  striated  muscle-fibres  arise  in  the 
vicinity  of  non-striated  fibres  but  are  never  continuous  with  them.  Bundles  of  these  fibres 
3/£  to  1  mm.  in  diameter  run  transversely  across  the  vein  toward  the  auricle,  gradually 
converging  into  larger  bundles,  which  are  separated  from  one  another  by  a  tissue  rich  in 
lymph-  and  blood-vessels.  In  the  angle  (sulcus)  formed  between  the  auricle  (atrium)  and 
vena  cava  these  bands  of  striated  muscle  become  much  thinner  and  contain  numerous 
tortuous  fibres  resembling  Purkinje  fibres.  In  this  region  there  is  a  considerable  deposit 
of  fat,  lymphoid  and  connective  tissue,  forming  a  more  or  less  definite  border-line.  The 
muscle-fibres  of  the  auricle  (atrium)  are  inserted  in  the  connective  tissue  here.  The 
connection  between  the  musculature  of  the  vena  cava  and 
that  of  the  auricle  is  made  by  the  numerous  small  bundles 
of  striated  muscle-fibres  lying 
just  beneath  the  endocardium,  which  pass 
across  this  junction  and  end  in  the  fibres  of 
auricular  muscle.      "In    the    macro- 


AURICULOVENTRICULAR 
BUNDLE.    (HIS) 

LEFT  BRATICH 

RIGHT  BRANCH 


RIGHT  BRANCH 


Fig.  10. — The  sinus  region  of  the  heart  and  the  auriculoventricular  bundle.  (Schematic,  constructed 
from  the  findings  of  Keith  and  Flack,  Tawara  and  later  investigators.)  A,  seen  from  the  right.  The 
broken  line  marks  off  the  area  corresponding  to  the  region  of  the  embryonic  sinus.  B,  the  same  region 
seen  from  the  front.     CS,  mouth  of  coronary  sinus. 


scopic  preparations  it  is  almost  always  readily  seen  that 
the  sulcus  is  bridged  at  its  posterior  lateral  third  by  a 
muscle-bundle  which  ascends  upwards  and  backwards  from 
the  auricle  (atrium)  to  the  superior  vena  cava,  where  it  is 
strengthened  by  fibres  from  the  circular  musculature  of 
the  lower  part  of  the  vein.  This  bundle  is  also  well  seen  microscopically, 
but  numerous  other  smaller  muscle  bundles  are  seen  as  well.  It  corresponds  quite  well  with 
that  described  by  Keith  and  Flack,  and  Wenckebach. 

Schonberg  found  that  the  region  of  the  sulcus  is  particularly  rich  in  nerve-fibres, 
ganglion-cells,  blood-vessels,  and  lymphoid  tissue,  and  is  therefore  particularly  liable  to 
pathological  infiltrations  and  cicatrizations. 

It  is  worthy  of  note  that  the  sulcus  noted  by  Schonberg  does  not  repre- 
sent the  sino-auricular  junction  but  the  veno-sinal  junction.  The  strands 
of  striated  muscle  which  he  describes  are  derived  from  the  sinus.  The  sino- 
auricular  (sino-atrial)  junction,  on  the  other  hand,  is  actually  situated  within 
the  body  of  the  auricle  (atrium). 

Role  of  the  Sinus  in  Mammals. — There  is  a  considerable  amount  of 
physiological  as  well  as  anatomical  evidence  that  in  the  adult  mammal  as 
well  as  in  the  amphibian  this  is  the  region  in  which  the  cardiac  impulse  arises. 


8  DISEASES  OF  THE  HEART  AND  AORTA. 

Knoll  and  also  Fredericq  have  shown  by  graphic  records  that  the  right  auricle 
begins  to  contract  .01  to  .03  second  before  the  left  auricle, 
and  the  latter  as  well  as  Langendorff  and  Lohmann  demonstrated  upon  the  excised  heart 
that  the  left  auricle  ceases  to  contract  when  the  right  auricle  is  cut  away  from  the  septum. 
Erlanger  and  Blackman  were  able  to  constrict  off  the  region  of  the  vense  cavse  by  a  suitable 
clamp,  and  also  by  torsion  of  this  part  of  the  auricle,  and  obtained  a  slight  degree  of  block 
(2:1)  between  the  sinus  and  the  atrial  portions  of  this  chamber  by  this  means;  but  neither 
Hirschfelder  and  Eyster  nor  Erlanger  and  Blackman  were  able  to  produce  such  a  sino- 
auricular  block  in  the  heart  in  situ.  Erlanger  has  shown,  however,  that 
the  tissue  in  this  region  responds  more  readily  to  induc- 
tion ducts  than  the  rest  of  the  auricle,  showing  a  higher 
irritability. 

Quite  recently  Wybauw  has  shown,  by  means  of  the  electrocardiogram,  that  the 
region  of  Keith  and  Flack's  node  becomes  negative  before  any  other  part  of  the  auricle; 
and  this  observation  has  been  confirmed  by  Lewis.  Lewis  and,  later,  Wybauw 
have  shown  also  that  when  artificial  stimuli  are  applied 
to  any  other  part  of  the  auricle  the  resultant  electrocardio- 
gram is  atypical,  but  when  it  is  applied  to  the  node  of  Keith 
and    Flack    the    electrocardiogram    is    normal. 

A.  E.  Cohn  and  Kessel  have  found  that,  although  multiple  incisions  elsewhere  in  the 
auricle  did  not  affect  the  rate,  when  the  node-bearing  area  was  entirely  cut  away  the  heart 
stopped  entirely  in  ten  out  of  sixteen  experiments,  and  in  two  other  experiments  the  rate 
fell  30  to  50  per  cent.  The  stoppage  after  the  excision  lasted  from  7  to  92  seconds,  after 
which  the  rate  gradually  quickened  but  always  remained  slower  than  before  the  cut. 

Eyster  and  Meek  (Heart,  1913-1914,  v,  119)  attempted  to  study  the  same  question 
from  a  different  angle,  by  determining  directly  the  point  at  which  the  electrical  wave  of 
negative  variation  first  makes  its  appearance.  The  point  at  which  this  occurs  would  of 
course  first  be  negative  to  any  other  point  on  the  surface  of  the  heart  or  blood-vessels,  so 
that  when  they  placed  one  electrode  over  the  sino-auricular  node  and  one  over  the  auricle 
it  was  easy  to  determine  the  point  at  which  the  impulse  arose  and  to  map  out  the  electrical 
sequence  over  the  whole  surface  of  the  heart.  They  found  that  in  the  dog  the  sino-auricular 
node  was  the  first  one  to  become  negative,  then  the  superior  vena  cava,  then  the  coronary 
sinus  and  right  auricle,  indicating  that  the  cardiac  impulse  travelled  in  this  order. 

Course  of  the  Impulse  after  Leaving  the  Sinus. — From  the  sinus  region 
the  cardiac  impulse  travels  to  the  walls  of  the  auricles  and  gives  rise  to  the 
auricular  contraction.  It  is  also  propagated  downward  toward  the  ventricles, 
which  it  reaches  about  one-fifth  of  a  second  later. 

The  discovery  of  nerve-fibres  (Tawara)  and  ganglion-cells  (Wilson)  in  this  bundle 
has  raised  the  question  as  to  whether  the  conduction  occurs  through  nerve  or  muscle  tissue. 
The  preponderance  of  evidence  seems  to  be  in  favor  of  the  latter.  In  the  frog  Bond  has 
been  able  to  see  that  the  muscle-fibres  of  the  auriculoventricular  ring  actually  contract 
whenever  an  impulse  passes  from  the  auricles  to  the  ventricles.  V.  Tabora  has  found 
that  the  vagi  do  not  act  upon  the  ventricles  in  mammals  after  the  conduction  has  been 
completely  cut  off  by  means  of  an  Erlanger  clamp  or  by  poisoning  with  digitalis.  This 
observation  is  in  opposition  to  the  work  of  Garrey  upon  the  terrapin's  heart,  using  a 
similar  method.     He  found  the  vagi  active  after  clamping. 

Kent,  His,  Retzer,  Braeunig,  Keith,  and  Tawara  have  shown  that  the 
cardiac  impulse  is  propagated  from  auricles  to  ventricles  through  the  system 
of  Purkinje  fibres,  which  forms  a  A  whose  shaft  arises  in  the  right  auricle 
at  or  near  the  sinus,  runs  in  the  membranous  septum  (auriculoventricular 
bundle)  downward  to  the  muscle  septum,  where  it  divides  into  two  branches 
which  straddle  the  muscular  septum  and  then  pass  to  the  right  and  left  ven- 
tricles. Within  these  chambers  the  branches  divide  into  numerous  ramifi- 
cations which  lie  just  beneath  the  endocardium  and  pass  downward  as  a 


PHYSIOLOGICAL  CONSIDERATIONS.  9 

meshwork  of  light-colored  translucent  strands  to  the  papillary  muscles  and 
walls  of  the  ventricles.  Occasionally  instead  of  following  the  walls  they  cross 
the  ventricular  cavity  to  the  papillary  muscle  as  isolated  strands  (mode- 
rator  bands,   T.  W.  King,  Tawara) . 


COORDINATION    OF   THE    CARDIAC    CHAMBERS. 

Under  all  circumstances  the  contractions  of  both  auricles  and  of  both 
ventricles  are  almost  synchronous,  or  under  vagus  stimulation  or  injury  to 
the  conduction  system,  the  chambers  of  the  right  heart  contract  one  or  two 
hundredths  of  a  second  before  those  of  the  left.  Even  under  these  circum- 
stances the  contractions  are  exactly  similar  in  the  two  parts  of  the  heart  and 
there  is  no  real  dissociation.  Biggs  and  Barker,  Hirschfelder  and  Bond  cut 
the  left  branch  of  the  conduction  system  (His  bundle),  and  found  that  the 
two  ventricles  continued  to  contract  coordinately  and  that  extrasystoles 
produced  in  the  one  were  communicated  at  once  to  the  other.  These  obser- 
vations have  been  confirmed  by  Trendelenburg  and  Cohn  and  by  Rothberger 
and  Eppinger,  who  showed  that  the  same  thing  was  true  for  the  right  branch 
of  the  bundle.  Rothberger  and  Eppinger  have  shown  that,  although  the 
mechanical  factors  of  the  contraction  are  not  altered,  great  changes  occur  in 
the  electrocardiogram. 

Arrangement  of  Muscle=fibres  in  the  Ventricle. — This  is  not  surpris- 
ing, on  account  of  the  peculiar  arrangement  of  the  muscle-fibres  within  the 
ventricle.  It  must  be  borne  in  mind  that 
the  heart  is  developed  from  the  original 
cardiac  tube,  a  vessel  provided  like  other 
vessels  with  a  loDgitudinal  and  a  circular 
muscle  coat.  In  the  process  of  develop- 
ment this  tube  at  first  is  twisted  into  a 
U  shape,  and  the  development  of  the  in- 
terventricular septum  transforms  the  U 
arrangement  into  more  or  less  of  a  W, 
the  arms  of  which  are  twisted  as  one 
might  twist  a  rope  or  wring  out  a  wet 
towel  (Borelli,  Mall).  The  final  course 
of  the  muscle-fibres  is  rather  complex, 
and,  as  stated  by  Mall,  it  "  must  be  due 
to  functional  adaptation  from  the  time 
the  heart  begins  to  beat." 

Borelli  and  the  other  workers  who 
followed  him,  notably  Haller,  Wolff, 
Gerdy  and  Ernst  Heinrich  Weber,  rec- 
ognized the  fact  that  the  walls  of  the 
heart  were  composed  of  bundles  of  fibres 
encircling    the    ventricles,    and    Borelli 

found  that  those  at  the  apex  penetrated  the  walls  to  spread  out  within  the 
cavity  of  the  ventricles.  Ludwig  and,  later,  Krehl  described  what  they  believed 
was  a  very  important  bundle  of  fibres  which  surrounded  the  cavity  of  the 
left  ventricle  like  a  ring.    They  supposed  that  these  fibres  were  the  principal 


Fig.  11. — Diagram  showing  the  arrange- 
ment of  the  strands  of  muscle-fibres  in  the 
ventr'cle  (modified  from  Mall).  PULM,  pul- 
monary artery;  MIT,  mitral  valve;  TRIC, 
tricuspid  valve;  AVB,  auriculoventricular 
bundle;  LV,  left  ventricle;  RV,  right  ven- 
tricle. The  sinospiral  bands  are  shaded  dark, 
the  bulbospiral  bands  are  light. 


10  DISEASES  OF  THE  HEART  AND  AORTA. 

factors  concerned  in  squeezing  the  blood  out  of  the  cavity  of  the  left  ventricle, 
and  hence  designated  them  as  the  "driving  apparatus"  (Triebwerk).  J. 
B.  MacCallum,  under  Mall's  direction,  was  able  to  show,  however,  that  the 
heart  of  the  pig's  embryo  could  be  unrolled  like  a  scroll,  and  Knower  found 
that  the  same  was  true  of  the  hearts  of  man  and  all  other  adult  mammals. 
Mall  has  continued  these  studies,  and  has  found  that  the  musculature  of 
the  two  ventricles  is  composed  of  two  distinct  spirals,  one  running  from  the 
tricuspid  or  sinus  portion  of  the  heart  to  the  apex  of  the  right  ventricle  (sino- 
spiral),  and  the  other  from  the  aortic  and  mitral  orifice  to  the  apex  of  the 
left  ventricle  (bulbospiral) .  These  two  spirals  are  each  composed  of  a  deep 
and  a  superficial  layer  of  fibres,  which,  as  Ludwig  demonstrated,  run  at  right 
angles  to  one  another,  and  they  are  connected  with  one  another  by  the  twisted 
strands  which  run  from  the  papillary  muscles  of  one  ventricle  to  those  of 
the  other  (Fig.  11).  He  found  that  Krehl's  Triebwerk  belongs  to  this  sys- 
tem, and  that  it  encircles  the  left  ventricle  like  a  spiral  and  not  like  a  ring, 
and  it  does  not  have  a  separate  existence. 

The  system  of  auriculo ventricular  conduction  fibres  (Purkinje-Tawara 
system)  is  not  derived  from  the  muscular  cardiac  tube,  like  these  ventricular 
muscular  strands,  but  is  derived  from  the  fibres  which  lie  in  the  loose  meshes 
between  the  endocardial  tube  and  the  muscular  tube,  from  which  arise  also 
the  auriculoventricular  valves  and  the  papillary  muscles.  In  the  develop- 
ment of  the  interventricular  septum  these  fibres  are  caught  and  pushed  up 
by  the  latter.  They  therefore  unite  with  the  system  of  spiral  fibres  of  the 
ventricles  which  run  in  the  septum,  not  included  in  this  structure,  but  rather 
superposed  upon  it,  and  straddle  the  septum  like  a  man  on  horseback,  whose 
head  is  the  node  of  Tawara,  whose  body  the  His  bundle  in  the  membranous 
septum,  and  whose  legs,  the  shafts  of  the  bundle,  pass  down  within  the  spiral, 
to  enter  the  walls  and  papillary  muscles  like  the  feet  within  the  stirrups. 

EMPTYING   AND    FILLING    OF   THE   HEART,    AND   MOVEMENTS 
OF   THE    VALVES. 

The  Presphygmic  Period. — The  instant  before  the  beginning  of  ven- 
tricular systole  the  mitral  and  tricuspid  valves  are  open,  while  the  aortic 
and  pulmonic  valves  are  closed.  When  the  ventricular  contraction  begins, 
it  at  once  raises  the  pressure  within  the  ventricles  above  that  in  the  auricles, 
causing  the  mitral  and  tricuspid  valves  to  close  with  a  snap.  There  is  thus 
a  short  interval,  the  presphygmic  (.07-.09  sec),  at  the  very  beginning  of 
systole,  during  which  all  four  valves  are  closed  and  movement  of  blood  ceases 
in  all  four  chambers.  This  period  lasts  until  the  pressure  within  the  ventricles 
rises  above  the  arterial  pressures  (minimal  pressure),  after  which  the  blood 
is  driven  out  during  the  rest  of  systole. 

Marey  has  shown  on  mechanical  models  that  the  presphygmic  period  is 
prolonged  in  mitral  insufficiency  and  shortened  in  aortic  insufficiency;  and 
Robinson  and  Draper  have  found  it  lengthened  in  cases  of  cardiac  weak- 
ness. In  extreme  cases  it  may  last  .168  sec.  In  cases  of  arrhythmia  the 
presphygmic  periods  of  the  weaker  beats  may  be  very  much  prolonged,  and 
this  may  produce  an  effect  upon  the  tracing  which  simulates  prolonged  con- 
duction time. 


PHYSIOLOGICAL  CONSIDERATIONS. 


11 


CAGp, 


Fig.  12. — Apparatus  for  registering  the  volume  of 
the  ventricles.     CARDIOM.,  cardiometer. 


Method  of  Recording  the  Volume  Curve.  —  Yandell  Henderson  has  recorded  the 
emptying  and  filling  of  the  ventricles  by  means  of  a  specially  constructed  cardiac  plethys- 
mograph  or  cardiometer  like  that  of  Tigerstedt  and  Johannson.  Henderson's  cardiometer 
was  made  from  an  ordinary  rubber  ball,  out  of  which  a  large  window  was  cut  and  then 
closed  hermetically  by  cementing  on  a  curtain  of  rubber  dam.  In  the  centre  of  the  rubber 
dam  a  hole  was  cut  just  large  enough  for  it  to  fit  air-tight  in  the  auriculoventricular  groove. 
The  heart  was  then  pushed  in  through  the  hole  until  the  dam  slipped  into  the  groove. 
The  changes  of  pressure  within  the  air  space 
surrounding  the  heart  were  communicated 
to  a  recording  tambour  through  a  glass  tube 
cemented  in  the  opposite  surface  of  the 
ball  (Fig.  12).  Dr.  Cameron  and  the  writer 
have  found  it  most  convenient  to  have  the 
recording  tambour  inverted,  so  that  up- 
strokes record  systole  and  down- 
strokes  diastole,  while  a  general 
rise  in  the  curve  indicates 
diminution  in  volume,  and  a 
general  fall  indicates  dilatation  . 

W.  G.  MacCallum  has  controlled  this  method  by  recording  the  amount  of  blood 
flowing  out  of  a  tube  whose  proximal  end  is  inserted  into  the  aorta  and  whose  distal  end  is 
elevated  to  a  level  corresponding  to  the  diastolic  pressure.  The  results  obtained  by  this 
method  indicate  that  the  results  obtained  with  the  cardiometer  have  an  error  of  not  more 
than  ten  per  cent.,  an  accuracy  sufficient  for  all  experimental  purposes. 

Outflow  during  Systole. — By  this  means  Henderson  has  found  that 
during  systole  the  ventricles  do  not  empty  themselves  with  a  rush  at  the 
beginning  of  systole,  but  that  the  outflow  continues  quite  uniform  through- 
out at  least  nine-tenths  of  the  latter  period  (outlasting  the  rise  of  the  arterial 
pulse-wave)  and  begins  to  slow  only  toward  the  very  end  (slight  rounding 
of  the  crest  of  the  curve).  At  the  cessation  of  outflow  there  is  an  instant 
during  which  the  ventricular  pressure  is  falling,  in  which  no  inflow  takes 
place,  but  this  is  only  one  or  two  hundredths  of  a  second  and  is  difficult  to 
estimate  accurately.  This  instant  corresponds  to  the  dicrotic  notch  upon 
the  aortic  pulse-wave. 

Filling  of  the  Ventricles. — The  ventricles  then  begin  to  fill  at  a  rapid  and 
uniform  rate  until  they  are  almost  completely  distended.  If  the  pulse-rate  is 
rapid,  the  next  systole  takes  place  before  the  filling  is  as  complete  as  possible, 
and  cutting  short  the  filling  diminishes  the  volume  of  the  heart ;  not  only  the 
total  volume,  but  the  amount  of  blood  discharged  at  each  systole  (Fig.  13). 

Diastole  and  Diastasis. — If,  on  the  other  hand,  the  heart  rate  is  slow 
(Fig.  13),  as  after  stimulation  of  the  vagus,  the  influx  begins  at  the  same 
rate  as  before  and  continues  uniformly  for  about  two-fifths  of  a  second  (steep 
ascent  of  the  curve)  until  the  ventricles  are  distended,  after  which  scarcely 
any  blood  flows  into  the  ventricles  no  matter  how  long  the  interval  to  the 
next  beat.  The  diastolic  period  is  thus  divided  into  two  parts:  (1)  the  phase 
of  diastole  proper  during  which  filling  of  the  ventricles  takes  place; 
(2)  the  phase  of  diastasis  in  which  little  or  no  filling  occurs.  The 
slower  the  heart  the  greater  is  the  diastolic  filling  and  the  longer  its  duration. 
The  greatest  amount  of  output,  in  unit  time  occurs  at 
a  rate  which  just  allows  the  phase  of  diastolic  filling 
to  be  complete  but  in  which  the  next  beat  occurs  before  diastasis  sets 
in.    Any  rate  above  or  below  this  brings  about  some  slowing  of  the  circulation. 


12 


DISEASES  OF  THE  HEART  AND  AORTA. 


AORTIC     PRESSURE 


Fig.  13. — Diagram  showing  the  events  of  a  single  cardiac  cycle.  The  upper  curve  indicates  the 
pulse  in  the  aorta.  The  black  rectangles  indicate  the  incidence  of  the  heart  sounds.  The  hearts,  shown 
semi-schematically  below  indicate  the  relative  volumes  at  different  phases  of  the  cardiac  cycle  correspond- 
ing to  the  normal  volume  curve  which  constitutes  the  lowest  curve  in  the  figure.  These  hearts  are  drawn 
by  referring  the  corresponding  points  upon  the  volume  curve  to  a  common  base-line,  and  taking  the 
ordinates  as  the  long  axis  of  the  heart.     The  changes  in  appearance  are  slightly  exaggerated. 

Downstrokes  represent  filling,  upstrokes  represent  emptying  of  the  ventricles.  The  sketch  at  the 
transition  from  diastole  to  diastasis  represents  the  probable  position  of  the  mitral  and  tricuspid  valves  at 
that  instant.  The  sketch  at  the  right  indicates  the  period  of  auricular  systole.  The  heavily  shaded  zone 
indicates  the  amount  of  residual  blood.     (Kindness  of  the  Interstate  Medical  Journal.) 


Position  of  the  Valves  and  Diastole. — Baumgarten  (1843)  has  been  able  to  demonstrate 
upon  the  excised  heart  that  the  cusps  of  the  mitral  and  tricuspid  valves  are  floated  together 
by  the  influx  of  blood  and  the  valves  close  spontaneously  when  the  inflow  ceases.  The 
writer  has  been  able  to  show  that  the  occurrence  of  diastasis  is  not  necessarily  caused  by 
the  valves  being  closed,  but  by  the  fact  that  the  heart  fills  for  a  time  before  the  walls  are 


PHYSIOLOGICAL  CONSIDERATIONS. 


13 


put  upon  a  stretch,  and  then  the  passive  elasticity  of  the  walls  prevents  further  filling. 
If  the  venous  pressure  is  materially  increased,  further  increase  in  volume  then  takes  place. 
The  closure  of  the  valves  in  early  diastole  depends  chiefly 
upon  the  suddenness  both  of  the  filling  and  of  its  cessation. 

A  very  pretty  and  instructive  demonstration  of  the  opening  and  closing  of  the  heart 
valves  has  been  devised  by  J.  Gad  by  an  experiment  shown  in  Fig.  14,  A,  which  can  be 
very  nicely  performed  upon  a  sheep's  heart  as  bought  at  a  butcher  shop. 

The  left  auricle  is  cut  away  and  the  bowl  of  a  large  thistle  tube  tied  in  the  place  by 
a  circular  ligature.  A  large  glass  tube  is  thrust  through  the  aorta  into  the  ventricle  and 
ligatured  in  place.  Both  the  thistle  tube  and  the  aortic  cannula  are  connected  with  fun- 
nels by  means  of  rubber  tubes,  and  the  chambers  of  the  heart  may  be  then  completely 
filled  with  water.  The  opening  and  closing  of  the  valves  may  be  brought  about  by  raising 
and  lowering  one  or  the  other  of  the  funnels,  and  may  be  watched  through  the  wall  of  the 
bulb.  Insufficiency  of  the  valve  may  be  produced  by  cutting  or  stretching  one  of  the  chordae 
tendineae,  but  after  the  experiment  has  been  repeated  a  few  times  upon  the  same  heart  a 


Fig.   14. — Methods    for   demonstrating  the  movements   of   the  heart  valves. 

Baumgarten's  method. 


A,   Gad's  method;    R, 


certain  amount  of  insufficiency  usually  sets  in  spontaneously.  The  sounds  produced  by 
the  valves  and  blood  stream  independently  of  the  contraction  can  be  well  studied  by  plac- 
ing the  stethoscope  upon  such  a  heart,  provided  all  the  air  has  been  removed  from  the 
cardiac  chambers.  A  very  interesting  experimental  study  of  the  forces  involved  in  this 
diastolic  closure  has  recently  been  made  by  Yandell  Henderson  and  F.  E.  Johnson  (Heart, 
1912-1913,  iv,  69).    The  article  is  illustrated  by  excellent  photographs  and  diagrams. 

Still  simpler  is  the  older  method  of  Baumgarten  (1843)  of  cutting  away  the  auricles 
to  expose  the  valves  and  then  pouring  in  water  from  a  beaker  (Fig.  14,  B). 


RELAXATION    OF   THE    HEART,    AND    TONICITY    OF    THE    CARDIAC    MUSCLE. 

It  has  been  supposed  by  some  writers  that  the  diastolic  dilatation  of 
the  heart  is  brought  about  by  some  active  muscular  contraction,  since  the 
pressure  within  both  ventricles  becomes  negative,  even  to  the  extent  of  -55 
mm.  Hg.  More  recent  studies,  however,  have  shown  that  this  negative 
pressure  is  probably  an  artefact,  and,  on  the  other  hand,  Newell,  Martin 
and  Donaldson  have  shown  that  the  heart  does  not  fill  unless  there  is  a  slight 
positive  pressure  in  the  veins.  The  rigidity  of  the  walls  of  the  heart  and  the 
pressure  in  the  coronary  arteries  do  not  hold  the  ventricle  distended,  for  A.  L. 


14  DISEASES  OF  THE  HEART  AND  AORTA. 

Prince  (Am.  Jour.  Physiol.,  1915,  xxxvii,  43)  has  shown  that  the  ventricles 
fill  as  rapidly  at  a  coronary  pressure  of  50  mm.  Hg  as  at  one  of  275  mm.1 
Therefore  the  heart  has  no  suction-pump  action. 

The  heart  muscle  is  quiescent  and  the  heart  walls  are  relaxed  during 
the  entire  period  of  diastole,  so  that  neither  the  most  delicate  recording 
levers  nor  the  most  sensitive  galvanometers  reveal  the  slightest  signs  of  con- 
traction. Nevertheless,  as  will  be  seen,  the  degree  of  this  diastolic  relaxa- 
tion of :  the  walls  varies  considerably  under  different  circumstances  depend- 
ent upon  the  tonicity  of  the  heart  muscle.  This  is  shown  by  variations  in 
the  length  of  strips  of  cardiac  muscle  under  a  constant  load,  as  well  as  by 
variations  in  the  cardiac  volume. 

Tonicity. — T  onicity  may  be  defined  as  the  resist- 
ance of  the  heart  muscle  tostretching  in  diastole; 
or,  less  accurately,  as  its  diastolic  rigidity. 

The  force  which  stretches  the  heart  walls  in  diastole  is  the  pressure  at 
which  the  blood  enters  the  heart  from  the  great  veins,  namely  the  venous 
pressure,  so  that  with  a  high  venous  pressure  (unless  antagonized  by  a  high 


Fig.  1 5. —Volume  curves  of  the  ventricles  at  increasing  pulse  rates.  The  shaded  zone  indicates  the 
amount  of  blood  within  the  heart  at  each  instant,  the  sketches  at  right  and  left  indicating  the  size  of  the 
heart  pictorially.  The  light  broken  line  indicates  the  volume  curve  as  it  would  appear  if  the  heart  rate 
were  slow.     (Kindness  of  the  Interstate  Medical  Journal.) 

tonicity)  they  will  be  stretched  considerably  (dilatation),  while  with  a  low 
venous  pressure  comparatively  little  blood  will  enter  and  the  heart  will  remain 
small.  In  all  cases  filling  will  continue  until  an  equilib- 
rium is  reached  between  the  venous  pressure  and 
the  cardiac  tonicity,  unless  the  heart  rate  is  so  rapid  that  the 
filling  is  interrupted  by  the  next  systole.  A  high  tonicity  will,  however, 
antagonize  a  high  venous  pressure  and  prevent  overfilling. 

Moreover,  Howell  and  Donaldson  have  shown  that  the  systolic  output 
of  the  heart  depends  to  a  great  extent  upon  the  amount  entering  the  latter 
from  the  great  veins,  and,  hence,  upon  the  venous  pressure.  If  the  venous 
pressure  falls  below  a  certain  level,  the  heart  fills  incompletely,  and  the  ven- 
tricles are  unable  to  pump  enough  blood  into  the  arteries  to  maintain  the 
blood-pressure  at  the  usual  level. 

The  rate  of  filling  of  the  heart  is  accelerated  (curve  of  filling  steeper) 
(Fig.  16)  when  either  the  venous  pressure  is  high  or  the  tonicity  is  low;  the 

xFor  a  detailed  account  of  the  various  theories  of  the  cardiac  relaxation,  with  full 
bibliography,  consult  E.  Ebstein,  Die  Diastole  des  Herzens,  Ergebnisse  der  Physiol., 
Wiesb.,  1904,  iii,  2  Abth. 


PHYSIOLOGICAL  CONSIDERATIONS. 


15 


filling  is  slowed  (curve  more  oblique)  when  either  the  tonicity  is  high  or  the 
venous  pressure  is  low.  So  that,  as  regards  filling  of  the  heart,  a  high  tonic- 
ity is  equivalent  to  a  low  venous  pressure,  and  conversely,  a  low  tonicity 
is  equivalent  to  a  high  venous  pressure  (Fig.  16). 

Influences  which  affect  tonicity  may  be  studied  objectively  in  isolated 
strips  of  cardiac  muscle  by  means  of  their  shortening  or  lengthening,  or  upon 
the  intact  heart  by  changes  in  the  volume  curve. 


venous  pressure: 


! 


VOLUME  OF 

VENTRICLES 


Fig.  16. — Diagram  showing  the  effect  of  varying  venous  pressures  upon  the  volume  of  the  heart, 
upon  the  rapidity  of  filling  of  the  ventricles  (volume  curve),  and  upon  the  position  assumed  by  the  mitral 
and  tricuspid  valves  at  the  end  of  the  first  inflow  into  the  ventricles.  The  figure  to  the  left  shows  the 
valves  remaining  open,  that  in  the  middle  shows  partial  closure  (functional  stenosis),  that  upon  the  right 
complete  diastolic  closure. 


The  total  volume  of  the  heart  at  any  given  instant  may  be  regarded  as 
follows : 

Volume  of  heart  =  volume  of  heart  walls  +  volume  of  blood  within  cardiac  chambers. 
Volume  of  walls  =--  volume  of  muscle  +  coronary  blood  +  lymph.      (The  two  latter 

factors  vary  somewhat,   though  relatively  slightly,  the  lymph 

increasing  considerably  in  cardiac  stasis.) 
Volume  of  blood  within  chambers  =  output  at  each  systole  +  blood  remaining  at  end 

of  systole  (residual  blood) . 

Residual  Blood. — The  residual    blood    undergoes    great 
variations.    In  dilated  hearts  it  may  attain  to  several  times  the  amount 


16 


DISEASES   OF  THE  HEART  AND  AORTA. 


of  the  systolic  output  (cf.  Fig.  17),  while  in  small  hearts  it  may  be  only  a 
fraction  of  the  latter. 

Henderson  and  Prince  (Am.  Jour.  Physiol.,  1914,  xxxv,  116)  have  shown  that  in  a 
normal  man  the  systolic  discharge  of  the  left  ventricle  is  about  100  to  150  cubic  centimetres. 

The  changes  in  tonicity  may  be  measured  by  the  volume  of  the  heart 
at  the  end  of  diastole,  i.e.,  when  the  filling  is  most  complete,  a  large  diastolic 
volume  representing  low  tonicity  (when  venous  pressure  and  pulse-rate  are 
constant),  a  small  volume  indicating  a  high  tonicity. 

Nature  of  Changes  in  Tonicity. — Porter  has  found  that  a  strip  of  heart 
muscle  can  be  made  to  remain  elongated  (diminished  tone),  or  can  then  be 
made  to  remain  shortened  when  not  receiving  any  stimuli  whatever  (in- 
creased tone).  Several  degrees  of  this  permanent  shortening  can  be  super- 
posed on  one  another  with  great  similarity  to  the  tetanus  of  skeletal  muscle 
("tetanus  of  tone,"  Porter).  Barcroft  and  Dixon  have  shown  that  the  muscle 


Fig.  17. — Diagram  showing  the  condition  of  the  heart  with  varying  degrees  of  tonicity  but  with 
systolic  output  (amount  of  blood  forced  out  per  beat)  normal.  The  volume  at  the  end  of  diastole  consti- 
tutes the  index  of  tonicity  which,  at  the  end  of  systole,  indicates  the  amount  of  residual  blood.  High 
venous  pressure  has  the  same  effect  as  low  tonicity.      (Kindness  of  the  Interstate  Medical  Journal.) 

when  in  tone  gives  off  more  CO2  than  when  at  rest,  further  supporting  this 
view  of  the  role  of  increase  and  decrease  in  tone. 

Factors  Producing  Changes  in  Tonus. — F.  B.  Hoffmann  has  demon- 
strated that  there  are  two  separate  sets  of  fibres  in  the  frog's  vagus.  One 
set  influences  the  heart-rate  only  (chronotropic  effect)  and  also  increases 
the  size  and  force  of  contraction  (augmentor  effect)  and  also  increases  the 
cardiac  tonus  but  does  not  affect  the  rate  at  all.  This  group  of  fibres  is 
found  only  in  the  interauricular  and  interventricular  septum  (septal  nerves) 
in  the  frog.  In  other  animals  the  two  groups  of  fibres  pass  side  by  side 
and  cannot  be  dissociated,  though  it  is  frequent  in  weak  stimulation  of  the 
vagus  to  find  one  effect  occurring  without  the  other. 

P.  D.  Cameron,  in  the  writer's  laboratory,  has  found  that  in  dogs  the 
intravenous  administration  of  digitalis,  strophanthus,  nitroglycerin,  and 
calcium  salts  increases  cardiac  tonicity.     The  effect  of  small  (therapeutic) 


PHYSIOLOGICAL  CONSIDERATIONS.  17 

doses  of  these  drugs  is  exerted  almost  entirely  upon  the  tonic  fibres  in  the 
vagus,  and  fails  to  appear  if  the  vagi  have  been  cut  or  paralyzed  with  atro- 
pine. Larger  doses,  however,  exert  similar  effects  by  direct  action  on  the 
heart  muscle.  Atropine  itself  illustrates  these  effects  by  causing  a  primary 
depression  of  tonus  as  the  vagi  become  paralyzed,  which  is  followed  by  an 
increase  in  tonicity  from  direct  action  on  the  heart  muscle.  Potassium  salts, 
asphyxia,  formic  acid,  adrenalin  depress  tonicity.  Aconite  in  therapeutic 
doses  affects  rate  more  than  tonus  in  the  dog. 

Since  the  exact  volume  of  the  heart  cannot  be  determined  clinically, 
the  area  of  the  cardiac  shadow  in  diastole  furnishes  the  best  index  of  the 
tonus,  especially  when  combined  with  study  of  the  venous  pressure.  Com- 
paratively little  investigation  has  been  carried  on  in  this  field.  Moritz  and 
Dietlen  have  shown  that  exercise  usually  increases  tonus  in  healthy  persons. 
The  study  of  tonus  has  also  proved  of  value  in  the  study  of  exercise  and  in 
the  controlling  of  hydrotherapy  and  drug  treatments,  as  well  as  in  the  study 
of  myocardial  insufficiency. 

ACTION  OF  THE  CARDIAC  NERVES. 

The  nerve  supply  of  the  heart  is  derived  from  two  sets  of  extracardiac 
nerves,  the  vagi  connecting  it  with  the  medulla  and  the  so-called  accelerator 
nerves  which  connect  it  with  the  sympathetic  system.  These  in  turn  divide 
into  branches  which  run  to  the  intrinsic  ganglia  of  the  heart  itself,  the  course 
of  these  nerves  and  their  relations  to  the  rest  of  the  central  nervous  system 
being  indicated  in  Fig.  18. 

Each  vagus  and  each  accelerator  is  distributed  chiefly  over  the  corre- 
sponding half  of  the  heart,  but  the  free  anastomosis  of  the  cardiac  plexuses 
permits  the  impulses  from  one  side  to  spread  more  or  less  freely  to  the  other, 
and  only  occasionally  does  a  preponderance  of  effect  upon  one  side  of  the 
heart  become  evident.     (See  page  18.) 

The  vagi  contain  two  sets  of  fibres,  the  afferent  or  sensory  fibres,  whose 
ganglion-cells  are  located  in  the  ganglia  and  which  carry  the  sensory  impulses 
from  the  heart;  and  the  motor  or  cardio-inhibitory  fibres,  whose  cells  are  located 
in  the  nucleus  and  which  carry  the  impulses  down  to  affect  the  heart-rate. 

Afferent  Impulses. — As  regards  the  afferent  impulses,  the  tracings  of 
Einthoven,  Flohil,  and  Battaerd  have  demonstrated  that  a  wave  of  electro- 
negativity passes  upward  at  each  heart-beat  similar  to  the  slower  negative 
wave  which  accompanies  each  respiration  (see  page  213  and  Fig.  125).  The 
nature  of  the  afferent  impulses  and  their  relation  to  cardiac  symptoms  are 
discussed  on  pages  213  and  214. 

Efferent  Impulses. — The  efferent  impulses  which  pass  down  the  vagi 
are  of  various  types:  (1)  Cardioinhibitory,  which  slow  or  stop  the  heart- 
beat by  preventing  the  genesis  of  cardiac  impulses.  (2)  Negatively  dromo- 
tropic,  which  depress  conductivity  either  by  action  on  the  His  bundle  or  by 
depressing  the  irritability  of  the  ventricles  themselves.  (3)  Impulses  which 
affect  tonicity,  sometimes  depressing,  sometimes  increasing  it.  As  Cameron 
has  shown,  paralyzing  the  vagi  with  atropine  prevents  the  tonus  changes 
resulting  from  the  administration  of  most  drugs. 

Right  and  Left  Vagal  Effects, — Like  the  accelerators,  each  vagus  acts 
upon  the  corresponding  side  of  the  heart,  and  certain  differences  between 
2 


18 


DISEASES  OF  THE  HEART  AND  AORTA. 


the  action  of  the  two  vagi  seem  to  be  due  to  this  localized  action.  In  a  series 
of  experiments  performed  by  the  writer  in  collaboration  with  Dr.  H.  A. 
Stewart,  in  which  the  left  vagus  was  the  nerve  usually  stimulated,  it  was  noted 
chat  vagal  heart-block  was  produced  with  great  frequency,  and  often  over- 
shadowed the  inhibitory  effect  upon  the  auricles;  whereas  in  most  physio- 
logical experiments,  in  which  for  greater  convenience  the  right  vagus  is  used, 
the  inhibition  predominates  and  the  block  is  absent.  Drs.  G.  C.  Robinson 
and  Draper  have  recently  obtained  similar  results  from  pressure  on  the  vagi 
in  man.    The  right  vagus  usually  slows  the  heart,  the  left  induces  block. 


Fig.  18. — Origin  and  course  of  the  cardiac  nerves,  and  cutaneous  distribution  of  the  corresponding 
branches.  (Schematic;  modified  from  Douglas  Powell  and  Gibson.)  MOT  SENS,  nuclei  of  the  efferent 
(motor)  and  afferent  (sensory)  fibres  of  the  vagus;  C  1,  2,  3,  4,  5,  6,  7,  8,  and  T  1,  2,  3,  4,  5,  6,  7,  8, 
cervical  and  thoracic  (dorsal)  spinal  nerves  and  tbeir  cutaneous  distribution;  SCG,  MCG,  ICG,  superior, 
middle,  and  inferior  cervical  ganglia;    REC  LAR,  recurrent  laryngeal  nerve;    C  PL,  cardiac  plexus. 


A  very  extended  series  of  experiments  has  recently  been  performed  by 
Garrey  upon  the  heart  of  the  turtle.  Garrey  has  found  that  when  the  vagi 
are  stimulated  with  very  weak  stimuli,  only  the  corresponding  side  of  the 
heart  is  affected,  but  if  the  stimulation  is  stronger  it  affects  both  sides,  the 
impulse  then  crossing  to  the  other  side  of  the  heart  within  the  cardiac  plexus. 
The  right  vagus  inhibits  because  it  acts  upon  the  right  precaval  and  post- 
caval veins  and  the  sinus  which  under  ordinary  circumstances  beat  twice  as 
fast  as  the  veins  on  the  left  and  are  the  "  pacemakers  "  of  the  heart;  but  if 
the  right  veins  are  slowed  by  cooling  and  the  left  veins  accelerated  by  warm- 
ing, the  left  side  of  the  heart  may  become  the  "  pacemaker,"  and  weak  stimu- 
lation of  the  left  vagus  now  produces  slowing  of  the  rate  instead  of  block. 


PHYSIOLOGICAL  CONSIDERATIONS. 


19 


Accelerator  and  Sympathetic  Nerves. — All  the  branches  of  the  cervical 
and  the  upper  four  thoracic  nerves  give  off  rami  communicantes  which  pass 
to  the  cervical  and  stellate  ganglia.  From  these  ganglia  branches  pass  out 
down  along  the  arteries  and  vena  cava  to  the  heart,  constituting  the  second 
group  of  extracardiac  nerves — the  so-called  accelerator  nerves. 

Pawlow  has  shown,  however,  that  this  action  is  not  common  to  all  the 
branches  of  those  nerves,  but  is  very  much  more  marked  in  the  case  of  the 
right  than  of  the  left  annulus  of  Vieussens,  probably  because  it  supplies  the 
sinus  region  of  the  heart.  This  fact  has  been  confirmed  by  Bayliss  and  Star- 
ling, Reid  Hunt,  and  others. 

Rothberger  and  Winterberg  studied  these  effects  with  the  electrocar- 
diograph, and  from  the  form  of  the  latter  were  able  to  demonstrate  that: 

1.  Acceleration  of  the  heart  is  a  function  of  the  right  accelerator,  or 
right  annulus  of  Vieussens,  probably  because  its  fibres  are  distributed  chiefly 
to  the  region  of  the  embryonic  sinus  (sino-auricular  node  of  Keith  and  Flack 
and  neighboring  regions). 

2.  Stimulation  of  the  various  branches  of  the  right  cervical  sympathetic 
gave  rise  to  an  electrocardiogram  typical  of  overaction  of  the  right  ventricle, 
and,  conversely,  stimulation  of  the  left  cervical  sympathetic  branches  gave 
rise  to  electrocardiograms  with  inverted  R  and  T  waves  indicating  overaction 
of  the  left  ventricle. 

3.  Stimulation  of  certain  cardiac  branches  of  the  left  cervical  sympa- 
thetic gave  rise  to  simultaneous  contractions  of  the  auricles  and  ventricles, 
by  causing  impulse  to  arise  in  the  atrioventricular  bundle  (nodal  rhythm, 
cf.  page  118),  with  or  without  the  occurrence  of  tachycardia. 

Tonic  Action  of  the  Vagi  and  Accelerators. — The  recent  studies  of  Ep- 
pinger,  Falta,  and  their  collaborators  have  shown  that  in  many  pathological 
and  borderline  conditions,  especially  those  in  which  there  is  a  disturbance  in 
the  glands  of  internal  secretion,  there  is  also  an  alteration  of  the  balance 
which  normally  exists  between  the  autonomic  (vagi,  phrenic  and  splanchnic) 
and  the  sympathetic  nervous  system;  so  that  sometimes  the  influence  of  the 
former  predominates  (vagotonie)  and  sometimes  the  latter  (sympathicotonie). 
Many  cases  of  hyperacidity,  bronchial  asthma,  ulcer  of  the  stomach,  and  cer- 
tain forms  of  tuberculosis  show  manifestations  of  overaction  of  the  vagi;  while 
Basedow's  disease  and  its  formes  frustes,  as  well  as  certain  cases  of  diabetes 
mellitus,  represent  typical  examples  of  overaction  of  the  sympathetic  system. 

In  some  conditions  there  occurs  overaction,  in  others  underaction,  of 
both  systems  simultaneously.  Eppinger,  Hess  and  A.  H.  Hopkins  have  given 
the  following  tabulation  of  tonic  nerve  effects : 


Vagotonie 

Sympathico- 
tonie 

Vagotonie 

Sympathico- 
tonie 

Pupil 

Dilated 

Stomach 

.  Pylorospasm 

Atonic 

Face 

. .  .Flushed 

Pale 

Intestine 

.  Diarrhoea  or 

Stasis 

Skin 

. . .  Moist 

Dry 

spastic  con- 

Eyeballs  

. . .Sunken 

Prominent  (ex- 

stipation 

ophthalmus) 

Pulse 

.Slow 

Accelerated 

Dry 

HC1  secretion . 

. Increased 

Diminished 

Bronchi 

Tendency  to 

Glycosuria 

.  Diminished 

Increased 

asthma 

.  Contracted 

Relaxed 

Cardia 

. .  .Contracted 

Relaxed 

Eosinophiles .  . 

. Increased 

Decreased 

Stomach 

. . . .  Contracted 

Relaxed 

20  DISEASES  OF  THE  HEART  AND  AORTA. 

Patients  in  whom  there  is  overaction  of  the  vagi  show  particularly 
marked  effects  from  the  administration  of  atropine  (1  mg.,  gr.  1/60,  sub- 
cutaneously,  in  men;  0.75  mg.,  gr.  1/75,  in  women)  and  pilocarpine  (10  mg., 
gr.  1/6,  subcutaneously,  in  men,  7.5  mg.,  gr.  1/8,  in  women).  Those  with 
overaction  of  the  sympathetic  are  particularly  sensitive  to  adrenalin  (1  cc, 
15  minims,  of  the  1/1000  solution,  equal  to  1  mg.,  gr.  1/60,  of  the  crystalline 
substance,  subcutaneously,  in  men;  0.75  cc,  12  minims,  in  women). 

Cardiac  Plexus. — The  intrinsic  nerves  of  the  heart  exist  in  the  form  of 
a  plexus  or  plexus  system  grouped  especially  around  the  coronary  vessels 
and  their  branches. 

The  simplest  form  of  intrinsic  nerve  supply  is  seen  in  the  frog  tadpole, 
where  it  has  been  studied  by  His,  Jr.  This  observer  found  that  the  first 
ganglia  pass  out  toward  the  heart  as  outgrowths  from  the  vagosympathetic 
chain  and  lie  on  each  side  of  the  pulmonary  vein,  along  which  they  gradually 
wander  to  the  heart  and  come  to  lie  between  the  layers  of  the  interauricular 
septum.  A  second  group  of  ganglia  arises  from  the  so-called  intestinal  branch 
of  the  vagosympathetic  nerve  and  follows  the  superior  vena  cava  down  into 
the  heart  to  the  sinus  venosus,  where  it  lies  close  to  the  pulmonary  vein  and 
anastomoses  with  the  pulmonary  plexus  described  above.  This  group  of 
ganglion-cells  forms  the  sinoauricular  ganglion  first  described  by  Remak  in 
1848.  From  this  ganglion  the  cells  wander  further  down  the  septum,  form- 
ing the  two  septal  nerves  of  Ludwig  (1848),  and  each  of  these  in  turn  ends  in  a 
ganglion  (described  by  Bidder  in  1852)  at  the  auriculo ventricular  junction. 
From  Bidder's  ganglia  one  set  of  fibres  passes  down  over  the  endothelial 
surfaces  of  the  valves,  to  distribute  themselves  among  the  muscle-fibres  of 
the  ventricular  walls;  another  passes  over  between  the  auricles  and  the  bul- 
bus  and  distributes  itself  to  the  region  of  the  bulbus  and  the  walls  of  the  auri- 
cles and  ventricles. 

F.  Hoffmann  has  cut  these  nerves  away  from  the  rest  of  the  vagi  and 
shown  that,  while  stimulation  of  the  vagus  fibres  passing  to  the  sinus  and 
auricles  caused  slowing  or  stoppage  of  the  heart,  stimulation  of  the  septal 
nerves  caused  no  change  in  rate,  but  did  cause  an  increase  in  the  force  of  the 
ventricular  beat  and  in  the  tonus  of  the  walls  (inotropic  effect). 

An  observation  made  by  Cameron  in  the  writer's  laboratory  has  ren- 
dered it  probable  that  similarly  distributed  fibres  are  present  in  the  mamma- 
lian heart;  for  he  found  that  substances  (digitalis,  strychnine  and  potassium, 
calcium)  which  cause  increase  or  diminution  in  the  tonus  of  the  ventricular 
muscle  of  the  intact  heart  no  longer  exert  these  effects  in  small  doses  when 
the  vagi  are  paralyzed  with  atropine. 

Both  vagi  and  accelerators  are  normally  in 
tonic  activity.  Reflex  quickening  of  the  pulse-rate,  as  from  emotion, 
pain,  sensation,  and  other  reflex  causes  (Reid  Hunt),  and  moderate  exercise 
(Hering  and  Bowen),  is  due  partly  to  diminution  of  tonic  activity  of  the 
vagi,  partly  to  direct  stimulation  of  the  accelerators  (Hooker);  while  the 
acceleration  after  violent  exercise  is  due  to  stimulation  of  the  accelerators 
(Hering,  Bowen).  Acceleration  upon  mild  exercise  can  also  be  obtained  in 
patients  whose  vagi  are  made  inactive  by  0.5  to  1.0  mg.  (T\-^  to  or  gr.) 
atropine  (Hirschf elder).  On  the  other  hand,  exercise  caused  no  accelera- 
tion but  a  slight  slowing  of  the  pulse  in  a  dog  from  which  Friedenthal  had 
removed  all  the  cardiac  nerves. 


PHYSIOLOGICAL  CONSIDERATIONS  21 

The  mode  of  action  of  the  cardiac  nerves  has  been  shrouded  in  mystery,  especially 
that  of  the  inhibition  by  the  vagus.  Howell  and  Duke  in  a  most  brilliant  series  of  researches 
have  shown  that  potassium  is  given  off  from  the  heart  muscle  and 
can  be  found  in  increased  quantity  in  the  perfusion  liquid 
after  the  vagus  has  been  stimulated.  Controls  without  vagus  stimula- 
tion show  no  such  increase.  It  would  therefore  appear  that  vagus  inhibition  is 
a  true  potassium  effect,  a  fact  further  borne  out  by  the  close  analogy  between 
the  action  of  this  element  and  stimulation  of  the  vagus,  as  well  as  by  the  marked  increase 
in  the  action  of  the  vagus  after  the  administration  of  large  quantities  of  potassium  or  after 
increase  of  potassium  in  the  blood. 

These  observers  were  unable  to  demonstrate  any  effect  of  the  accelerators  upon  the 
liberation  of  calcium,  potassium,  or  nitrogen. 

In  order  to  explain  the  act  of  inhibition,  Erlanger  has  suggested  the  very  ingenious 
theory  that  the  motor  impulses  for  the  cardiac  contraction  arise  in  the  vagus  itself.  These 
impulses  he  supposes  to  arise  at  the  normal  rate  of  discharge  of  nerve-cells,  namely  10  to 
50  per  second,  to  some  but  not  all  of  which  the  heart  responds  with  a  contraction.  When  the 
vagus  is  stimulated  the  rate  of  impulses  becomes  faster  and  the  impulses  become  smaller, 
and  the  heart  responds  to  fewer  nerve  impulses,  with  corresponding  slowing  of  the  rate. 

BIBLIOGRAPHY. 

Physiology. 

Bowditch,  H.  P.:  Ueber  die  Eigenthumlichkeiten  der  Reizbarkeit,  welche  die  Muskel- 
fasern  des  Herzens  zeigen,  Ber.  d.  math.  phys.  CI.  d.  k.  sachs.  Gesellsch.  d. 
Wissensch.,  Leipzig,  1871. 

Engelmann,  Th.  W.:  Ueber  den  Ursprung  der  Herzbewegungen,  Arch.  f.  d.  ges.  Physiol., 
Bonn,  1897,  lxv,  109. 

Mackenzie,  James:  A  Preliminary  Inquiry  into  the  Tonicity  of  the  Muscle-fibres  of  the 
Heart,  Brit.  M.  J.,  London,  1905,  ii,  1689. 

Merunowicz.    Quoted  from  Schaefer's  Physiology. 

Ringer,  S.:  Concerning  the  Influence  Exerted  by  Each  of  the  Constituents  of  the  Blood 
on  the  Contractions  of  the  Ventricle,  J.  Physiol.,  Camb.,  1882,  iii,  380.  A  Further 
Contribution  Regarding  the  Influence  of  the  Different  Constituents  of  the  Blood  on 
the  Contraction  of  the  Heart,  J.  Physiol.,  Cambr.,  1884,  iv,  29.  A  Third  Contribution 
Regarding  the  Influence  of  the  Inorganic  Constituents  of  the  Blood  on  Ventricular 
Contraction,  ibid.,  p.  222. 

Howell,  W.  H.:  On  the  Relation  of  the  Blood  to  the  Automaticity  and  Sequence  of  the 
Heart-beat,  Am.  J.  Physiol.,  Bost.,  1898,  ii,  47. 

Greene,  C.  W. :  On  the  Relation  of  the  Inorganic  Salts  of  Blood  to  the  Automatic  Activity 
of  a  Strip  of  Ventricular  Muscle,  ibid.,  p.  82. 

Howell,  W.  H.:  The  Cause  of  the  Heart-beat,  J.  Am.  Assoc,  Chicago,  1906,  xlvi,  Nos. 
22  and  23. 

Erlandsen,  A.:  TJntersuchungen  ueber  die  lecithinartigen  Substanzen  des  Myocardiums 
und  der  quergestreiften  Muskeln.,  Ztschr.  f.  physiol.  Chem.,  Strassb.,  1907,  li,  71. 

Loeb,  J.:  Ueber  Ionen  welche  rhythmische  Zuckungen  des  Skelettmuskels  hervorrufen, 
Beitrage  zur  Physiologie  (Festschr.  f.  A.  Fick),  Braunschweig,  1899,  p.  101.  The 
Dynamics  of  Living  Matter,  N.  York,  Columbia  Univ.  Press,  1906,  for  complete  dis- 
cussion of  work  upon  the  comparative  physiology  of  salt  action. 

Lingle,  D.  J.:  The  Action  of  Certain  Ions  on  Ventricular  Muscle,  Am.  J.  Physiol.,  Bost., 
1900,  iv,  265. 

Moore,  A. :  The  Effect  of  Ions  on  the  Contractions  of  the  Lymph  Hearts  of  the  Frog,  Am. 
J.  Physiol.,  Bost.,  1901,  v,  87. 

Locke,  F.  S.:  Die  Wirkung  der  Metalle  des  Blutplasmas  und  verschiedener  Zucker  auf 
das  isolirte  Saugethierherz.,  Centralbl.  f.  Physiol.,  Leipz.  u.  Wien.,  1901,  xiv,  670. 

Langendorff,  O.:  Untersuchung  am  iiberlebenden  Saugethierherzen,  Arch.  f.  d.  ges.  Phy- 
siol., Bonn,  1895,  lxi,  291. 

Rusch,  H.:  Experimentelle  Studien  liber  die  Ernahrung  des  isolirten  Saugethierherzens, 
ibid.,  1898,  lxxiii,  535. 


22  DISEASES  OF  THE  HEART  AND  AORTA, 

Kuliabko,  A.:  Wiederbelebung  des  menschlichen  Herzens,  Centralbl.  f.  Physiol.,  Leipz. 
und  Wien,  1902,  xvi,  330. 

d'Hallion,  M.:  Reviviscence  d'un  cceur  d'enfant  36  heures  apres  la  mort,  J.  d.  sc.  m6d.  de 
Lille,  1903,  ii,  481. 

Deneke,  Th.,  and  Adam,  H. :  Beobachtungen  am  isolirten  iiberlebenden  menschlichen 
Herzen,  Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  1906,  ii,  491. 

Gaskell,  W.  H.:  Ok  the  Rhythm  of  the  Heart  of  the  Frog  and  the  Nature  of  the  Action 
of  the  Vagus  Nerve,  Phil.  Trans.  Roy.  Soc,  London,  1882,  p.  993.  On  the  Innerva- 
tion of  the  Heart,  with  Especial  Reference  to  the  Heart  of  the  Tortoise,  J.  Physiol., 
Cambridge,  1884,  iv,  43.  The  Contraction  of  Cardiac  Muscle,  Schafer's  Text-book  of 
Physiol.,  Edinb.  and  Lond.,  1900,  ii,  169. 

His,  W.,  Jun.:  Die  Thatigkeit  des  embryonalen  Herzens  und  deren  Bedeutung  fur  die 
Lehre  von  der  Herzbewegung  beim  Erwachsenen,  Arb.  a.  d.  med.  Klin,  zu  Leipz., 
1893,  14. 

Bond,  G.  S. — Unpublished  experiments. 

Erlanger,  J. :  Irregularities  of  the  Heart  Resulting  from  Disturbed  Conductivity,  Am.  J. 
M.  Sc,  Phila.,  1908,  n.  s.  cxxxv,  797. 

Keith,  A.,  and  Flack,  M.  W.:  The  Auriculoventricular  Bundle  of  the  Human  Heart,  Lan- 
cet, Lond.,  1906,  ii,  359. 

Keith,  A. :  An  Account  of  the  Structures  Concerned  in  the  Production  of  the  Jugular  Pulse, 
J.  Anat.  and  Physiol.,  Lond.,  1908,  xlii,  1. 

Koch,  W. :  Weitere  Mittheilungen  ueber  den  Sinusknoten  des  Herzens,  Verhandl.  d.  deutsch. 
path.  Ges.,  Jena,  1909,  xiii,  85. 

Lewis,  T.,  Oppenheimer,  B.  S.,  and  Oppenheimer,  A.:  The  Site  of  Origin  of  the  Mammalian 
Heart  Beat:  The  Pacemaker  in  the  Dog  Heart,  1910,  ii,  147. 

Adam,  H.:  Experiment elle  Untersuchungen  ueber  den  Ausgangspunkt  der  automatischen 
Herzreize  beim  Warmbluter,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1906,  cxi,  607. 

Langendorff,  O.,  and  Lehmann,  C:  Der  Versuch  von  Stannius  am  Warmbluterherzen, 
Arch.  f.  d.  ges.  Physiol.,  Bonn,  1906,  cxii,  352. 

Erlanger,  J.,  and  Blackman,  J.  R. :  A  Study  of  the  Relative  Rhythmicity  and  Conductiv- 
ity in  Various  Regions  of  the  Auricles  of  the  Mammalian  Heart,  Am.  J.  Physiol., 
Bost.,  1907,  xix,  125. 

Wybauw,  R.:  Etude  de  certaines  conditions  dans  lesquelles  le  nerf  pneumogastrique  cesse 
d'agir  sur  le  coeur,  Arch.  Internat.  de  Physiol.,  Liege,  1904-05,  ii,  198. 

Jager,  T.:  Ueber  die  Bedeutung  des  Keith-Flackschen  Knotens  fur  den  Herzrhythmus, 
Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1910,  c,  1. 

Flack,  M.:  An  Investigation  of  the  Sino-auricular  Node  of  the  Mammalian  Heart,  J.  Phy- 
siol., Camb.,  1910,  xli,  64. 

Retzer,  R. :  Some  Results  of  Recent  Investigations  on  the  Mammalian  Heart,  Anat.  Rec, 
Phila.,  1908,  ii,  149. 

Schonberg,  S.:  Ueber  Veranderungen  im  Sinusgebiet  des  Herzens  bei  chronischer  Arrhyth- 
mie,  Frankf.  Ztschr.  f.  Path.,  Wiesb.,  1908,  ii,  153. 

De  Witt,  L.  M. :  Observations  on  the  Sino-ventricular  Connecting  System  of  the  Mammalian 
Heart,  Anat.  Rec,  Phila.,  1909,  hi,  475. 

McWilliam,  J.  A.:  On  the  Rhythm  of  the  Mammalian  Heart,  J.  Physiol.,  Camb.,  1888, 
ix,  167. 

Hering,  H.  E.:  Ueberleitungsstorungen  am  Saugethierherzen  mit  zeitweiligem  Vorhofs- 
systolenausfall,  Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  1906,  iii,  511;  and  Ueber 
die  Automatie  des  Saugethierherzens,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907,  cxvi,  143. 

Bond,  G.  S. :  Unpublished  observations. 

V.  Tabora,  D.:  Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  iii. 

Garrey,  W.  E.:  Dissociation  of  Nerve  Impulse  from  Normal  Conduction  in  the  Heart  by 
Means  of  Compression,  Am.  J.  Physiol.,  Bost.,  1911. 

Hirschfelder,  A.  D.,  and  Eyster,  J.  A.  E.:  Extrasystoles  in  the  Mammalian  Heart,  Am.  J. 
Physiol.,  Bost.,  1907,  xviii,  222. 

Langendorff,  O.,  and  Lehmann,  C:  Der  Versuch  von  Stannius  am  Warmbluterherzen, 
Arch.  f.  d.  ges.  Physiol.,  Bonn,  1906,  cxii,  352. 

Fredericq,  L. :  La  pulsation  du  cceur  du  chien  est  une  onde  de  contraction  qui  debute  dans 
l'oreillette  droite,  etc.,  Arch,  internat.  de  physiol.,  Liege,  1906,  iv,  57. 


PHYSIOLOGICAL  CONSIDERATIONS.  23 

Lohmann,  A.:  Ueber  die  Funktion  der  Briickenfasern,  an  Stelle   der  grossen  Venen  die 

Fuhrung  der  Herztatigkeit  beim  Saugetiere  zu  iibernehmen,  Arch,  f.  d.  ges.  Physiol., 

Bonn,  1908,  cxxiii,  628. 
Kent,  His,  Retzer,  Braunig,  Tawara.    See  Part  III,  Chapter  XI. 
King,  T.  W.    See  Part  III,  Chapter  VII. 
Wilson,  J.  G. :  The  Nerves  of  the  Atrioventricular  Bundle,  Proc.  Roy.  Soc.,  Lond.,  1909, 

ser.  B,  vol.  Ixxxi,  151. 
Barker,  L.  F.,  and  Hirschfelder,  A.  D.:  The  Effect  of  Cutting  the  Branch  of  the  His  Bundle 

Going  to  the  Left  Ventricle,  Arch.  Int.  Med.,  Chicago,  1909,  iv,  193. 
Eppinger,    H.,   and   Rothberger,   J.:  Ueber  die  Folgen   der  Durchschneidung  der  Taw- 

araschen  Schenkel  des  Reizleitungs-systems,  Ztschr.  f.  klin.  Med.,  Berl.,  1910,  Ixx,  1. 
Cohn,  A.  E.,  and  Trendelenburg,  W.:    Untersuchungen  zur  Physiologie  des  Uebergangs- 

bundels  am  Saugetierherzen  nebst  mikroskopischen  Nachprufungen,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1910,  cxxxi,  1. 
Ludwig,  C:  Ueber  den  Bau  und  die  Bewegungen  der  Herzventrikel,  Ztschr.  f.  rat.  Med., 

Heidelb.,  1849,  vii,  189. 
Krehl,  L. :  Beitrage  zur  Kenntniss  der  Fullung  und  Entleerung  des  Herzens,  Abhandl. 

d.  kgl.  sachs.  Gesellsch.  d.  Wissensch.,  Math.-phys.  Kl.,  Leipz.,  1891,  xvii,  341. 
MacCallum,  J.  B.:  On  the  Muscular  Architecture  and  Growth  of  the  Ventricles  of  the 

Heart,  Contrib.  Sc.  Med.  dedic.  to  W.  H.  Welch,  Baltimore,  1900,  307. 
Borelli:  De  motu  animalium,  Romae,  1681. 
Wolff,  C.  F.:  Acta  Acad.  Sc.  Imp.  Petropal.,  1780-92,  vols.  ii-x. 
Gerdy:  Recherches  discussions  et  propositions,  These,  Paris,  1823. 

Weber,  E.  H.:  Hildebrandt's  Handbuch  der  Anatomie  des  Menschen,  Braunschweig,  1831. 
Knower,  H.  McE.:  Demonstration  of  the  Interventricular  Muscle-bands  of  the  Adult 

Human  Heart,  Anat.  Rec,  Phila.,  1908-9,  ii,  204;  Johns  Hopkins  Hosp.  Bull.,  Bait., 

1908,  xix,  208. 
Mall,  F.  P. :  On  the  Muscular  Architecture  of  the  Ventricles  of  the  Human  Heart,  Am.  J. 

Anat.,  Phila.,  1911,  xi,  211. 
Robinson,  G.  C,  and  Draper,  G.:  A  Study  of  the  Presphygmic  Period  of  the  Heart,  Arch. 

Int.  Med.,  Chicago,  1910,  v,  168,  and  Deutsches  Arch.  f.  klin.  Med.,  Leipz. 
Baumgarten,  A. :  Ueber  den  Mechanismus  durch  welchen  die  venosen  Herzklappen  geschlos- 

sen  werden,  Arch.  f.  Anat.,  Physiol,  u.  wissensch.  Med.,  Berl.,  1843,  463. 
Howell,  W.  H.,  and  Donaldson,  F. :  Experiments  upon  the  Heart  of  the  Dog,  Phil.  Tr.  Roy. 

Soc,  Lond.,  1884,  Part  I,  139. 
Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough  and  F.  P.  Chillingworth) : 

The  Volume  Curve  of  the  Ventricles  of  the  Mammalian  Heart  and  the  Significance 

of  this  Curve  in  Respect  to  the  Mechanics  of  the  Heart-beat  and  the  Filling  of  the 

Ventricles,  Am.  J.  Physiol.,  Bost.,  1906,  xvi,  325. 
Gad,  J.:  Klappenspiel  im  Ochsenherzen,  Arch.  f.  Physiol.,  Leipzig,  1886,  p.  380. 
Hooker,  D.  R.:  May  Reflex  Cardiac  Acceleration  Occur  Independently  of  the  Cardio-inhib- 

itory  Center?    Am.  J.  Physiol.,  Bost.,  1908,  xix,  417. 
Stewart,  H.  A.:  A  Clinical  and  Experimental  Study  of  the  Blood-pressure  and  Pulse  in 

Aortic  Insufficiency,  Thesis,  Edinb.,  1907;  also  Arch.  Int.  Med.,  Chicago,  1908,  i. 
Porter,  W.  T.:  Observations  on  the  Tonus  of  Heart  Muscle,  Am.  J.  Physiol.,  Bost.,  1906, 

xv,  1. 
Barcroft,  J.,  and  Dixon,  W.  E.:  The  Gaseous  Metabolism  of  the  Mammalian  Heart,  J. 

Physiol.,  Cambr.,  1907,  xxxv,  182. 
Hofmann,  Fr.:  Ueber  die  Function  der  Scheidewandnerven  des  Froschherzen,  Arch.  f.  d. 

ges.  Physiol.,  Bonn,  1895,  lx,  139. 
Cameron,  P.  D.:  Physiological  and  Pharmacological  Studies  upon  the  Tonicity  of  the 

Mammalian  Heart,  Thesis,  Edinb.,   1908,  and  Johns  Hopkins  Hosp.  Rep.,  Bait., 

1911,  xvi,  549. 
Bayliss,  W.  M.,  and  Starling,  E.  H.:  On  Some  Points  in  the  Innervation  of  the  Mammalian 

Heart,  J.  Physiol.,  Camb.,  1892,  xiii,  407. 
Hunt,  Reid:  Direct  and  Reflex  Acceleration  of  the  Mammalian  Heart,  with  Some  Obser- 
vations upon  the  Relations  of  the  Inhibitory  and  Accelerator  Nerves,  Am.  J.  Physiol., 

Bost.,  1899,  ii,  395. 
MacCallum,  W.  G. :  The  Changes  in  the  Circulation  in  Aortic  Insufficiency,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1911,  xxii,  197. 


24  DISEASES  OF  THE  HEART  AND  AORTA. 

Martin,  H.  N.,  and  Donaldson,  F.:  Experiments  on  the  Supposed  Suction-pump  Action 
of  the  Mammalian  Heart.    Stud,  from  the  Biol.  Lab.,  Johns  Hopkins  University, 
1890,  iv,  37. 
Einthoven,  W,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A. :  On  Vagus  Currents  Examined  with 
the  String  Galvanometer.  Quart.  J.  Exper.  Physiol.,  Lond.,  1908,  i,  243;  Nebro  Vag- 
usstrome,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxiv,  246. 
Hirschfelder,  A.  D.,  and  Stewart,  H.  A.:  Unpublished  observations. 
Robinson,  G.  Canby:  Personal  communication. 

Garrey,  W.  E. :  Experiments  about  to  be  published  in  the  American  Journal  of  Physiology. 
Pawlow,  J.  P.:  Ueber  die  Zentrifugalen  Nerven  des  Herzens,  Arch.  f.  Phvsiol     Lehoz 

1887,  498. 
Rothberger,  J.,  and  Winberger:  Ueber  die  Beziehung  der  Herznerven  zur  Form  des  Elek- 

_  trokardiogramms,  Arch.  f.  d.  ges.  Physiol.,  i,  Bonn,  1910,  cxxxv,  506. 
Eppinger,  H.,  Falta,  W.,  and  Rudinger,  C.:  Ueber  die  Wechselwirkung  der  Drusen  mit 

innerer  Sekretion,  Ztschr.  f:  klin.  Med.,  Berl.,  1908,  lxvi,  1;  1909,  lxvii,  380. 
Eppinger,  H.,  and  Hess,  L.:  Zur  Pathologie  der  vegetativen  Nervensystems,  ibid.,  1909, 

lxvii,  345. 
Falta,  W.,  Newburgh,  L.  H.,  and  Nobel,  E.:  Ueber  die  Wechselwirkung  der  Drusen  mit 

innerer  Sekretion,  IV  Mitth.     (Ueber  Beziehungen  der  Ueberfunktion  zur  Konsti- 

tution),  ibid.,  1911,  lxxii,  97. 
Falta,  W.,  and  Kahn,  F.:    Klinische  Studien  ueber  Tetanie,  mit  besonderer  Beriicksichti- 

gung  des  vegetativen  Nervensystems,  ibid.,  1911,  lxxiv,  108. 
Hopkins,  A.  H. :  A  Clinical  Study  of  Vagotonia,  Arch.  Int.  Med.,  1913,  xii,  586. 
Wolfsohn,  J.  M.:  The  Vegetative  Nervous  System  with  Especial  Reference  to  Vagotonia 

and  Sympathicotonie,  J.  Am.  Med.  Assoc,  Chicago,  1914,  lxii,  1535. 
Hering,  H.  E.:  Ueber  die  Beziehungen  der  extracardialen  Herznerven  zur  Steigerung  der 

Herzschlagzahl  bei  Muskeltatigkeit,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1895,  lx,  429. 
Bowen,  W.  P.:  A  Study  of  the  Pulse-rate  in  Man  as  Modified  by  Muscular  Work,  Contrib. 

to  Med.  Research  (Vaughan),  Ann  Arbor,  1903,  p.  462. 
Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Johns  Hopkins  Hosp, 

Bull.,  Bait.,  1906,  xvii,  337. 
Friedenthal,  H.:  Ueber  die  Entfernung  der  extracardialen  Herznerven  bei  Saugethieren., 

Arch.  f.  Physiol.,  Leipz.,  1902,  p.  135. 
Howell,  W.  H.,  and  Duke,  W.  W.:  The  Effect  of  Vagus  Inhibition  on  the  Output  of  Potas- 
sium from  the  Heart,  Am.  J.  Physiol.,  Bost.,  1908,  xxi,  51.    Note  upon  the  Effect 

of  Stimulation  of  the  Accelerator  Nerve  upon  the  Calcium,  Potassium,  and  Nitrogen 

Metabolism  of  the  Isolated  Heart,  ibid.,  1908-1909,  xxiii,  174. 
Erlanger,  J.:  Mammalian  Heart  Strips,  together  with  a  Theory  of  Cardiac  Inhibition, 

Proc.  Am.  Physiol.  Soc,  Bost.,  1910,  in  Am.  J.  Physiol,  1910,  p.  16. 
Keith,  A.,  and  Flack,  M.:  The  Form  and  Nature  of  the  Muscular  Connections  between 

the  Primary  Divisions  of  the  Mammalian  Heart,  J.  Anat.  and  Physiol.,  1907,  xli,  172. 
His,  W.,  Jr. :  Quoted  on  page  22. 
Ludwig,  C. :  Ueber  die  Herznerven  des  Frosches,  Arch.  f.  Anat.  u.  Physiol,  u.  wissensch. 

Med.,  Berl.,  1848,  139. 
Bidder,  F.,  and  Rosenberger,  G.:  Ueber  functionell  verschiedene  und  raumlich  Getrennte 

Nervencentra  im  Froschherzen,  ibid.,  1852,  163. 
Hoffmann,  F. :  Ueber  die  Function  der  Scheidewandnerven  des  Froschherzens,  Arch,  f .  d= 

ges.  Physiol.,  Bonn,  1895,  ex,  139, 


II. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 

THE  BLOOD-PRESSURE  IN  HEALTH  AND  DISEASE. 

Definition. — The  blood-pressure,  or  "  arterial  tension,"  is  the  pressure 
which  the  blood  is  exerting  upon  the  walls  of  the  vessel  in  which  it  is  to  be 
measured  (lateral  pressure),  or  upon  the  column  of  blood  ahead  of  it  in  the 
direction  in  which  it  is  flowing  (end  pressure). 

The  end  pressure  is  equal  to  lateral  pressure  +  velocity  head,  but  as  a  rule  differs 
by  only  a  few  millimetres  from  the  lateral  pressure.  The  end  pressure  in  the  branch  of  a 
vessel  is  equal  to  the  lateral  pressure  in  the  vessel  from  which  it  branches. 


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Fig.  19. — Curve  of  intraventricular  and  aortic  pressures.  (After  Huerthle.)  A ,  aortic  pressure ; 
V,  intraventricular  pressure;  D,  curve,  taken  with  a  differential  manometer,  showing  the  differences  of 
pressure  between  left  ventricle  and  aorta. 


Pressure  within  the  Left  Ventricle. — It  is  evident  that  in  a  system  of 
elastic  tubes  like  the  arteries,  the  pressure  of  the  blood  in  any  segment  of 
artery  is  brought  about  by  the  tendency  of  the  inflow  (from  the  heart)  to 
remain  in  excess  of  the  outflow  through  the  capillaries.  The  inflow  to  the 
arteries  is  maintained  by  the  pumping  action  of  the  heart,  that  is,  by  the 
intraventricular  pressure  during  systole.  As  shown  by  Huerthle  and  Porter, 
the  pressure  within  the  ventricle  remains  tolerably  constant  throughout 
systole  and  takes  the  form  of  a  plateau  more  or  less  independent  ,of  the  pulse 
curve  in  the  aorta  (Fig.  19),  though  the  floor  of  the  plateau  slopes  down- 
ward with  peripheral  dilatation  and  upward  with  constriction. 

If  the  systole  is  too  weak  to  open  the  aortic  valves,  and  the  heart  con- 
tracts without  change  in  volume  (isometrically),  the  curve  does  not  remain 
a  plateau,  but  has  a  rounded  apex  like  ;that  of  _the  isometric  contraction 
of  skeletal  muscle.    The  pressure  within  the  ventricle  when  the  aortic  valves 

25 


26  DISEASES  OF  THE  HEART  AND  AORTA. 

are  open  is  slightly  in  excess  of  that  within  the  aorta,  that  is,  very  little  above 
the  maximal  pressure  as  measured  in  the  latter,  and  it  remains  at  this  height 
until  the  end  of  systole,  when  the  aortic  valves  close. 

Huerthle  and  others  have  shown  that  the  intraventricular  pressure  is  not  always 
constant  throughout  systole,  but  that  when  the  peripheral  resistance  is  very  low  it  falls 
toward  the  end  of  systole,  while  if  the  peripheral  resistance  is  very  high  it  rises  toward  the 
end  of  systole. 

The  Maximal,  Minimal,  and  Pulse  Pressures. — Accordingly,  when  the 
aortic  valves  open  (.07  to  .09  second)  after  the  beginning  of  ventricular 
systole  (see  Fig.  13,  page  12),  the  pressure  in  the  aorta  soon  rises  to  its  max- 
imum, and  from  that  time  until  the  beginning  of  the  next  systole  it  dimin- 
ishes more  or  less  gradually  as  the  excess  of  blood  flows  out  from  the  arterial 
tree  through  the  capillaries  and  into  the  veins.  The  minimal  pressure 
is  reached  just  before  the  beginning  of  the  next  systole.  The  pulse-pres- 
sure is  the  difference  between  the  maximal  and 
minimal  pressures. 

Characteristics  of  the  Pulse. — It  is  evident  that  the  maintenance  of 
the  circulation  depends  upon  the  head  of  pressure  in  the  arteries,  and  accord- 
ingly much  attention  was  paid  by  the  older  clinicians  to  the  "  arterial  ten- 
sion "  and  the  "  quality  of  the  pulse,"  which  they  thought  were  manifesta- 
tions of  it.  The  arterial  tension  was  judged  by  the  force  necessary  to  obliterate 
the  pulse  at  the  wrist  when  the  fingers  are  pressed  upon  the  radial  artery. 

A  still  more  accurate  method  of  feeling  the  pulse  is  to  empty  the  artery  for  a  few 
centimetres  by  "milking"  out  the  blood  with  two  fingers  of  one  hand,  while  obliterating 
the  artery  above  the  wrist  with  the  fingers  of  the  other  hand.  The  pressure  of  the  latter 
is  then  gradually  diminished  until  the  return  of  the  pulse  is  felt,  this  point  marking  the 
maximal  or  systolic  pressure.  By  careful  training  of  the  sensations  and  comparing 
the  observation  with  the  results  of  a  good  sphygmomanometric  determination  made  at 
the  same  time,  a  great  degree  of  skill  in  judging  pressures  may  be  attained;  one  of  the 
"writer's  teachers,  who  has  cultivated  this  perception  to  a  remarkable  degree,  voices  the 
general  experience  in  saying,  "I  can  estimate  the  blood-pressure  with  the  fingers  alone 
quite  accurately  in  about  eight  cases  out  of  ten,  but  those  in  which  it  is  of  real  importance 
are  always  the  other  two." 

The  minimal  pressure  may  also  be  judged,  but  even  less  accurately,  by  estimating 
the  amount  of  pressure  at  which  the  size  of  the  pulse  just  begins  to  decrease  as  one  raises 
the  pressure  in  the  artery. 

Determination  of  Maximal  Blood=pressure. — Instruments  for  deter- 
mining the  blood-pressure  date  from  1855,  when  K.  Vierordt  determined 
the  weight  that  could  be  placed  over  the  radial  artery  before  the  pulse  was 
obliterated. 

Marey  (1876)  devised  the  first  useful  apparatus  for  estimating  the  blood-pressure  in 
man.  He  placed  the  hand  in  a  plethysmograph  connected  with  a  bottle  for  raising  the 
pressure  and  a  sphygmoscope  tambour  for  recording  the  size  of  the  pulse-waves.  He  states 
(1878)  that  the  maximal  pressure  may  be  determined  as  the  point  where  the  pulsation 
disappears,  the  minimal  as  the  point  where  the  oscillations  are  largest.  It  is  worthy  of 
note  that  Marey  was  twenty-five  years  in  advance  of  the  times,  and  that  his  methods 
and  conclusions  are  almost  exactly  those  of  the  best  modern  methods  (Erlanger  and  v. 
Recklinghausen).  Unfortunately,  the  work  of  Marey  was  little  known,  and  the  first  appa- 
ratus to  attain  general  use  was  that  of  v.  Basch  (1887).  Unlike  Marey,  v.  Basch  studied 
only  the  maximal  pressures,  but  much  good  pioneer  work  was  done  with  this  instrument. 
It  consisted  of  a  small  rubber  bulb  filled  with  water  and  communicating  with  a  mercury 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


27 


manometer.  The  bulb  was  pressed  upon  the  radial  artery  until  the  pulse  below  it  was 
obliterated,  and  the  pressure  necessary  was  read  off  upon  the  manometer.  V.  Basch  modi- 
fied the  apparatus  later  by  using  a  spring  manometer,  and  Potain  substituted  air  for 
water  in  the  bag  with  an  aneroid  barometer. 
This  method  is  still  almost  universal  in 
France,  but  the  possible  error  with  v.  Basch's 
as   well   as   Potain's   methods   is   as    much 

as  78  mm.  Hg  (Tigerstedt).  Fig.  20. — Diagram  showing  the  effect  of  com- 

pression upon  arteries  of  various  types.     A,  nor- 
mal; B,  hypertrophied  media  ;  C,  atheromatous. 


HOLLOW 

SPRING     ANEROID 


ANEROID 
CHAMBER 


Fig.  21. — Types  of  manometer  used  for  determining  blood-pressure. 


pressure 


However,  Marey   (I.e.)   had  shown  that 
pulse-wave    was    obtained  when   the 
an  organ  was  equal  to  the 
tery    supplying  it   (i.e.,  the 
minimal  pressure — Ho  well  and  Brush). 

Modern  methods  for  the  clini- 
cal study  of  blood-pressure  depend 
upon  the  obliteration  of  the  pulse 
in  the  brachial  artery.  This  was 
first  accomplished  by  Riva-Rocci 
(1896)  and  Hill  and  Barnard  (1897), 
who  compressed  the  upper  arm  by 
inflating  a  rubber  bag  which  was 
wrapped  around  the  arm  with  a 
wide  silk  bandage  (Riva-Rocci)  or 
a  leather  cuff  (Hill  and  Barnard). 
When  the  bag  is  inflated  at  a  pres- 
sure above  the  maximal  pressure  in 
the  artery,  the  walls  of  the  latter 
radial  pulse  at  the 
(Riva-Rocci).  The 
air  in  the  bag  is 
a   manometer   and 


the  maximal 
pressure  about 
within    the     ar  - 


collapse  and  the 
wrist   disappears 
pressure    of   the 
measured  off    on 


read  in  millimetres  of  mercury  (Riva- 
Rocci)  or  in  centimetres  of  water  (v. 
Recklinghausen) . 1 


Fig.  22. — Erlanger  blood-pressure  apparatus 
with  Hirschfelder  polygraph  attachment.  (Kind- 
ness of  Schneider  Bros.) 


1  R.  Mohr  (Muenchen.  med.  Wchnschr.,  1912,  lix,  759)  cites  a  case  of  thrombosis  of 
the  arm  veins  following  compression  with  sphygmomanometer  cuff. 


28  DISEASES  OF  THE  HEART  AND  AORTA. 

Sources  of  Error  in  the  Compression  of  the  Artery . — 
Even  with  wide  cuffs,  however,  the  pressure  in  the  compressing  bag  may  be  somewhat 
greater  than  that  within  the  artery;  although,  as  v.  Recklinghausen  and  Janeway  have 
shown,  the  soft  tissues  of  the  limb  do  not  play  any  role  in  bringing  this  about,  unless  the 
muscles  are  being  actively  contracted  or  the  limb  is  cedematous.  Either  of  these  conditions 
may  introduce  a  considerable  error.  Under  ordinary  circumstances,  however,  the  chief 
source  of  error  lies  in  the  tone  of  the  arterial  wall.  V.  Basch 
and  Martin  and  Scholtyssek  and  Schmidt  found  that  1-7  mm.  Hg  was  sufficient  to  collapse 
the  normal  artery  completely. 

W.  Russell,  on  the  other  hand,  claims  upon  purely  physical  grounds  that  the  thick- 
ness and  terms  of  the  arterial  wall  may  greatly  increase  this  discrepancy,  and  that,  since 
an  artery  may  contract  to  one-third  its  original  diameter,  its  wall  may  thicken  and  the 
resistance  to  compression  may  increase  in  a  corresponding  degree.  This  claim  has  been 
substantiated  by  the  experiments  of  Herringham  and  Wamack  and  Janeway  and  Park. 
The  latter  have  shown  upon  the  excised  artery  that,  when  the  wall  of  the  vessel  (human 
and  ox  carotid  artery)  is  thrown  into  a  state  of  constriction  by  painting  with  epinephrin 
or  barium  chloride,  it  was  necessary  to  obtain  an  excess  of  pressure  amounting  sometimes 
to  30  mm.  of  mercury  in  order  to  obliterate  the  lumen.  To  collapse  a  boiled  artery  164  mm.- 
Hg  was  necessary.  MacWilliam  and  Kesson  (Heart,  1912-1913,  iv,  279)  report  similar  results. 

All  these  observations  furnish  support  to  Russell's  claims  that  within  certain  limits 
the  sphygmomanometer  may  record  "not  blood-pressure,  but  arterial  resistance." 

This  source  of  error  is  common  to  all  the  present  methods  for  the  clinical  determina- 
tion of  blood-pressure,  and  it  must  always  be  borne  in  mind  in  interpreting  the  results 
obtained;  although,  it  must  be  confessed,  the  magnitude  of  the  error  cannot  be  estimated 
in  any  individual  case.  It  is  greatest  in  thickened,  leathery  arteries  of  small  calibre,  least 
in  arteries  which  are  large  and  dilated,  and  it  may  possibly  account  for  much  of  the  hyper- 
tension recorded  in  arteriosclerosis  and  nephritis  as  well  as  for  the  apparently  tremendous 
changes  in  pressure  recorded  when  the  arteries  pass  from  relaxation  to  constriction  with 
the  onset  of  the  vascular  crises  (p.  368). 

Hoover  has  also  shown  in  man  that  immersion  of  one  arm  of  a  normal  man  in  ice- 
water  may  cause  the  blood-pressure  recorded  in  that  arm  to  appear  as  much  as  180  mm.  Hg 
higher  than  that  recorded  simultaneously  in  the  other  arm.  MacWilliam  and  Kesson 
report  differences  of  30  to  90  mm.  Hg  between  the  two  arms. 

Atheromatous  or  calcified  plaques  may  also  prevent  the  complete  collapse  of  the 
artery,  as  v.  Recklinghausen  has  claimed ;  but  Janeway  and  Park  have  shown  such  plaques 
are  rarely  continuous  for  more  than  one  or  two  centimetres  of  the  lumen;  and,  since  they 
do  not  affect  the  compression  of  the  vessel  elsewhere,  they  do  not  increase  the  reading  as 
much  as  does  mere  vasoconstriction. 


GRAPHIC   METHODS   FOR   THE   DETERMINATION   OF  MAXIMAL  AND   MINIMAL 
BLOOD=PRESSTJRE   IN   MAN. 

Erlanger's  Sphygmomanometer. — The  first  and  most  accurate  of  the 
modern  instruments  for  the  graphic  recording  of  both  maximal  and  minimal 
blood-pressures  was  that  of  Erlanger.  It  is  constructed  upon  the  same  gen- 
eral principles  as  the  original  apparatus  of  Marey,  but  the  pulse-wave  is 
obtained  from  a  v.  Recklinghausen  brachial  cuff  instead  of  a  hand  plethys- 
mograph.  It  differs  from  the  ordinary  apparatus  of  the  Riva-Rocci  type 
with  broad  v.  Recklinghausen  cuff  only  in  the  fact  that  by  means  of  a  T-tube 
the  cuff  is  connected  also  with  a  rubber  pressure-bag  in  a  glass  case.  The 
oscillations  of  pressure  in  the  cuff  are  thus  communicated  to  the  pressure 
bag,  and  the  oscillations  of  this  bag  are  communicated  to  the  air  in  the  glass 
case  around  it,  and  are  recorded  by  the  movements  of  a  Marey  tambour 
upon  the  smoked  paper  on  a  small  drum.  He  is  also  able  to  let  the  pressure 
flow  out  very  slowly  by  a  series  of  capillary  outlets  of  different  bores.  A 
complicated  stop-cock  allows  any  of  these  to  be  used  at  will. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


29 


In  using  the  Erlanger  apparatus,  one  turns  the  stop-cock  to  the  point  marked  "In," 
then  raises  the  pressure  in  the  bag  to  well  above  the  maximum  arterial  pressure,  and  turns 
the  stop-cock  to  the  point  marked  1  or  2,  which  corresponds  to  capillary  outlets  of  different 
sizes.  The  pressure  in  the  bag  falls  gradually,  and  soon  small  oscillations  of  the  lever  are 
seen,  due  to  the  impact  of  the  compressed  artery  upon  the  upper  margin  of  the  bag.  A 
sudden  increase  in  the  size  of  these  wavelets  soon  takes  place  and  marks  the  maximal 
pressure,  which  is  read  off  on  the  manometer;  it  is  just  a  trifle  below  the  maximal  pressure 
that  the  first  pulse-wave  passes  completely  through  under  the  cuff  and  causes  the  larger 
wave,  upon  which  also  a  small  shoulder  is  usually  seen.  Below  this  point  the  oscillations 
continue  to  increase  in  size  and  then  to  de- 
crease, the  manometer  being  watched  all  the 
while.  The  point  at  which  the  oscillations 
are  maximal  is  the  minimal  or  dias- 
tolic blood-pressure.  Sometimes,  especially 
in  arteriosclerotics,  the  oscillations  decrease 
a  little  and  then  again  increase  at  about  10 
mm.  lower  pressure.  In  that  case  Erlanger 
has  shown  that  the  lower  point  or  second 
maximum  of  oscillations  is  the  one  cor- 
responding to  the  minimal  pressure. 

In  order  to  keep  these  records  perma- 
nent, Fontaine  marks  off  on  the  drum  the 
points  which  correspond  to  each  fall  of  5  or 
10  mm.  Hg  in  the  manometer.  These  marks 
are  made  by  means  of  one  of  the  tambours 
upon  the  polygraph  (Hirschf  elder)  attachment 
which  is  caused  to  vibrate  by  squeezing  a  small 
pipette  inserted  into  the  long  rubber  tube. 

This  apparatus  has  been  carefully  tested,  both  upon  animals  and  upon  mechanical 
models,  and  has  been  shown  to  give  accurate  results.  Of  course  it  cannot  be  used  unless 
the  muscles  of  the  arm  are  at  rest,  but  neither  can  any  other  sphygmomanometer,  without 
introducing  a  large  error.  The  readings  obtained  in  determining  both  maximal  and  mini- 
mal pressures  in  arteriosclerotics  are  too  high, 
but  this  error  is  also  universal  and  at  present 
unavoidable.  At  times  the  systolic  increase 
in  size  is  not  sudden,  but  this  can  usually  be 
remedied  by  pressing  the  lever  a  little  more 
tightly  than  before  against  the  drum.  Occa- 
sionally a  larger  or  smaller  capillary  outlet  is 
required  and  these  may  be  readjusted.    The 


Fig.  23. — Auscultatory  method  of  determin- 
ing blood-pressure,  as  used  with  the  Oliver  ap- 
paratus.    (Kindness  of  Hawksley  and  Son.) 


PW 


115 


Fig.  24a. — Diagram  showing  arrangement  of  Erlanger  apparatus.      (After  Howell.) 
Fig.  24b. — Curve  taken  with  the  Erlanger  blood-pressure  apparatus,  showing  the  points  of  maximal 
and  minimal  presssure. 

readings  obtained  by  Erlanger's  method  are,  as  a  rule,  about  5  mm.  higher  for  the  maximal 
(systolic)  pressure  than  by  the  broad  cuff  Biva-Rocci,  and  for  the  minimal  (diastolic) 
within  about  5  to  10  mm.  of  the  readings  by  the  method  of  Masing  and  Strasburger  as 
modified  by  the  writer  (Hirschf elder,  also  Brush).  Erlanger's  method  gives  results  suffi- 
ciently unequivocal  to  form  the  basis  for  a  research,  although  the  other  method  is  often 
quite  satisfactory. 


30 


DISEASES  OF  THE  HEART  AND  AORTA. 


Uskoff  s  Sphygmotonometer. — Uskoff  has  devised  a  slight  modification  of  this  instru- 
ment in  which  the  sphygmomanometer  and  the  Jaquet  cardiosphygmograph  are  combined. 
It  is  smaller  and  more  compact  than  the  original  instrument  of  Erlanger,  and  is  provided 
with  an  excellent  time-marker.  The  absolute  blood-pressure  is  recorded  automatically  by 
means  of  a  float  upon  the  mercury  manometer.  The  rod  extending  upward  from  the  float 
contains  perforations  corresponding  to  millimetres  of  mercury.  As  each  perforation  passes 
the  top  of  the  manometer  bulb  it  is  caught  by  a  pin  projecting  from  a  tambour,  which 
registers  upon  a  second  tambour  by  air  transmission.  Every  five  millimetres  a  wider  mark 
is  made.  Knowing  the  starting-point  the  absolute  pressure  corresponding  to  each  pulsa- 
tion is  easily  ascertained  and  the  record  thus  made  permanent.  Erlanger,  however,  has 
shown  that,  owing  to  the  construction  of  the  pressure  bulb,  it  is  not  as  accurate  as  his 
instrument. 

The  polygraph  tambours  and  time-marker  are  those  of  the  Jaquet  cardiosphygmo- 
graph, and,  though  not  of  the  greatest  delicacy,  they  are  quite  satisfactory  for  general  use. 
As  a  combined  instrument  the  Uskoff  apparatus  thus  presents  many  excellent  features. 

Gibson  (1907)  and  Sahli  (sphygmobolometer,  1907)  record  the  pulsations  in  the  cuff 
directly  by  the  movement  of  the  mercury  manometer,  by  which  they  do  away  entirely 
with  the  pressure  bag  and  the  tambour  of  the  other  instruments  and  record  the  pressure 


A 

B 

c 

D 

SOUND 

FAINT   SOUND 
OB  MURMUR 

LOUD, 

SHARP    SOUND 

DULL  THUDDING  SOUND, 
OR  SOUND    ABSENT 

Fig.  25. — Diagram  showing  the  effect  of  varying  degrees  of  compression  upon  the  excursion  of  the 
arterial  wall.  A,  pressure  in  the  cuff  above  the  maximal  arterial  pressure;  B,  between  the  maximal  and 
minimal  arterial  pressure;  C,  at  the  minimal  pressure;  D,  below  the  minimal  pressure. 

directly  in  millimetres  of  mercury.  For  pulses  of  large  amplitudes  their  instruments  are 
entirely  satisfactory,  but  with  smaller  pulses  the  inertia  of  the  mercury  column  is  too  great 
to  transmit  the  vibrations. 

Numerous  other  sphygmomanometers  have  been  devised,  notably  the  sphygmo- 
scope  of  Pal  for  visual  determination  of  pressure  by  the  movement  of  a  drop  of 
colored  liquid,  and  the  visual  (tonometer)  and  graphic  (tonograph)  methods  of  v.  Reckling- 
hausen, upon  the  same  principle  as  Erlanger's,  but  they  do  not  possess  any  special  advan- 
tages in  their  respective  spheres  of  usefulness  over  the  methods  given  above.  V.  Reckling- 
hausen's manometer  is,  moreover,  a  simple  metal  spring  manometer,  and  in  the  writer's 
experience  is  liable  to  undergo  great  deterioration. 


SIMPLER    METHODS    FOR    THE    DETERMINATION    OF    BLOOD-PRESSURE. 

Although  the  graphic  methods  are  indispensable  for  purposes  of  research, 
numerous  simpler  and  more  convenient  methods  of  considerable  accuracy 
are  available  for  the  determination  of  both  maximal  and  minimal  blood- 
pressure  in  ordinary  clinical  work.  Instruments  used  for  this  purpose  are 
in  the  main  mechanical  variations  of  the  original  Riva-Rocci  type  with  a 
cuff  not  less  than  12  cm.  wide.  The  greatest  difference  in  the  various  instru- 
ments lies  in  the  construction  of  the  manometer.  The  manometers  in  use 
in  the  various  instruments  are  of  four  types : 

1.  Ordinary  mercury  manometers : 

(a)  With  reservoir  (Riva-Rocci,  Cooke,  Stanton,  Lockhard-Mummery) . 

(b)  With  U-shaped  mercury  manometer  (Janeway,  Martin,  Faught). 

2.  Compressed-air  manometers  (Oliver,  Benedick). 

3.  Spring  manometers  (v.  Recklinghausen). 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


31 


PLATE  I. 


Rogers'  "Tycos"  aneroid  sphygmo- 
manometer. (Kindness  of  Taylor  In- 
strument Co.) 


Riva-Rocci  blood-pressure   apparatus  as  modified  by  Stanton. 
(Kindness  of  the  A.  H.  Thomas  Co.) 


Oliver's  compressed  air  sphygmomanometer.     (Kind-        V.  Recklinghausen  apparatus.  (After  v.  Reckling- 
ness  of  Hawksley  &  Son.)  hausen,  Arch.  f.  exper.  Path.  u.  Pharmacol.,  \v.) 


32  DISEASES  OF  THE  HEART  AND  AORTA. 

4.  Aneroid  (corrugated  metal  chamber  manometers)  (Rogers  (Tycos), 
Lauder  Brunton,  Pachon). 

Little  can  be  said  against  the  instruments  with  mercury  manometer 
except  that  their  size  (they  must  be  at  least  a  foot  in  length)  renders  them 
rather  cumbersome  for  house-to-house  practice.  There  is,  moreover,  with 
many  of  the  instruments  a  certain  liability  to  lose  some  of  the  mercury  in 
transportation  or  where  setting  up  the  instrument,  although  it  may  be  re- 
placed with  only  a  few  minutes'  inconvenience. 

Compressed=Air  Manometers. — The  compressed-air  manometers  consist  of  a  fine 
glass  tube  ending  in  a  glass  bulb.  The  tube  is  sealed  with  a  drop  of  mercury,  oil,  or  alcohol, 
which  moves  to  and  fro  in  answer  to  the  pressure  on  either  side  of  it.  A  scale  along  the 
tube  indicates  the  amount  of  pressure  corresponding  to  the  position  of  the  drop.  The  pres- 
sure of  a  cock  enables  the  observer  to  equalize  the  pressure  with  the  outside  air,  so  as  to 
remove  the  effects  of  change  in  temperature  and  barometric  pressure,  before  beginning 
the  compression.  These  air  manometers  are  absolutely  accurate, 
and  instruments  of  this  type  are  smaller  and  more  portable  than  the  mercury  manometers; 
but,  on  the  other  hand,  a  certain  amount  of  inconvenience  may  be  met  with  at  times  in 
adjusting  the  drop  which  serves  as  an  indicator. 

Spring  Manometers. — The  manometer  in  v.  Recklinghausen's  tonometer  is  con- 
structed on  the  same  principle  as  v.  Basch's  hollow  spring  manometer.  It  is  a  bent  tube 
of  metal  with  high  elasticity  and  is  closed  at  one  end.  When  the  pressure  of  air  within 
this  tube  is  increased,  the  tube  tends  to  straighten,  causing  the  free  end  to  move  through  an 
amplitude  which  varies  with  the  pressure.    This  movement  is  recorded  on  a  calibrated  dial. 

In  the  v.  Recklinghausen  apparatus,  in  contrast  to  most  of  the  others,  the  dial  is 
calibrated  in  centimetres  of  water  instead  of  millimetres  of  mercury;  and  hence  the  readings 
must  be  multiplied  by  1.36,  in  order  to  be  translated  into  the  usual  terms  of  blood-pressure 
recording;  or,  for  ordinary  purposes,  £-  of  the  Recklinghausen  reading  =  reading  in  milli- 
metres of  mercury. 

The  v.  Recklinghausen  instrument  is  rather  bulky  for  private  practice,  but  in  other  ways 
very  convenient  for  determination  both  of  maximal  and  of  minimal  blood-pressure.  The  chief 
objection  to  it  lies  in  the  fact  that,  like  all  spring  manometers,  the  metal  of  the  spring  is  liable 
in  the  course  of  time  to  undergo  changes  in  elasticity  so  that  it  no  longer  corresponds  even 
remotely  to  the  scale.  In  an  instrument  used  by  the  writer  at  the  Johns  Hopkins  Hospital 
this  error  amounted  in  less  than  two  years  to  more  than  thirty  centimetres  of  water. 

Aneroid  Manometers. — ■  The  aneroid  manometer,  in  which  the  pressure  acts  not  on 
a  spring  but  by  pressing  apart  the  walls  of  a  corrugated  metal  chamber  (Fig.  21),  was 
introduced  by  Marey  (1878).  It  is  smaller  and  more  convenient  of  construction  than  the 
spring  manometer,  so  that  instruments  of  this  type  may  be  carried  in  the  pocket,  and,  at 
the  same  time,  when  adequate  care  is  taken  in  the  preparation  of  metal,  it  retains  its 
accuracy  for  a  long  time.  For  the  personal  security  of  the  observer,  they  should  from  time 
to  time  be  compared  with  mercury  manometers.  The  writer  has  found  instruments  of 
the  Tycos  construction  entirely  free  from  variation  for  over  two  years,  and  still  longer 
periods  for  absolute  accuracy  are  on  record.  On  the  other  hand,  Bachmann  has  found 
differences  of  as  much  as  40  mm.  in  pressure  between  the  readings  made  with  Pachon  and 
the  Stanton.  Since  the  error  with  the  latter  should  not  be  more  than  10-15  mm.,  this 
shows  a  considerable  error  in  the  calibration  or  the  durability  of  the  Pachon  instrument. 
Drs.  Dandy  and  Engle  have,  moreover,  controlled  the  Tycos  instrument  with  the  Erlanger 
and  have  found  the  readings  to  be  accurate  within  5  mm.  of  mercury. 

Palpatory.— The  oldest  of  the  simpler  methods  for  the  determination  of  maximal 
or  systolic  pressure  consisted  in  determining  the  point  of  pressure  in  the  cuff  at  which  the 
radial  pulse  could  no  longer  be  felt  at  the  wrist  while  the  pressure  was  being  raised,  or  the 
point  at  which  it  returned  when  the  pressure  was  allowed  to  fall. 

This  method  is  in  most  cases  quite  satisfactory,  but,  as  shown  by  control  with  the 
Erlanger  apparatus,  it  usually  gives  results  5-10  mm.  too  low,  probably  because  the  radial 
artery  must  be  distended  somewhat  before  the  pulse  can  be  felt. 

The  minimal  or  diastolic  pressure  can  also  be  determined  by  palpation 
either  at  the  radial  (Strasburger)  or  at  the  brachial  near  the  bend  of  the  elbow  (Ehret). 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  33 

The  minimal  pressure  is  represented  by  the  point  above  which  the  pulse  begins  to  decrease 
in  size  as  the  pressure  in  the  brachial  is  gradually  raised,  or  that  at  which  the  pulse  is  of 
largest  volume  and  most  collapsing  quality  as  the  pressure  in  the  cuff  is  allowed  to  fall. 

This  method  is  often  quite  accurate  for  minimal  pressure,  but  the  estimation  is  highly 
subjective.  In  palpation  at  the  wrist  the  best  results  are  obtained  by  pressing  the  finger 
tips  against  the  radius  and  allowing  the  artery  to  beat  against  the  pads  of  the  fingers. 

Oscillatory  Determination. — By  watching  the  oscillations  of  the  column  of  mercury  in 
one  of  the  mercury  manometer  instruments,  or,  still  better,  by  watching  the  movement  of  the 
needle  or  indicator  drop  in  the  other  forms  of  instrument,  it  is  usually  possible  to  determine 
the  minimal  or  diastolic  blood-pressure  with  great  accuracy  at  the  point  at  which  the  oscilla- 
tions are  of  greatest  excursion  (Janeway,  1901).  When  the  pulse  is  very  small,  however, 
this  method  is  not  satisfactory  in  instruments  with  the  mercury  manometer,  but  it  is  of 
very  general  application  in  those  with  aneroid  chamber  and  dial  (Rogers'  "Tycos,"  Lauder 
Brunton,  Pachon),  in  which  the  estimation  can  be  made  quickly  and  with  great  certainty. 

The  maximal  pressure  is,  as  a  rule,  less  definite,  but  is  represented  by  the  point  at 
which  the  excursions  suddenly  increase  in  size  as  the  pressure  falls.  As  for  the  minimal 
pressure,  this  method  of  determination  is  most  satisfactory  in  instruments  without  mercury. 

Auscultatory  Method. — Korotkow  (1905)  introduced  a  very  ingenious  method  for 
determining  both  the  maximal  and  the  minimal  pressure,  which  is  the  quickest  and  most 
accurate  of  all  the  clinical  methods  now  in  use.  He  called  attention  to  the  fact  that  when 
the  pressure  within  the  cuff  is  raised  above  the  maximal  pressure,  no  sound  can  be  heard 
with  a  stethoscope  placed  over  the  brachial  artery  at  the  bend  of  the  elbow.  As  the  pres- 
sure falls  below  the  maximal,  however,  a  beat  comes  through  beneath  the  cuff,  expands  the 
artery  beneath  the  stethoscope,  and  causes  a  clicking  or  faint  pistol-shot  tone  to  be  heard 
in  the  stethoscope.  As  the  pressure  falls  and  the  artery  expands  more  and  more  with  each 
beat,  the  sound  increases  in  magnitude  and  is  often  accompanied  or  replaced  by  a  murmur 
as  the  blood  flows  through  a  narrowed  stream-bed.  Where  the  pressure  within  the  cuff  is 
just  at  the  diastolic,  however,  the  artery  is  alternately  completely  collapsed  in  diastole  and 
filled  to  its  utmost  in  systole,  so  that  at  this  point  the  sound  becomes  loudest  and  sharpest. 
Below  the  diastolic  pressure  the  artery  remains  filled  during  diastole  and  the  sound  sud- 
denly changes  from  a  sharp  to  a  dull  and  booming  quality.  It  usually  diminishes  and  dis- 
appears a  few  millimetres  below  the  diastolic  pressure. 

The  auscultatory  method  is  very  accurate  indeed.  In  a  series  of  1200  determinations 
by  Schumpf  and  Zabel  it  coincides  almost  exactly  with  oscillatory  and  graphic  determina- 
tions with  the  von  Recklinghausen  apparatus;  in  another  by  Drs.  Engle  and  Allen,  at  the 
Johns  Hopkins  Hospital,  in  which  it  was  controlled  with  the  Erlanger  instrument,  the 
maximal  pressure  was  found  to  be  absolutely  accurate  and  the  minimal  within  5  mm.  of 
the  Erlanger.  Hooker  and  Southworth  (Arch.  Int.  Med.,  1914,  xiii,  384)  recorded  the 
arterial  sounds  graphically  and  found  the  readings  in  close  accord  with  records  made  simul- 
taneously with  the  Erlanger  apparatus.  Ehret,  who  has  reported  over  1000  cases,  finds 
that  in  aortic  insufficiency  the  point  at  which  the  pulse  in  the  brachial  artery  at  the  elbow 
(arteria  cubitalis)  is  maximal  represents  the  exact  minimal  or  diastolic  pressure.1 

For  the  exigencies  of  private  practice,  therefore,  the  most  satisfactory  apparatus  is  the 
small  pocket  instrument  with  the  aneroid  type  ("Tycos,"  Lauder  Brunton),  using  both  the 
auscultatory  and  oscillatory  methods  for  the  determination  of  maximal  and  minimal  pressure. 

Normal  Blood=pressures. — For  young  persons  (19  to  25  years  old)  in  the  reclining 
posture  the  average  blood-pressure,  according  to  Erlanger,  is  maximal  110  mm.,  minimal 
65  mm.,  pidse-pressure  45  mm.  In  general,  the  limits  in  normal  individuals  at  rest  are 
maximal  110  to  135  mm.,  minimal  60  to  90  mm.,  pulse-pressure  30  to  45  mm. 

Woley  records  the  following  figures  obtained  from  the  examination  of  1000  healthy 
individuals  with  the  Tycos  instrument: 

Age 15  to  30      31  to  40      41  to  50      51  to  60 

Average  maximum  pressure 122  127  130  132 

The  upper  limit  of  the  normal,  according  to  his  figures,  ranges  from  140  between 
15  and  30  years  to  155  at  60  years.  Barach  and  Marks  (Arch.  Int.  Med.,  1914,  xiii,  648) 
found  maximal  blood-pressure  below  150,  minimal  below  100  in  90  per  cent,  of  656  normal 
young  men. 

1  Warfield  has  shown  that  with  high  diastolic  pressures  (130-160  mm.)  the  auscultatory 
reading  is  often  20  mm.  too  low. 
3 


34  DISEASES  OF  THE  HEART  AND  AORTA. 

In  females  the  average  blood-pressures  were  8  mm.  lower  than  in  males.1 
According  to  Musgrave  and  Simson,  a  low  blood-pressure  is  common  in  the  tropical 
countries,  probably  owing  to  increased  vasodilation. 

Trumpp  has  found  that  the  blood-pressure  in  infants  is  80  mm.  Hg.  In  early  child- 
hood and  throughout  the  first  decade  it  is  usually  below  90  mm.,  and  before  puberty  ranges 
between  90  and  110  mm. 

MECHANISM    OF   THE    CIRCULATION. 

Pressure  in  Different  Parts  of  the  Vascular  System. — Dawson  has  shown 
that  the  mean  pressure  is  very  constant  throughout  the  arterial  system, 
while  the  maximal  pressure  falls  greatly  as  one  approaches  the  periphery. 
The  minimal  pressure  is  also  quite  constant.  As  one  approaches  the  periph- 
ery the  maximal  pressure  falls  quite  rapidly  to  meet  the  minimal,  and  in 
the  smallest  arteries  they  are  practically  equal.  Hence  the  pressure 
in  these  arterioles  does  not  differ  greatly  from 
the  minimal  pressure  in  the  aorta,  although  it  is  certainly 
a  few  millimetres  less.  The  minimal  arterial  blood-pres- 
sure therefore  represents  the  peripheral  resistance 
(vasomotor  changes),  while  the  maximal  pressure  approxi- 
mates the  intraventricular  pressure.  Marey  (1.  c.)  has 
shown  that  his  approximation  is  closest  when  peripheral  resistance  is  high. 
Accordingly  the  pulse-pressure,  or  difference  between  the  two,  represents 
the  head  of  pressure  tending  to  drive  the  blood  from  the  heart  through  the 
aorta  and  large  arteries  onward  into  the  peripheral  arterioles.  The  fall 
in  pressure  may  be  compared  to  a  cascade  whose 
first  descent  is  from  heart  to  arterioles,  whose 
second  from  arterioles  to  capillaries,  and  whose 
third  is  from  the  capillaries  back  to  the  heart.  The 
actual  head  of  pressure  at  any  point  in  the  arteries  is  never  equal  to  the 
total  head  (maximal  pressure)  which  would  be  active  if  the  fall  were  unin- 
terrupted by  interposed  resistance,  but  is  more  nearly  equal  to  the  pulse- 
pressure. 

Hill  and  his  collaborators  Flack  and  Rowlands  have  shown  that  the  pressure  recorded 
over  the  femoral  arteries  of  healthy  men  is  higher  than  that  recorded  in  the  brachial 
arteries  when  the  subject  is  sitting  up.  The  difference  is  then  due  to  the  height  of  the 
arm  above  the  thigh  and  is  represented  by  a  column  of  mercury  which  would  exactly 
balance  this  column  of  blood.  When  the  subject  is  lying  horizontal,  the  difference  dis- 
appears, although  Dawson  has  found  that  in  dogs  the  maximal  pressure  in  the  femoral 
artery  is  slightly  higher  than  that  in  the  brachial.  This  is  due  in  part  to  the  fact  that  the 
femoral  pressure  is  an  end-pressure,  while  the  brachial  pressure  is  a  lateral  pressure  with 
reference  to  the  aorta,  and  in  part  due  to  conditions  of  elasticity  and  oscillation  of  the 
arterial  walls. 

In  persons  with  aortic  insufficiency  or  arteriosclerosis,  however,  the  difference  still 
remains  when  the  subject  lies  down,  partly  owing  to  the  fact  that  the  large  pulse-waves 
in  the  femoral  artery  are  conducted  better  than  the  smaller  ones  in  the  brachial  artery, 
and  partly  owing  to  the  increased  tonus  of  the  arterial  walls.  The  latter  condition  can 
cause  a  discrepancy  of  over  100  mm.  Hg,  much  of  which  can  be  made  to  disappear  when 
the  arteries  are  relaxed  by  immersing  the  limb  in  hot  water.  In  a  case  recorded  by  Hoover, 
owing  to  local  arterial  spasm,  the  blood-pressure  in  the  brachial  arteries  was  245  mm., 
while  that  in  the  legs  was  162  mm. 

1  Excitement  or  worry,  accompanying  the  first  examination,  may  raise  the  blood- 
pressure  temporarily  to  150  or  160  mm.  Hg,  though  it  may  be  normal  hours  later. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


35 


FACTORS  DETERMINING  MAXIMAL  AND   MINIMAL   PRESSURE. 

The  fall  in  blood-pressure  during  diastole  continues  until  the  next  sys- 
tole takes  place.  If  the  pulse-rate  is  rapid  the  diastole  is  short  and  the  blood- 
pressure  has  not  time  to  fall  much ;  hence,  other  things  being  equal,  minimal 
pressure  rises  and  pulse-pressure  falls  as  pulse- 
rate  increases. 


jpIG>  26. Diagram  showing  the  maximal  and  minimal  pressures  in  various  parts  of  the  circulatory  system. 

Erlanger  and  Hooker  have  claimed  that  under  ordinary  conditions  the  product  of 
pulse-pressure  multiplied  by  pulse-rate  is  tolerably  con- 
stant, and  represents  roughly  the  velocity  of  blood  flow,  although  Y.  Henderson,  the 
writer,  and  others  have  proved  that  this  is  very  inaccurate  and  may  involve  an  error  of 


Fig.  27. — Diagram  showing  effects  of  vasoconstriction,  vasodilation,  increased  and  decreased  force 
of  ventricular  contraction  upon  the  maximal  and  minimal  blood-pressures  and  upon  the  form  of  the  pulse. 
SYS,  systole;    DIAS,  diastole;    ART,  large  arteries;    AOL,  arterioles;    CAP,  capillaries. 


more  than  50  per  cent.  The  curves  of  Dawson  and  Gorham,  who  claim  that  the  pulse- 
pressure  is  a  "reliable  index"  of  the  systolic  output  (per  beat)  of  the  ventricles,  indicate 
that  these  writers  referred  to  qualitative  rather  than  quantitative  changes.  Henderson 
has  shown,  however,  that  within  a  certain  range  of  pulse-rate  the  ventricular  output  per 
beat  varies  inversely  as  the  pulse-rate.    Within  this,  the  usual,  range  the  velocity  of  blood 


36  DISEASES  OF  THE  HEART  AND  AORTA. 

flow  is  greatest.  At  rates  below  it  time  is  lost  during  the  periods  of  diastasis;  above  it  the 
successive  systoles  encroach  upon  the  period  of  ventricular  filling  and  cut  short  the  inflow. 
Within  the  limits  indicated  by  Henderson,  Erlanger  and  Hooker's  index  of  velocity  may 
often  be  correct,  especially  when  there  are  no  extreme  vasomotor  changes. 

If  the  peripheral  vessels  dilate,  more  blood  can  flow  through  in  the  same  time,  and 
hence,  when  the  pulse-rate  is  constant,  vasodilation  brings  about  fall  in 
minimal  pressure,  rise  in  pulse-pressure;  vasoconstriction 
brings  about  rise  in  minimal  pressure,  fall  in  pulse-pres- 
sure, but  a  change  in  maximal  pressure  following  the  change  in  minimal  usually  occurs 
reflexly.  Fig.  26  shows  the  various  relations  of  maximal,  minimal,  and  pulse-pressures  to 
the  state  of  the  intraventricular  pressure. 

Lauder  Brunton  has  shown  that  the  arterioles  and  capillaries  in  man  dilate  and  con- 
tract rhythmically  at  a  rate  of  about  once  in  twenty  seconds.  This  can  be  observed  by 
watching  the  changes  in  the  breadth  of  the  red  streak  left  upon  the  forehead  after  rubbing 
it  with  the  finger-nail. 

Changes  in  the  peripheral  vessels  can  be  recorded  by  placing  the  patient's  hand  in  a 
plethysmograph  which  is  sealed  hermetically  about  the  forearm  by  means  of  a  rubber 
cuff.  The  free  space  in  the  plethysmograph  is  filled  with  water,  which  runs  in  or  siphons 
out  of  a  tube  leading  to  a  movable  test-tube.  Changes  in  volume  of  the  arm  are  recorded 
by  upward  or  downward  movements  of  the  test-tuba. 

Determination  of  the  Velocity  of  Blood  Flow  in  the  Arm. — By  the  use  of  a  slight 
modification  of  the  plethysmograph  it  is  possible  to  make  quantitative  studies  of  the  amount 
of  blood  flowing  through  the  arm.  This  method,  first  suggested  by  Brodie  and  Russell, 
has  been  applied  clinically  by  Hewlett  and  van  Zwaluwenburg  with  excellent  results.  The 
usual  form  of  arm  plethysmograph  is  connected  with  a  Brodie's  bellows  recorder  or  a  large 
tambour,  and  a  narrow  Riva-Rocci  blood-pressure  cuff  is  placed  on  the  upper  arm  just 
above  the  plethysmograph.  The  pressure  in  this  cuff  is  suddenly  raised  to  a  level  a  little 
below  the  diastolic  arterial  pressure  by  opening  a  stop-cock  from  a  pressure  bottle.  When 
the  cuff  is  thus  inflated,  blood  can  enter  the  arm  through  the  arteries  but  cannot  leave  it 
through  the  veins,  and  the  amount  of  increase  in  size  corresponding  to  this  stagnation  is 
indicated  by  a  rise  of  the  recording  lever  of  the  bellows.  The  amount  of  the  rise  can  be 
calibrated  by  letting  water  flow  into  the  tambour  or  into  a  suitably  connected  vessel. 

This  rise  is  at  first  quite  sudden,  and  when  controlled  by  a  time-marker  it  may  be 
used  as  an  index  of  the  velocity  of  flow  through  the  arm.  Soon,  however,  the  pressure  in 
the  veins  rises,  reaches  the  diastolic  pressure,  and  blood  begins  to  flow  off  beneath  the  cuff, 
and  the  slope  of  the  curve  becomes  more  gradual.  The  steep  portion  of  the  curve  may  be 
used  to  determine  the  volume  of  blood  flow  per  second  or  per  minuie.  The  normal  figures 
may  be  regarded  as  between  2  and  8  cc.  per  minute  per  100  Gm.  of  arm  (determined  by 
the  volume  of  water  displaced  by  the  arm  up  to  the  level  to  which  it  is  inserted  in  the 
plethysmograph).  The  velocity  may  increase  up  to  10  or  12  cc.  during  perspiration  or 
after  exercise,  or  it  may  fall  to  about  1  cc.  upon  exposure  to  the  cold. 

G.  N.  Stewart  (Heart,  iii)  has  obtained  figures  for  velocity  of  flow  which  accord  well 
with  Hewlett's  by  calculating  the  velocity  from  the  amount  of  heat  given  off  by  the  hand 
when  immersed  in  a  calorimeter.  This  is  constructed  of  a  copper  tin  inner  vessel  separated 
from  an  outer  tin  jacket  by  a  space  filled  with  broken  cork.  The  inner  vessel  is  filled  with 
water  at  30°  C,  the  hand  immersed  in  it  and  escape  of  heat  from  above  is  prevented  by 
a  tightly-fitting  collar  of  saddle  felt  fitting  tightly  about  the  wrist.  Velocity  of  flow  is 
calculated  according  to  the  following  formula: 

D       ft       f  hi     H  fl       _  Rise  of  temperature  (in  6  minutes) 1 

^  Rectal  temperature  (C.)  minus  30    Specific  heat  of  blood  (about 

0.9) 

Both  these  methods  are  relatively  simple  and  easy  of  application  and  both  give  data 
which  are  quite  as  important  as  those  which  are  obtained  from  blood-pressure  and  pulse. 
Hewlett's  method  is  of  further  value  because  it  enables  one  to  determine  the  actual  move- 
ment of  blood  into  and  out  of  the  arm  with  each  heart-beat.  In  other  words,  it  reveals  also 
the  significance  of  the  pulse-wave  (see  page  65),  whereas  Stewart  gives  only  the  measure 
of  the  total  blood  flow  without  imparting  further  information. 

Work  of  the  Heart. — Since  the  intraventricular  pressure  is  almost  con- 
stant throughout  systole,  it  is  evident  that  the  work  done  by  the  heart  is 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


37 


tolerably  constant  through  this  period;  and  since  no  work  is  done  during 
diastole,  it  is  evident  that  the  work  of  the  heart  per  minute  may  be  esti- 
mated, at  least  roughly,  by  the  product  of  intraventricular  pressure  X  dura- 
tion of  systole  X  pulse-rate.1 

Martin  and  Donaldson,  and  later  W.  G.  MacCallum,  have  shown  that  the 
work  of  the  heart  is  more  or  less  proportional  to  the  amount  of  blood  flowing 
through  the  coronary  arteries,  and  G.  S.  Bond  has  found  that  usually  the 
latter  runs  almost  entirely  parallel  to  the  general  blood-pressure;  so  that  a 
rise  in  general  blood-pressure  thus  compensates  at  once  up  to  a  certain  limit 
for  the  increased  work  that  it  is  imposing  on  the  heart. 


Fig.  28. — Diagram  of  apparatus  for  determining  the  rate  of  blood  flow  through  the  arm.  (A.  W. 
Hewlett  and  G.  Van  Zwaluwenburg.)  The  arm  is  placed  in  the  plethysmograph,  P,  the  opening  of  which 
is  closed  by  a  piece  of  rubber  dam,  D,  and  the  connection  with  the  skin  made  tight  with  soapsuds.  The 
narrow  pressure  cuff,  C,  is  placed  around  the  arm  about  3  cm.  above  the  opening  into  the  plethysmograph. 
The  pressure  cuff  is  inflated  by  opening  the  stop-cock  connecting  it  with  the  large  bottle,  A,  in  which  the 
pressure  has  previously  been  raised  by  the  rubber  bulb,  B.  Pressures  are  read  by  the  spring  manometer,  M . 
The  plethysmograph  is  connected  with  the  volume  recorder,  V,  which  writes  upon  a  moving  drum.  Air  can 
be  let  out  of  the  system  by  the  stop-cock,  X,  and  water  can  be  introduced  from  the  burette,  Y,  so  that  the 
writing  point  of  the  volume  recorder  can  be  adjusted  at  will.  The  stop-cock,  Z,  serves  to  disconnect  the 
plethysmograph  from  the  recording  apparatus  during  adjustments  of  the  former.  The  recording  apparatus 
is  graduated  by  allowing  5  cc.  of  fluid  at  a  time  to  flow  in  from  the  burette,  and  marking  the  elevation  of 
the  volume  recorder  thus  produced. 

The  value  of  blood-pressure  determinations  as  an  index  of  the  func- 
tional power  of  the  heart  will  be  discussed  on  page  199  in  relation  to  exercise 
and  cardiac  overstrain. 


VARIATIONS  IN  BLOOD-PRESSURE  UNDER  PHYSIOLOGICAL 
CONDITIONS. 

1.  Change  of  position.  Erlanger  and  Hooker  have  shown  that  the  minimal 
pressure  usually  rises  considerably  and  the  pulse-pressure  always  decreases 
upon  standing  after  having  lain  down.  The  pulse-rate  increases  accordingly.  They  have 
shown  that  these  effects  are  entirely  due  to  the  rule  of  gravity. 

1  For  more  complicated  and  perhaps  more  accurate  formulae  cf.  Tigerstedt  (1.  c). 

Pulse-pressure 
The  ratio  Maximal    (systolic)  pressure  or  Blood-pressure  coefficient  is  used  more  or 
less  as  an  index  of  circulatory  conditions.    Its  significance  may  be  given  as  follows: 
P.  P.  =  P.  Rate  =  Velocity)  . 

ovsf  p  =p  Rate  =  Work  C  =  Efficiency  of  heart  as  a  pump.    In  a  normal  individual 

this  coefficient  is  25  per  cent,  to  35  per  cent. 


38  DISEASES  OF  THE  HEART  AND  AORTA. 

2.  After  meals  the  maximal  pressure  and  pulse-pressure 
are  increased,  also  the  pulse-rate,  and  the  minimal  pressure  may  be  increased,  but 
to  a  less  extent.    The  circulation  is  accelerated. 

3.  After  exercise  the  effect  is  the  same  as  after  meals,  only  more  marked. 
When  exercise  is  continued  to  the  point  of  fatigue  the  pressures  fall,  the  pulse-rate  falls 
also,  and  the  circulation  is  slowed  (Schott,  Masing,  Cabot,  Bowen).    (See  page  197.) 

4.  Upon  sensory  stimulation  the  vasomotor  centre  in  the  medulla 
usually  responds  by  constricting  the  peripheral  vessels,  and  the  pressure,  especially  the 
minimal  pressure,  rises.  The  pulse-rate  usually  quickens  also.  There  are  great  variations 
in  the  response  of  different  healthy  individuals  to  pain  sensations.  Dr.  A.  Berg,  under  the 
writer's  direction,  has  tested  the  effect  of  pinching  the  ear  upon  the  blood-pressure  of 
healthy  individuals,  and  has  found  in  some  persons  a  rise  of  blood-pressure 
amounting  to  10  to  20  mm.  Hg,  in  others  no  effect,  in  others  a  fall  of  about  10  mm.  Too 
intense  stimuli  produce  shock.  Mental  exertion  has  a  similar  effect — a  definite 
vasoconstriction  setting  in,  which  is  shown  by  the  shrinkage  of  the  arm  in  a 
plethysmograph.  Zabel  has  shown  that  the  rise  in  blood-pressure  is  proportional  to  the 
amount  of  mental  effort.  For  example,  a  theological  student  could  translate  a  few  lines 
of  Caesar  to  which  he  was  accustomed  without  any  change  in  blood-pressure,  while  the 
calculation  of  17  X  18  caused  his  blood-pressure  to  rise  21  mm.  Hg  (28  cm.  H20).  On  the 
other  hand,  a  young  merchant  was  able  to  do  various  calculations  without  change  of  blood- 
pressure,  whereas  an  attempt  at  translation  caused  a  rise  of  16.5  mm.  (22  cm.  H20). 

Cannon  and  de  la  Paz  have  demonstrated  that  the  psychic  rise  in  blood-pressure  is 
due  to  a  true  psychic  secretion  of  adrenalin,  for  they  found  in  the  cat  that  the  blood  obtained 
from  a  cannula  which  they  introduced  through  the  femoral  vein  up  the  vena  cava  to  the 
level  of  the  adrenal  vein  contained  more  adrenalin  after  the  cat  had  been  excited  by  the 
presence  of  a  dog  than  it  did  when  the  cat  was  quiescent.  They  determined  the  amount 
of  adrenalin  by  the  inhibition  of  the  rhythmic  contractions  of  strips  of  perfused  origin 
uterine  muscle  which  occurs  whenever  adrenalin  is  added  to  the  perfusion  fluid  in  even 
infinitesimal  quantities. 

5.  I  n  sleep  the  opposite  effects  are  seen:  there  is  a  general  vasodilation 
and  a  fall  in  minimal  blood-pressure  (Howell,  Brush,  and  Fayerweather). 
There  is  probably  also  a  slight  fall  in  maximal  pressure. 

VARIATIONS  IN  BLOOD-PRESSURE  UNDER  PATHOLOGICAL 
CONDITIONS. 

ASPHYXIA   AND   THE   EFFECT   OF   EXCESS   OF   CO2. 

When  the  heart  fails  the  circulation  is  slowed  and  the  blood  becomes 
incompletely  aerated  and  overloaded  with  C02  (f.  Bohr).  These  conditions 
closely  simulate  the  conditions  present  in  asphyxia  (Traube),  or  after  breath- 
ing an  atmosphere  overladen  with  C02  (Klug  has  shown  that  the  effect  of 
these  is  quite  similar). 

Experimental  Asphyxia. — The  conditions  as  observed  in  experimental 
asphyxia  somewhat  foreshadow  those  due  to  accumulation  of  C02  from  heart- 
failure.  The  blood-pressure  changes  in  asphyxia  have  been  most  carefully 
studied  by  Konow  and  Stenbeck  in  Tigerstedt's  laboratory,  who  found  as- 
phyxiation in  rabbits  resulting  in  the  following  series  of  events : 

1 .  At  the  beginning  of  asphyxia  the  vasomotor  and  cardiac  centres 
in  the  medulla  are  stimulated,  as  is  also  the  inhibitory  centre.  Blood- 
pressure  rises  and  the  pulse  is  slowed.  (Cameron  has  shown  that,  on 
the  other  hand,  the  tonicity  of  the  heart  muscle  promptly  decreases  with  the 
first  stage  of  asphyxia  and  remains  diminished  throughout.) 

2.  As  asphyxia  continues,  the  effect  of  slowing  of  the  pulse  exceeds  that  of  the  rise 
of  pressure  and  the   blood-pressure   falls. 

3.  This  condition  slows  the  circulation  still  more,  C02  accumulates  in  the  blood, 
bathing  the  vasomotor  centre,  the  latter  stimulates  the  arterioles  to  still  further  constric- 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


39 


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tion,  the  vagus  can  no  longer  overcome  these  effects,  and  in  spite  of  its  continued  action 
the  pulse   quickens  and  blood-pressure   again   rises. 

4.  The  activity  of  the  vasomotor  centre  diminishes  while  the  vagus  centre  remains 
at  maximal  activity,  and  the  pulse-rate  again  slows  and  blood-pres- 
sure  again  falls. 

5.  The  vagus  centre  fatigues,  the  ac-  £ 
cessory  vasomotor  centres  in  the  spinal  =>  £ 
cord  are  again  stimulated,  and  blood-  <  " 
pressure    and    pulse-rate    again             zg 

•  2  o 

rise.  ^z 

6.  Conductivity  of  the  heart  dimin-  ={  < 
ishes,  occasional  beats  are  dropped  by  the  pj  a 
ventricle,     blood-pressure     and  !2  ** 
pulse-rate    fall,    and   the   animal 
dies   at   this   stage    unless  respiration  is 
promptly  restored. 

Occasionally  in  asphyxia  periodic 
changes  in  rhythm  of  the  heart  occur, 
such  as  have  been  described  by  Luciani 
in  frogs  and  by  Langendorff  in  cats. 
These  irregularities  occur  when  the  vagi 
are  sectioned  as  well  as  when  they  are 
active;  this  also  occurs  when  the  animal 
is  made  to  breathe  an  excess  of  CO2 
(Klug).  When,  however,  the  vagi  are 
inactive  (cut),  the  rise  of  blood-pressure 
in  asphyxia  is  continuous  from  the  onset 
until  the  vasomotor  centres  fail  (i.e.,  in 
the  fourth  stage).  When  the  cervical 
nerves  have  been  cut  and  the  vagi  are 
active,  there  is  an  immediate  fall  in  both 
blood-pressure  and  pulse-rate;  the  rise  in 
blood-pressure  sets  in  much  later  when 
the  accessory  vasomotor  centres  in  the  spinal  cord  are  stimulated,  or  the  animal  may 
die  if  these  fail  to  respond. 


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Fig.  29. — Diagram  showing  the  curve  of  blood- 
pressure  during  asphyxia.  (Schematic,  illustrating 
the  results  of  Konow  and  Stenbeck.)  N,  normal ; 
BP,  blood-pressure  ;   PR,  pulse-rate. 


BLOOD-PRESSURE  IN  VARIOUS  DISEASES. 

Importance  of  Determining  the  Mechanism  Producing  the  Change. — 

Variations  in  blood-pressure  occur  not  only  in  conditions  of  health  but  still 
more  under  pathological  conditions.  As  will  be  seen,  the  mechanism  which 
brings  these  changes  about  is  not  always  a  simple  one,  and  the  causal  factor 
may  not  be  affected  by  merely  resorting  to  therapeutic  methods  which  lower 
a  high  blood-pressure  or  raise  a  low  one.  It  is  therefore  necessary  for  the 
clinician  to  investigate  as  far  as  possible  the  condition  of  the  vasomotor 
nerves,  the  strength  of  the  heart-beat,  to  determine  also  whether  the  blood 
is  properly  aerated,  and  learn  whether  the  kidneys  are  performing  their 
function  properly,  before  proceeding  to  symptomatic  treatment  of  high  or 
low  blood-pressure  when  the  cause  is  in  any  way  obscure. 


DISEASES   WITH   HIGH   BLOOD-PRESSURE    (HYPERTENSION). 

The  following  represents  the  typical  blood-pressure  findings  in  various 
diseases.    In  exceptional  cases  more  extreme  variations  are  seen. 

1.  Nephritis  (discussed  below) ,  especially  the  chronic  forms  (maximal  pressure  160  to 
220,  minimal  120  to  160,  pulse-rate  50  to  80).     High  blood-pressure  is  common  in  both 


40  DISEASES  OF  THE  HEART  AND  AORTA. 

parenchymatous  and  interstitial  cases.  Passler  and  Heineke  found  that  in  animals  from 
which  almost  all  the  kidney  substance  had  been  removed,  blood-pressure  rose  pari  passu 
with  the  occurrence  of  signs  of  renal  insufficiency  in  the  metabolism. 

Excellent  reviews  of  this  subject  have  recently  been  published  by 
T.  C.  Janeway  and  by  Pearce.  There  seems  to  be  a  striking  parallelism 
between  continuous  high  blood-pressure  and  oversecretion  of  the  adrenals, 
sometimes  leading  to  an  hypertrophy  of  the  latter  (see  page  42). 

In  acute  nephritis  the  blood-pressure  may  not  rise,  but  Buttermann  reports 
a  case  of  scarlatinal  nephritis  where  a  rise  of  50  mm.  heralded  the  onset  of  the  nephritis. 
Here  it  is  of  diagnostic  and  prognostic  importance. 

In  uraemia  blood-pressure  rises,  at  the  beginning  of  the  attack,  but  may 
gradually  fall  a  few  days  before  a  fatal  termination  (Laqueur).  Gradual  fall  in  blood- 
pressure  also  accompanies  amelioration.  Engel  finds  that  there  is  no  rise  in  the  mildest 
cases  of  nephritis,  but  that  the  rise  of  pressure  runs  parallel  to  the  severity  of  the  disease 
until  the  terminal  fall  sets  in  from  cardiac  weakness. 

2.  Arteriosclerosis. — Increased  blood-pressure  (maximal  150  to  170,  minimal  110  to 
130,  pulse  60  or  over)  is  the  rule  in  arteriosclerosis,  though  there  are  occasional  exceptions 
where  the  maximal  pressure  does  not  exceed  or  even  reach  110  mm.  (Israel).  (See  also 
chapter  on  Arteriosclerosis.) 

3.  Lead  Poisoning  (plumbism). — Acute  and  chronic  forms  are  usually  associated  with 
high  blood-pressure,  as  in  arteriosclerosis,  often  with  vasomotor  crises. 

4.  Chronic  Hypertrophy  of  the  Heart  from  other  causes,  as  in  athletes,  or  as  the 
result  of  smoking  in  excess,  of  compensated  heart  lesions,  etc.  (maximal  pressure  may  reach 
145  mm.,  minimal  90  to  110  mm.,  pulse-rate  normal  or  increased). 

5.  Aortic  Insufficiency  is  often  but  not  always  associated  with  high  maximal  pres- 
sure (maximal  pressure  170  to  220  mm.  Hg,  minimal  60  to  140,  pulse-rate  usually  increased, 
being  even  as  high  as  120).  This  is  usually  associated  with  arteriosclerosis.  In  young 
individuals,  as  in  experimental  aortic  insufficiency  in  animals,  the  maximal  pressure  is 
usually  little  changed,  the  minimal  pressure  lowered  (maximal  120  to  130,  minimal  50  to 
60,  pulse-rate  normal  or  increased). 

6.  Conditions  associated  with  increased  pressure  in  the  cranial 
cavity  (meningitis,  apoplexy,  cerebral  thrombosis,  frac- 
ture of  the  skull,  intracranial  hemorrhage,  rapidly  growing 
brain  tumors,  some  cases  of  uraemia,  Jacksonian  epilepsy). 
Maximal  blood-pressure  may  rise  to  300  or  400  mm.  Hg,  minimal  pressure  to  160  or  over, 
pulse-rate  slow,  60  or  under.  Cushing  has  shown  that  when  the  intracranial  pressure  is 
raised  above  the  blood-pressure,  the  ansemia  of  the  vasomotor  centre  brings  about  a  tre- 
mendous vasoconstriction  and  action  of  the  augmentor  fibres  in  increasing  the  strength 
of  the  heart-beat.  The  blood-pressure  rises  in  successive  stages  (Traube-Hering  waves) 
until  the  mean  pressure  exceeds  the  intracranial  pressure.  The  rise  of  blood- 
pressure  expresses  the  need  of  the  brain  for  blood;  to  coun- 
teract the  vasoconstriction  with  nitrites  or  other  vaso- 
constrictors or  by  venesection  only  increases  the  task  of 
the  heart.  The  only  medical  treatment  which  aids  it  at  all  is  administration  of 
atropine  to  paralyze  the  vagi,  quicken  the  heart,  and  permit  the  pressure  to  rise  more 
readily.  Lumbar  puncture  helps  somewhat  by  removing  the  excess  of  intracranial  fluid. 
If  this  does  not  suffice,  Cushing  advises  surgical  interference  in  many  cases,— a  flap  of  the 
skull  being  lifted  temporarily  in  order  to  relieve  the  intracranial  tension  and  to  allow  the 
blood-pressure  to  fall.  This  procedure  is  almost  devoid  of  danger  in  the  hands  of  a  surgeon 
whose  asepsis  is  perfect,  but  very  dangerous  if  it  is  imperfect,  and  this  point  alone  will 
often  decide  the  advisability  or  inadvisability  of  the  operation. 

7.  Attacks  of  Idiopathic  Epilepsy  are  associated  with  very  high  blood-pressure  and 
slow  pulse.  The  blood-pressure  falls  within  a  few  minutes  after  the  fit,  which  assists  to 
differentiate  it  from  uraemia  (Pilcz). 

8.  Vascular  Crises.— Pal  has  described  an  important  group  of  cases  associated  with 
crises  of  high  blood-pressure  due  to  vasoconstriction.  Among  these  he  classes  uraemia, 
certain  cases  of  arteriosclerosis,  especially  with  abdominal  and  cardiac  symptoms,  and 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


41 


especially  the  tabetic  visceral  crises  with  intense  pain.  He  has  shown  that  these  as  well  as 
attacks  of  lightning  pains  are  associated  with  marked  vasoconstriction  and  rise  in  blood- 
pressure,  and  states  that  they  are  even  relieved  by  the  administration  of  nitroglycerin. 
He  also  classes  angina  pectoris,  intermittent  claudication,  and  Raynaud's  disease  under 
this  head. 

9.  Some  Cases  of  Angina  Pectoris  during  Attacks. 

10.  Some  Cases  of  Adams=Stokes  Diseases  between  Attacks. — Gibson  reports  a  case 
with  maximal  pressure  270,  minimal  pressure  70,  pulse-rate  27.  The  pressure  may,  however, 
never  rise  materially.    During  the  attacks  it  always  falls  almost  to  zero  (see  page  565) . 

11.  Exophthalmic  Goitre  (Graves's  or  Basedow's  disease)  is  often  accompanied  by 
hypertrophy  of  the  heart  with  increased  maximal,  140  to  160  mm.,  minimal  90  to  110  mm., 


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Fig.  30. — Diagram  showing  typical  blood-pressures  in  various  diseases.     Solid  black,  minimal  pressure; 
striped  shading,  pulse-pressure;  dot,  pulse-rate. 


and  pulse-pressure  30  to  50  mm.,  pulse-rate  accelerated  to  120  and  over.    In  some  cases 
of  Graves's  disease  the  pressure  remains  low  (maximal  120,  minimal  90). 

12.  The  End  of  Pregnancy,  the  onset  of  labor,  and  the  puerperium  are  accompanied 
by  a  slight  (10-15  mm.)  rise  of  maximal  pressure  with  little  change  in  minimal  pressure 
(Slemons  and  Goldsborough;  see  Part  III,  Chapter  IX). 

13.  Chronic  Primary  Polycythaemia. — The  increased  number  of  red  corpuscles  in- 
creases the  viscosity  of  the  blood,  and  thereby  the  work  of  the  heart,  besides  arteriosclerosis 
is  usually  associated.  On  the  other  hand,  as  shown  by  W.  Erb,  Jr.,  increase  in  blood- 
pressure  causes  liquid  to  leave  the  vessels  and  thereby  increases  the  viscosity  of  the  blood 
further — introducing  a  vicious  cycle. 


42  DISEASES  OF  THE  HEART  AND  AORTA. 

14.  Cyanosis  in  Heart=failure  with  Broken  Compensation,  which  occurs  at  some 
stage  in  almost  all  failing  hearts.  The  blood  becomes  overloaded  with  C02,  and  vasocon- 
striction plus  augmentation  results  as  in  asphyxia  (see  page  315).  Usually  the  pulse  is 
quickened,  probably  from  fatigue  of  the  vagus  centre.  This  condition  is  of  great  clinical 
importance,  since  the  high  blood-pressure  increases  the  work  of  the  heart  and  accelerates 
its  failure.  Venesection,  nitrites,  digitalis,  anything  which  accelerates  the  velocity  of  blood 
flow  through  the  lungs,  brings  about  improvement  and  lowering  of  the  blood-pressure. 

CHEONIC    HYPERTENSION. 

One  of  the  most  interesting  and  important  conditions  from  the  clinical 
stand-point,  as  well  as  from  that  of  pathological  physiology,  is  the  condition 
of  persistent  high  blood-pressure  associated  with 
hypertrophy  of  the  left  ventricle.  As  will  be  seen,  this 
condition  or  syndrome  is  scarcely  to  be  regarded  as  a  single  clinical  entity, 
but  more  as  a  group  of  manifestations  secondary  to  a  variety  of  hetero- 
geneous clinical  conditions,  grouped  together  only  for  clinical  convenience 
and  for  convenience  in  discussion  of  their  pathogenesis  and  treatment.  They 
are  not  associated  with  primary  disease  of  the  heart,  but  arise  secondarily 
from  diseases  in  other  organs.  For  convenience  of  clinical  designation,  how- 
ever, they  have  been  grouped  under  terms  "  chronic  hypertension,"  "  hyper- 
piesis "  (Sir  Clifford  Allbutt)  and  "  presclerosis "  (Huchard) ;  but  these 
terms  are  usually  applied  to  the  high  blood-pressure  of  chronic  nephritis. 

Frequency  of  High  Blood=pressure  in  Chronic  Nephritis. — A  review  of 
the  cases  of  high  blood-pressure  in  association  with  either  arteriosclerosis 
or  chronic  nephritis  which  have  come  to  autopsy  from  the  Medical  Service 
of  the  Johns  Hopkins  Hospital  during  the  years  1905  to  1911  (total  admis- 
sions 7,000)  indicates  strongly  the  relation  of  chronic  nephritis  to  diffuse 
changes  in  the  kidneys.  Of  thirty-nine  cases  of  the  two  conditions  in  which 
the  blood-pressure  had  been  above  150  mm.  Hg  (Riva-Rocci  wide  cuff), 
only  four  were  free  from  diffuse  nephritic  changes,  and  in  none  of  these  was 
the  pressure  above  190  mm.  Hg,  while  in  fifteen  cases  of  chronic  nephritis 
the  blood-pressure  ranged  from  190  to  300  mm.  Hg,  eight  being  below  and 
seven  above  230  mm.  Similarly  T.  C.  Janeway  has  found  that  in  130  patients 
seen  in  private  practice  whose  blood-pressures  were  over  200  mm.  Hg,  at 
least  105  (81  per  cent.)  were  cases  of  outspoken  chronic  nephritis,  most  of 
the  others  being  cases  of  aortic  insufficiency.  Cohnheim  has  shown  that  in 
cases  of  kidney  stone  and  hydronephrosis,  hypertension  and  cardiac  hyper- 
trophy are  also  present,  as  they  are  in  chronic  nephritis. 

On  the  other  hand,  the  blood-pressure  is  by  no  means  always  elevated 
in  cases  of  chronic  nephritis,  as  shown  by  the  fact  that  it  was  below  135  mm. 
Hg  in  6  out  of  44  cases,  and  in  other  cases  fell  below  this  level  after  an  initial 
period  of  elevation.  The  low  blood-pressure  is  not  always  a  terminal  event 
even  in  cases  with  markedly  impaired  renal  function,  as  is  shown  not  only 
by  the  autopsy  records,  but  also  by  the  cases  whose  phenolsulphonphthalein 
excretion  has  been  found  by  Rowntree  and  Geraghty  to  be  greatly  diminished 
during  life. 

The  chief  other  conditions  in  which  very  high  blood-pressures  are  en- 
countered are  those  associated  with  increased  intracranial  pressure  (menin- 
gitis, fracture  of  the  skull,  brain  tumor,  apoplexy,  hemorrhagic  meningitis) 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  43 

and  aortic  insufficiency.  In  the  latter  condition,  though  the  maximal  pres- 
sure is  high  the  minimal  is  relatively  low  and  the  pulse-pressure  is  relatively 
large.  In  advanced  Basedow's  disease  the  blood-pressure  is  usually  con- 
siderably elevated,  though  it  rarely  reaches  190  mm.  and  never  towers  to 
the  extreme  heights  seen  in  chronic  nephritis.  In  contrast  to  the  latter  con- 
dition the  diastolic  pressure  is  not  extremely  elevated  and  the  velocity  of  the 
blood  flow  through  the  arm  is  very  considerably  increased  (Hewlett  and  van 
Zwaluwenburg) . 

Roughly  speaking,  the  cases  with  blood -pressure 
permanently  above  two  hundred  millimetres  of  mer- 
cury are  mainly  those  of  increased  intracranial  pres- 
sure, chronic  nephritis,  and  aortic  insufficiency; 
those  between  one  hundred  and  fifty  and  two  hundred 
millimetres,  besides  these  conditions  are  arterio- 
sclerosis, Basedow's  disease,  chronic  polycythemia, 
and    high    pressure    stasis    (Hochdruckstauung).* 

Possible  Sources  of  Error. — Just  how  much  of  the  high  reading  of  the  sphygmo- 
manometer in  chronic  hypertension  is  due  to  actual  elevation  of  blood-pressure  and 
how  much  is  due  to  the  incompressibility  of  the  arterial  wall  owing  to  increased  tonus  (see 
page  29)  is  difficult  to  determine.  George  Johnston,  Savill  and  Russell  have  shown  (see  page 
346)  that  in  many  of  these  cases  there  is  great  hypertrophy  of  the  media  of  the  peripheral 
arteries  (see  Plate  X) ;  and  Russell  claims  that  the  increased  tonus  of  the  hypertrophied 
media  imparts  to  the  vessel  wall  a  rigidity  which  makes  it  difficult  to  compress.  He  rather 
aptly  compares  the  artery  with  thickened  media  to  a  thin-walled  rubber  tube,  and  he  finds 
that  such  a  tube  of  the  same  diameter  as  the  radial  artery  may  require  a  pressure  of  150  mm. 
Hg  to  obliterate  it.  His  suggestions  have  been  confirmed  with  great  care  by  Janeway  and 
Park,  who  found  that  thickened  arteries,  especially  when  the  muscular  layer  is  rendered 
spastic  by  immersion  in  barium  chloride,  may  require  as  much  as  64  mm.  Hg  to  collapse 
them,  and  that  if  the  arteries  were  boiled  it  might  require  154  mm.  Hg.  The  actual  dis- 
crepancies in  human  beings  have  not  been  studied  on  a  large  scale,  but  Volhard  has 
found  the  readings  from  a  manometer  inserted  into  one  of 
the  large  peripheral  arteries  with  a  cannula  prior  to  an 
amputation  were  20  mm.  Hg  lower  than  those  obtained  with 
the  Riva-Rocci  method.  As  the  results  by  palpation  at  the  wrist  are  5-10 
mm.  Hg,  this  would  indicate  that  the  sphygmomanometric  reading  by  the  auscultatory 
method  would  have  been  25-30  mm.  Hg  too  high  in  this  case,  and  it  is  by  no  means  certain 
that  this  represented  one  of  extreme  grade.  It  is  possible  that,  as  Russell  claims,  this 
error  may  be  doubled  in  certain  cases,  and  that  the  high  readings  in  this  condition  may  be 
obtained  when  the  actual  blood-pressures,  which  are  60  mm.  or  more,  lower. 

There  is  at  present  little  conclusive  evidence  upon  which  to  substantiate  or  to  deny 
this  claim.  It  is  certain  that  when  the  diameter  of  the  arteries  is  reduced  by  vasoconstric- 
tion, the  resistance  of  their  walls  to  compression  is  correspondingly  increased,  so  that  this 
factor  probably  plays  a  much  greater  role  in  producing  errors  in  blood-pressure  readings 
in  conditions  of  vasoconstriction  than  in  the  normal  state,  or  in  states  of  arterial  dilata- 
tion, such  as  are  met  with  in  aortic  insufficiency.  On  the  other  hand,  the  tremendous  degree 
of  hypertrophy  of  the  heart  in  these  conditions  furnishes  good  evidence  that,  though  part 
of  the  high  readings  of  the  sphygmomanometer  may  be  due  to  this  error  in  the  method, 
the  greater  portion  is  unquestionably  due  to  a  true  elevation  of  the  blood-pressure. 

Causes  of  High  Blood=pressure  in  Nephritis. — The  cause  of  the  high 
blood-pressure  in  chronic  nephritis  has  been  the  subject  of  much  discussion. 

Traube  and  Cohnheim  believed  that  the  diminution  in  the  blood-channel 
through  the  kidneys  rendered  an  increased  blood-pressure  necessary,    i  n 

*  In  many  cases  the  periods  of  high  blood-pressure  may  be  transitory,  coming  on  under 
strain  and  excitement.    In  these  hypertension  usually  becomes  permanent  later. 


44  DISEASES  OF  THE  HEART  AND  AORTA. 

order  to  maintain  a  sufficiently  rapid  blood  flow 
through  these  organs;  for,  as  Cohnheim  put  it,  an  excess  of  ex- 
cretable  (harnfahige)  substances  in  the  blood  readily  brings  this  about.  That 
the  renal  vessels  were  sclerotic  and  their  walls  thickened  in  chronic  nephri- 
tis had  been  shown  by  George  Johnson  and  by  Gull  and  Sutton;  but,  as 
Cohnheim  showed,  mere  cutting  down  of  the  pathway  through  the  kidneys 
could  not  be  the  cause,  for  total  ligation  of  both  renal  ar- 
teries was  not  followed  by  rise  in  bloo  d-p  r  e  s  s  u  r  e. 
Numerous  writers  following  Cohnheim  have  believed  that  the  hypertension 
was  caused  by  the  action  of  substances  in  the  blood  which  are  excreted  by 
the  healthy  kidney  but  retained  when  the  organ  is  diseased,  notably  urea, 
the  purin  bodies,  and  the  ammonium  salts.  However,  hypertension  may  occur 
in  conditions  in  which  the  urea  output  is  normal  and  in  which  the  quantity 
present  in  the  blood  is  not  even  as  great  as  in  a  variety  of  other  conditions. 

Similarly  Erben  has  ascribed  it  to  the  non-coagulable  nitrog- 
enous bodies  (Reststickstoff)  in  the  blood,  among  which 
the  purin  bodies,  especially  xanthin  and  hypoxanthin,  seem  sufficient  to  cause 
hypertension  (Croftan).  The  relation  of  accumulation  of  these  substances 
in  the  blood  to  hypertension  does  not  seem  to  be  a  constant  one,  however 
(Strauss),  and  the  theory  requires  some  further  proof. 

Certain  it  is,  however,  that  reduction  of  the  amount  of  kidney  sub- 
stance alone  is  sufficient  to  bring  about  hypertension.  J.  Rose  Bradford 
demonstrated  that  if  more  than  half  the  substance  of  the  healthy  dog's  kid- 
ney is  removed  the  remaining  portion  secretes  a  very  abundant  and  very 
dilute  urine  resembling  that  found  in  chronic  contracted  kidney.  This  find- 
ing was  confirmed  by  Passler  and  Heineke,  who  removed 
more  than  a  kidney  and  a  half,  bit  by  bit,  and  pro- 
duced both  hypertrophy  of  the  heart  and  persist- 
ent high  blood-pressure,  and  these  observations  have  been 
confirmed  both  by  Sampson  and  Pearce  and  by  Carrel  and  Janeway.  The 
latter  investigators  reduced  the  renal  substance  by  ligating  successively  sev- 
eral branches  of  the  renal  artery  at  long  intervals;  and  found  not  only  hyper- 
trophy of  the  ventricles  of  these  dogs  but  also  a  rise  in  blood-pressure  of 
over  thirty  millimetres  of  mercury. 

Clinical  evidence,  too,  seems  to  confirm  the  results  of  these  experiments, 
for  Buttermann  has  encountered  a  rise  of  50  mm.  Hg 
within  48  hours  after  the  onset  of  nephritis  in 
scarlet-fever  patients. 

The  presence  of  an  internal  secretion  of  the  kidney 
has  also  been  suggested  by  Brown-Sequard  to  explain  the  hypertension,  and 
this  investigator,  as  well  as  Tigerstedt  and  Berg- 
mann,  has  shown  that  a  rise  of  blood-pressure  may 
be  produced  by  injecting  renal  extract  ("renin"), 
although,  as  Pearce  has  found,  this  rise  is  both  slight  and  inconstant.  Ex- 
tracts of  diseased  kidneys  show  no  striking  difference  from  those  of  normal 
organs  in  this  regard;  so  that  it  would  appear  that  evidence  in  favor  of  this 
theory  of  renal  internal  secretion  is  insufficient  to  admit  of  its  acceptance. 

Still  another  theory  which  has  gained  many  advocates  in  recent  years 
is  that  of  a   hypersecretion   of   adrenalin    (adrenalin aemia)  in 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  45 

these  cases;  and  this  theory  has  been  supported  by  the  observations  of  Josue, 
Vaquez  and  Aubertin,  Wiesel,  and  others  (see  page  356),  that  in  certain 
cases  of  hypertension  and  hypertrophy  of  the  heart  there  was  actual  hyper- 
trophy of  the  adrenal  cortex.  The  hopes  of  the  adherents  of  this  theory 
have  been  somewhat  blasted  by  the  fact  that  Cohn  has  found  the 
same  adrenal  hypertrophy  present  in  about  an 
equal  proportion  of  cases  in  which  there  was  no 
hypertension  or  hypertrophy  of  the  heart,  and,  on 
the  other  hand,  that  the  latter  conditions  were  by  no  means  always  accom- 
panied by  hypertrophy  of  the  adrenals. 

Physiological  evidence  also  has  pointed  in  the  same  way.  Schur  and 
Wiesel  found  that  the  serum  of  patients  with  hypertension  caused  contrac- 
tion of  the  pupil  of  the  excised  frog's  eye  (Ehrmann's  reaction  for  adrenalin), 
and  Frenkel  has  been  unable  to  produce  relaxation  of  the  muscle  of  the  mam- 
malian uterus  profused  with  oxygenated  Locke  solution  to  which  serum  of 
such  patients  had  been  added.  As  the  latter  represents  the  most  delicate  and 
certain  of  the  tests  for  adrenalin,  its  absence  may  be  taken  to  indicate  that 
in  these  cases  there  was  no  increased  amount  of  adrenalin  in  the  blood.  It 
will  appear  from  the  foregoing  that  the  hypertension  of  chronic  nephritis 
still  awaits  satisfactory  explanation. 

The  high  blood-pressure  of  chronic  nephritis  is  almost  certainly  accom- 
panied by  a  tremendous  vasoconstriction,  for  the  diastolic  blood-pressure 
also  remains  high,  and,  as  Hewlett  and  van  Zwaluwenburg  have  shown, 
the  velocity  of  blood  flow  through  the  arm  remains  normal  in  spite  of  the 
increased  pressure.  Keith,  Rowntree,  and  Geraghty  have  found  that 
the  volume  of  the  blood  plasma  may  remain  normal  or  even  be  dimin- 
ished in  chronic  hypertension,  so  that  plethora  cannot  play  a  role  in  its 
causation. 

Arteriosclerosis  and  Hypertension. — Hasenfeld  has  claimed  that  high 
blood-pressure  and  hypertrophy  of  the  heart  occur  in  those  cases  of  arterio- 
sclerosis in  which  there  are  lesions  in  the  splanchnic  arteries  or  the  aorta 
above  the  diaphragm,  and  Longcope  and  McClintock  have  shown  that  a 
distinct  rise  of  blood-pressure  may  be  produced  in  dogs  whenever  the  supe- 
rior mesenteric  artery  is  occluded.  Marchand  and  Jores,  on  the  other  hand, 
find  that  lesions  of  these  vessels  are  by  no  means  always  associated  with 
cardiac  hypertrophy  and  hypertension.  Jores  even  goes  so  far  as  to  claim 
that  they  occur  almost  exclusively  in  the  cases  with  small  red  kidney.  In 
this  form  he  finds  that  the  most  striking  change  is  an  arteriosclerosis  in  the 
renal  arteries  beginning  in  the  glomeruli  and  smaller  vessels  and  gradually 
involving  the  larger  branches  (arteriocapillary  fibrosis,  Gull  and  Sutton). 
The  autopsies  made  at  the  Johns  Hopkins  Hospital,  however,  do  not  bear 
out  Jores's  contention  that  the  small  red  kidney  is  the  only  form  associated 
with  high  blood-pressure  and  nephritis. 

If  the  patient  does  not  die  of  intercurrent  infection,  heart-failure  sets 
in  in  the  course  of  a  few  years,  with  gradually  developing  dyspnoea,  ana- 
sarca, hydrothorax,  progressive  dilatation  of  the  heart,  and  relative  tricuspid 
insufficiency. 

Effects  of  Chronic  Hypertension  upon  the  Circulation. — When  the 
blood-pressure  remains  elevated  to  the  heights  mentioned  above,  the  work 


46  DISEASES  OF  THE  HEART  AND  AORTA. 

of  the  heart  is  considerably  augmented.  If  this  be  calculated  simply  as  work 
of  heart  =  maximal  blood-pressure  X  pulse-rate,  it  will  be  seen  that  the  latter 
may  readily  be  more  than  doubled  without  bringing  about  any  improvement 
in  the  circulation,  and  in  the  course  of  several  years  this  overwork  usually 
impairs  the  strength  of  the  heart.  When  the  pulse-rate  becomes  more  rapid, 
which  usually  occurs  as  heart-failure  sets  in,  the  work  of  the  heart  may  be 
increased,  and  a  vicious  circle  is  introduced.  This  is  sometimes  accompanied 
by  a  fall  of  blood-pressure  shortly  before  death,  but  in  many  cases  the  pres- 
sure remains  elevated  until  the  end. 

Many  of  these  patients  are  entirely  free  from  symptoms  for  some  years 
after  the  onset  of  the  hypertension,  and  then  begin  with  only  occasional 
headaches,  frequent  micturition  at  night,  and  palpitation.  Sooner  or  later 
a  tendency  to  fatigue  and  lassitude  sets  in,  and  then  the  actual  failure  of 
the  heart.  In  not  a  few  of  the  cases  the  course  is  interrupted  by  the  onset 
of  uraemia,  resulting  in  death. 

In  patients  with  simple  arteriosclerosis  the  blood-pressure  rarely  if  ever 
rises  to  the  heights  reached  in  many  cases  of  nephritis,  and  it  is  almost  always 
well  below  190  mm.  Hg.  The  urine  may  contain  albumin  and  casts,  but 
the  phenolsulphonphthalein  excretion  is  undiminished  (Rowntree  and  Ger- 
aghty).  The  symptoms  are  usually  confined  to  those  of  circulatory  failure, 
although  headaches  may  arise  from  cerebral  arteriosclerosis  and  nocturnal 
micturition  may  be  due  to  impairment  of  the  general  circulation. 

Cerebral  Hemorrhage  and  Hypertension. — A  considerable  number  of 
cases  of  chronic  high  blood-pressure  are  sooner  or  later  associated  with  cere- 
bral hemorrhage,  owing  in  part  to  the  fact  that  mesarteritis  of  the  cerebral 
vessels  is  particularly  common  in  chronic  nephritis,  and  in  part  to  the  fact 
that  the  high  blood-pressure  imposes  a  very  severe  strain  upon  the  walls  of 
the  arteries  and  thus  leads  to  their  rupture.  The  rupture  in  turn  leads  to 
hemorrhage,  and  the  pressure  from  the  hemorrhage  upon  the  surrounding 
tissue  and  the  oedema  of  this  injured  tissue  lead  in  turn  to  increased  intra- 
cranial tension  and  thus  to  a  further  increase  in  the  blood-pressure  itself; 
so  that  a  vicious  circle  is  introduced : 


High  blood-pressure.      Cerebral  hemorrhage. 


Moreover,  as  Cushing  has  shown,  the  mere  anaemia  of  the  brain  leads 
reflexly  to  still  further  vasoconstriction  until  the  blood-pressure  is  increased 
above  the  intracranial  pressure  so  as  to  bring  sufficient  nourishment  to  the 
brain  in  spite  of  the  local  conditions. 

Treatment  of  chronic  hypertension  may  be  undertaken  in  two  ways, 
either  by  attempting  to  reduce  the  pressure  directly  by  dilating  the  periph- 
eral arterioles  with  drugs  of  the  nitrite  series  or  vasotonin  (yohimbin- 
urethane)  or  by  attempting  to  alleviate  the  factors  which  lead  to  the  vaso- 
constriction. 

The  advisability  of  attempting  to  dilate  the  arterioles  with  nitrites  or 
vasotonin  depends  upon  whether  the  high  blood-pressure  arises  incidentally 
or  whether  it  is  a  phenomenon  of  physiological  compensation.  For  example, 
in  conditions  accompanied  by  increased  intracranial  pressure,  as  Cushing 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  47 

has  shown,  the  vasoconstriction  goes  on  until  the  blood-pressure  rises  above 
the  intracranial  pressure  and  the  requisite  amount  of  blood  is  shunted  through 
the  brain.  If  this  vasoconstriction  is  antagonized  by  the  action  of  nitrites 
and  the  vasoconstriction  is  prevented,  the  heart  must  be  stimulated  to  far 
greater  efforts  in  order  to  nourish  the  brain,  and,  if  the  treatment  is  pushed 
still  further,  the  patient  may  suffer  distinctly  from  the  effects  of  cerebral 
anaemia.  In  the  past  decade,  before  this  fact  was  recognized,  the  writer  has 
seen  this  borne  out  in  patients  with  apoplexy,  whose  general  condition  and 
mental  condition  were  decidedly  worse  during  periods  when  the  pressure 
was  reduced  by  nitrites  than  it  was  during  those  when  the  hypertension  was 
not  interfered  with. 

On  the  other  hand,  as  seen  in  some  cases  of  vasomotor  crisis,  the  vaso- 
constriction may  also  be  merely  an  accessory  phenomenon  bearing  no  rela- 
tion at  all  to  any  physiological  need,  and  the  pressure  is  then  raised  merely 
in  order  to  force  the  blood  through  the  constricted  arteries  at  its  usual 
velocity. 

The  exact  mechanism  which  brings  about  the  rise  in  pressure  in  chronic 
nephritis  is  not  well  understood,  nor  has  it  been  conclusively  proved  whether 
this  is  a  toxic  or  a  compensatory  phenomenon,  though  Janeway  leans  to  the 
latter.  Fellner  believes  that  there  is  sometimes  an  over-compensation,  in 
which  a  slight  but  not  a  great  reduction  of  blood-pressure  is  beneficial. 
Whatever  be  the  explanation,  Matthews  has  shown  that,  though  the  hyper- 
tension can  be  reduced  by  comparatively  small  doses  of  nitrites  in  the  early 
stages  of  chronic  nephritis,  these  drugs  become  much  less  effective  after  the 
disease  is  far  advanced. 

On  the  other  hand,  some  benefit  may  be  obtained  by  modification  of 
the  diet,  especially,  as  Widal  has  shown,  by  reducing  the  amount  of  salt 
ingested.  With  the  decrease  in  salt  in  the  food,  there  follows  in  many 
cases  a  decreased  need  for  water,  for  Erich  Meyer  has  shown  that  the 
contracted  kidney  is  unable  to  excrete  more  than  a  certain  definite  con- 
centration of  salt  in  the  urine;  an  excess  of  water  is  needed,  therefore,  to 
carry  away  the  salt. 

Meats  should  be  either  entirely  eliminated  from  the  diet  or  taken  but 
once  a  day,  while  bouillon  and  meat  soups  and  the  glandular  organs  (sweet- 
breads, liver,  kidneys,  spleen,  lungs),  which  are  particularly  rich  in  purins, 
should  not  be  taken  at  all. 

The  patient  should  be  made  to  live  a  life  as  free  as  possible  from  over- 
exertion and  over-excitement,  and  he  should  take  hot  baths  rather  than  cold 
ones,  to  dilate  his  arteries  rather  than  constrict  them  more  than  is  necessary. 
For  the  same  reason  he  should  be  warmly  clothed  during  the  periods  when 
the  weather  is  at  all  cool. 

For  the  symptoms  of  cardiac  weakness  themselves,  or  in  order  to  ward 
them  off,  digitalis  may  be  administered,  either  in  the  tincture  or  the  more 
modern  special  preparations,  or,  on  the  other  hand,  be  given  as  the  infusion, 
which  is  preferred  by  many  clinicians  for  the  treatment  of  this  condition. 
In  cases  of  chronic  nephritis,  however,  the  effect  of  digitalis  is  at  best  only  pallia- 
tive, for  the  agent,  toxic  or  secretory,  which  has  led  to  the  hypertension  and 
the  hypertrophy  of  the  heart  has  already  exerted  an  action  quite  similar  to 
that  of  the  drug  itself;  and  the  effect  to  be  obtained  is,  therefore,  but  limited. 


48  DISEASES  OF  THE  HEART  AND  AORTA. 

Prognosis. — J.  W.  Fisher  has  found  from  the  extensive  statistics  of  the 
Northwestern  Mutual  Life  Insurance  Co. : 

I.  That  a  persistently  high  arterial  tension  will  result  in  an  excessive 
mortality  for  the  age  of  the  individual,  and  that  the  higher  the  arterial  ten- 
sion the  greater  is  the  mortality. 

II.  That  a  persistent  systolic  blood  tension  of  about  12  mm.  above  the 
average  for  the  age  would  seem  to  indicate  the  limit  of  normal  variation  in  man. 

pathological  conditions  associated  with  low  blood-pressure 

(hypotension). 

Although  the  occurrence  of  low  blood-pressure  is  usually  associated 
in  the  mind  with  the  idea  of  a  diseased  heart,  such  is,  as  a  rule,  not  the  case. 
In  fact,  in  most  chronic  diseases  of  the  heart  the  maximal  pressure  is  in- 
creased rather  than  decreased,  as  has  been  shown  above.  In  one  case  of 
aortic  insufficiency,  for  example,  the  writer  found  a  maximal  pressure  of 
150  and  a  minimal  pressure  of  110  two  minutes  before  death,  in  spite  of  in- 
tense heart  failure. 

A  low  blood-pressure  is  more  commonly  an  index  of  fail- 
ure of  the  vasomotor  centre  than  of  the  heart,  and  occurs  in  con- 
ditions where  the  strength  of  the  heart  is  uninjured  (Romberg  and  Passler,  Hasenfeld  and 
Fenevessy,  Crile). 

Conditions  in  which  low  blood-pressure  is  found  are: 

1.  Acute  infectious  diseases  except  meningitis  (where  the  blood-pressure  is  high 
from  increased  intracranial  tension).  Romberg  and  Passler  have  shown  that  bacterial 
poisons  (diminish  the  tonic  activity  of  the  vasomotor  centre,  and  may  even  paralyze  it. 
The  strength  of  the  heart  is  shown  to  be  undiminished  if  the  vasodilation  is  counteracted  by 
adrenalin,  compression  of  the  abdominal  aorta,  etc.  The  blood-pressure  falls  because  the 
arterioles  are  dilated  and  the  overflow  from  the  arteries  is  too  rapid  (maximal  pressure  90  to 
110,  minimal  pressure  50  to  90,  pulse-rate  increased,  see  table,  page  41). 

The  lowest  blood-pressure  isin  typhoid  fever  (Barach)  and  peritonitis, 
where  the  dilatation  of  abdominal  vessels  from  the  local  inflammation  add  their  effect  to 
that  of  the  cutaneous  vasodilation.  In  typhoid  fever  the  writer  has  seen  maximal  pressures 
as  low  as  65  mm.  Hg  (Riva-Rocci) ,  although  maximal  100  to  120  with  minimal  60  to  90  is 
more  common.  Crile  and  Briggs  have  described  rises  in  blood-pressure  at  the  onset  of  per- 
foration due  to  splanchnic  stimulation,  but  the  writer  has  had  two  cases  (one  of  which 
is  mentioned  by  Briggs)  in  which  inactivity  of  the  vasomotor  centre  prevented  this  rise 
from  occurring. 

In  pneumonia  the  blood-pressure  may  not  be  changed  much  (maximal  110  to 
130,  minimal  90,  pulse-rate  120) ;  it  may  rise  as  mild  asphyxia  sets  in,  or  it  may  fall  very 
low  from  vasomotor  paralysis. 

In  diphtheria,  scarlet  fever,  measles,  acute  rheumatism, 
and  in  fact  in  all  other  acute  infectious  diseases,  the  maximal  pressure  usually  falls  below 
100  during  the  height  of  the  fever  (Weigert). 

2.  Phthisis. — In  this  disease  all  ranges  of  blood-pressure  may  be  found.  John,  Nau- 
mann,  Burckhardt,  and  Stanton  have  found  uniformly  low  pressures,  90  to  100  mm.  with 
the  Gaertner  and  Riva-Rocci  apparatus.  Janeway  found  that  variations  of  maximal  pres- 
sure between  80  and  120  mm.  Hg  are  common  in  the  same  patient.  The  pulse-rate  is  usually 
rapid,  80  to  100  per  minute.  Peters  finds  that  there  is  usually  a  rise  of  blood-pressure 
when  improvement  sets  in,  and  a  fall  when  the  case  is  getting  worse. 

3.  Shock.— Goltz  in  1863  found  that  if  a  frog  were  tapped  upon  the  abdomen  the  heart 
stopped  beating  for  a  while  and  then  resumed  contraction,  but  the  arteries  were  then  pale 
and  small  and  the  circulation  very  much  retarded.  He  found,  on  the  other  hand,  that  the 
abdominal  veins  were  very  full,  and  that  the  vasomotor  nerves  supplying  the  abdominal 
vessels  were  no  longer  active.  He  regarded  this  vasomotor  paralysis  as  the  cause  of  trau- 
matic shock,  a"  view  which  was  further  applied  to  surgical  shock  by  various  clinicians, 
among  them  Keen,  Mitchell  and  Morehouse  (1864),  Lauder  Brunton  (1873),  and    Crile 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  49 

(1903).  Acting  upon  this  hypothesis,  Crile  attempts  to  counteract  the  vasomotor  paralysis 
by  putting  a  double-walled  rubber  suit  upon  the  patient  and  inflating  it  until  the  pressure 
upon  the  abdomen  and  lower  extremities  compensates  for  the  loss  of  vascular  tone.  The 
common  practice  of  elevating  the  feet  has,  of  course,  the  same  effect. 

The  conception  that  the  vasomotor  centre  is  paralyzed  in  shock  is  contradicted  by 
the  observations  of  Porter,  who  found  that  it  was  still  active ;  and  Seelig  and  Lyon  have  also 
shown  that  the  peripheral  vasoconstrictor  nerves  of  the  leg  are  in  tonic  activity  during 
severe  shock.  Still  further  they  have  shown  that  the  arteries  of  the  retina  are  distinctly 
contracted  during  shock,  and  that  various  organs  (kidney,  etc.)  removed  during  shock  are 
relatively  anaemic  as  compared  with  those  removed  with  a  normal  circulation. 

Moreover,  they  found  that  the  outflow  from  a  cannula  introduced  into  the  femoral 
vein  was  only  one-third  as  fast  when  the  animal  was  in  shock  as  when  it  was  normal.  Their 
observations  seem  to  substantiate  in  every  way  the  claim  of  Malcolm,  on  purely  clinical 
grounds,  that  the  trouble  could  not  be  due  to  dilatation  of  the  peripheral  vessels. 

More  recently  Yandell  Henderson  has  expounded  a  new  theory  for  the  production  of 
shock;  He  noticed  that  in  experiments  upon  animals  under  artificial  respiration  shock 
occurred  with  great  frequency  in  those  animals  in  which  the  ventilation  of  the  lungs  had 
been  excessive,  and  he  was  even  able  to  induce  death  from  shock  by  excessive  ventilation 
or  to  retain  a  slow  pulse-rate  and  a  high  blood-pressure  by  limiting  the  latter,  in  which  the 
animals  remained  in  good  condition  in  spite  of  severe  operative  procedures.  In  this  respect  he 
was  able  to  show  that  the  ill  effects  of  over-ventilation  were  due  to  the  washing  out  of  CO2 
from  the  blood,  bringing  about  the  condition  of  acapnia,  or  low  C02  in  the  blood,  which 
Mosso  had  found  to  produce  the  syncope  of  mountain  sickness,  and  which  Haldane  and  his 
collaborators  had  found  to  be,  responsible  for  many  conditions  of  weakness  in  man  as  result- 
ing from  too  rapid  breathing..  Henderson  believes  that  in  most  cases  of  surgical  shock  or 
clinical  syncope  the  rapid  breathing  (hyperpncea)  is  the  underlying  factor,  and  that  the 
sequence  of  events  is  as  follows:  (1)  pain  or  emotion;  (2)  hyperpncea;  (3)  overaeration  of 
the  blood  (lowering  of  the  CO2  content,  acapnia),  dilatation  of  the  veins,  accumulation  of 
the  blood  in  the  latter  and  transudation  of  fluid  into  the  tissues;  (4)  lowering  of  the  pressure 
in  the  veins  and  hence  diminished  entry  of  blood  into  the  heart;  (5)  fall  in  arterial  pressure, 
accompanied  by  loss  of  arterial  tone  (vasodilation) ;  (6)  cerebral  ansemia  and  syncope. 

Gatch  has  shown  that  rebreathing  expired  air  diminishes  the  ill-effects  of  anaesthesia 
upon  the  circulation. 

Though  Henderson's  studies  have  established  the  fact  that  the  condition  of  acapnia 
when  present  demands  symptomatic  treatment,  he  has  not  definitely  proved  that  it  is  the 
underlying  cause  of  all  shock.  Indeed,  H.  H.  Janeway  has  demonstrated  that  forced 
ventilation  of  the  abdominal  cavity  without  handling  of  the  intestines  does  not  lead  to 
shock.  Janeway's  experiments  have  been  confirmed  by  T.  Snodgrass  and  O.  H.  Klingen 
in  the  writer's  laboratory. 

Elliott  (Brit.  M.  J.,  1914,  i,  1393)  and  Corbett  (J.  Am.  M.  Assoc,  1915,  lxv,  380)  have 
shown  that  during  shock  the  adrenals  become  exhausted  of  adrenalin,  but  H.  C.  Jackson 
(Proc.  Soc.  Exper.  Biol,  and  Med.,  1916,  xiii,  85)  found  an  increased  amount  of  adrenalin 
in  the  vena  cava  after  shock  had  set  in,  proving  that  this  condition  is  not  due  to  adrenal 
exhaustion.  Corbett  and  Rowntree  and  also  Cannon  have  found  acidosis  present  in  sur- 
gical shock. 

In  fevers  the  high  temperature  gives  rise  to  a  slight  polypncea  and  also  f avore 
the  evaporation  of  C02  from  the  lungs,  and  Minkowski1  and,  later,  Caspari  and  Loewy2 
have  found  that  the  C02  content  of  the  blood  is  lowered,  as  well  as  the  02.  This  would 
strengthen  the  resemblance  between  the  circulatory  failure  of  fever  and  that  of  shock 
according  to  Henderson's  theory  of  acapnia.  Wolff3  has  shown  with  the  ferrocyanide  test 
that  the  velocity  of  the  circulation  through  the  body  is  about  30  per  cent,  slower  during 
fever  than  in  health. 

Newburgh  and  Lawrence  (Arch.  Int.  Med.,  1914,  xiii,  287)  have  shown  that  warming 
the  blood  bathing  the  medulla  causes  fall  of  blood-pressure. 

1  Minkowski,  O. :  Ueber  den  Kohlensauregehalt  des  arteriellen  Blutes  beim  Fieber, 
Arch.  f.  exper.  u.  Pharmakol.,  1885,  xix,  209. 

2  Caspari,  W.,  and  Loewy,  A. :  Ueber  den  Einfluss  gesteigerter  Korpertemperatur  auf 
das  Verhalten  der  Blutgasen.,  Biochem.  Ztschr.,  Berl.,  1910,  xxvii,  405. 

3  Wolff,  E. :  Ueber  die  Umlaufsgeschwindigkeit  des  Blutes,  Arch,  f .  exper.  Path.  u. 
Pharmakol.,  Leipz.,  1885,  xix,  265. 


50  DISEASES  OF  THE  HEART  AND  AORTA. 

4.  Collapse  from  various  poisons,  carbolic  and  salicylic  acid,  arsenic,  phosphorus, 
drugs  of  the  antipyretic  series,  etc.,  is  due  to  the  same  cause — failure  of  the  vasocon- 
strictor centre — and  likewise  is  accompanied  by  low  blood-pressure. 

5.  After  extensive  hemorrhage  a  fall  of  blood-pressure  sets  in  (except  after  vene- 
section in  some  cases  where  a  failing  heart  is  relieved),  owing  to  lack  of  blood  to  fill  out  the 
arteries.  This  is  usually  relieved  by  subcutaneous  or  intravenous  NaCl  infusion,  or  even 
by  direct  arterial  transfusion  (Crile). 

6.  In  diarrhoea,  dysentery,  cholera,  or  after  profuse  vomiting,  as  from  cancer 
of  the  stomach,  intestinal  obstruction,  peritonitis,  etc.,  when  large  amounts  of  fluid  have 
left  the  body,  the  arteries  may  also  be  depleted  of  fluid  and  a  very  low  blood-pressure  result. 
This  is  also  relieved  by  infusion. 

7.  In  pleurisy,  especially  pleurisy  with  effusion,  blood-pressure  is  uni- 
formly low. 

8.  Pericarditis  is  accompanied  by  low  blood-pressure  (maximum  100  to  120,  mini- 
mum 70  to  90,  pulse-rate  increased)  unless  complicated  by  hypertrophy  of  the  heart  or 
some  other  factors. 

9.  Acute  cardiac  diseases  of  all  types,  which  have  not  been  preceded  by  chronic  proc- 
esses and  are  not  associated  with  marked  cyanosis.  Here  the  above-mentioned  toxic  action 
on  the  vasomotor  centre  is  usually  present  if  the  endocarditis  is  of  the  infectious  variety, 
and  besides  there  is  some  weakening  of  the  heart.  The  quickened  pulse-rate  prevents 
CO2  from  accumulating  in  the  blood  and  the  asphyxial  rise  in  pressure  does  not  occur. 
K.  Weigert  reports  all  ranges  of  pressure  between  95  and  140  mm.  Hg. 

10.  In  chronic  mitral  stenosis  the  maximal  and  minimal  pressures  are  usually  normal 
or  a  little  below  normal,  when  the  left  ventricle  does  not  hypertrophy;  but  this  may  vary 
considerably. 

11.  Chronic  wasting  diseases,  cancer,  chronic  phthisis,  anaemias,  etc.,  are  associated 
with  brown  atrophy  of  the  heart  muscle  (see  page  289)  with  weakened  heart  action,  hence 
with  lowered  blood-pressure  (10  to  20  mm.  lower  than  normal,  pulse-rate  usually  increased). 

BLOOD-PRESSURE  IN  THE  VEINS. 

Various  methods  have  been  devised  for  the  determination  of  the  venous 
blood-pressure  in  man,  the  first  being  introduced  by  v.  Basch  and  being 
but  a  slight  variation  of  his  arterial  sphygmomanometer. 

A  very  similar  apparatus  has  been  constructed  recently  by  Sewall,  but  this  gives 
rather  unsatisfactory  results  in  practice.  V.  Frey  and  later  Gaertner  also  determined 
the  pressure  by  considering  it  equal  to  the  height  above  the  angle  of  Ludwig  at  which 
the  veins  of  the  hand  could  be  seen  to  collapse.  This  method  is  not  quite  as  good  as  the 
former.  A  considerable  advance  was  made  by  v.  Recklinghausen,  who  compressed  the 
vein  by  inflating  a  small  rubber  capsule  provided  with  a  glass  window  in  the  top  and  a 
rubber-dam  floor  having  a  hole  in  its  centre.  This  dam  was  coated  with  glycerin  so  as  to 
insure  perfect  contact.  It  is  then  placed  over  a  vein,  preferably  upon  the  back  of  the  hand 
or  wrist,  and  the  system  blown  up  until  the  vein  can  be  seen  to  disappear,  at  which  point 
the  pressure  is  read  off  upon  a  water  manometer.  Eyster  and  Hooker  have  modified  this 
chamber  by  constructing  one  of  aluminum  with  the  entire  top  of  glass  and  the  two  ends 
concave  so  as  to  avoid  pressure  upon  the  veins,  and  their  apparatus  seems  to  give  results 
concordant  within  1  cm.  H20.  They  find  that  the  normal  venous  pressure  at  the  sterno- 
xiphoid  articulation  is  5-10  cm.  H2O.1  It  is  increased  by  exercise  and  in  cardiac  cases 
with  broken  compensation,  when  it  may  rise  to  27  cm.  or  over.  When  the  veins  are  not 
sufficiently  distended  at  that  level  the  hand  may  be  lowered  a  known  distance,  the  pres- 
sure read;  and  the  distance  lowered  subtracted  from  the  amount  of  the  reading  will  repre- 
sent the  venous  pressure.  In  cases  where  phlebosclerosis  is  present  no  satisfactory  deter- 
minations could  be  made. 


1  These  figures  agree  well  with  direct  manometric  determinations  recently  made  in 
man  by  Moritz  and  v.  Tabora  (Verhandl.  d.  Kong.  f.  innere  Med.,  1909,  xxvi,  378). 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


51 


The  pressure  in  the  capillaries  of  vascular  areas,  especially  of  the  lips, 
may  be  determined  in  the  same  way,  using  the  point  of  blanching  as  the 
criterion. 

The  study  of  the  venous  pressure  is  of  undoubted  importance  as  an  index 
of  accumulation  of  the  blood  in  the  systemic  circulation  and  thus  as  an  index 
of  heart-failure.  Moreover,  it  is  the  most  important  physiological  factor 
bringing  about  variations  in  the  volume  of  the  heart;  a  high  venous  pressure 
causing  dilatation,  a  low  venous 
pressure  causing  diminution  in 
volume  (insufficient  filling).  This 
may  prove  to  be  an  important 
factor  in  bringing  about  certain 
conditions  in  which  there  is  "ar- 
terial anaemia"  (shock,  cardiac 
neurosis,  etc.). 

THE  PULMONARY  CIRCULATION. 

Before  birth  the  resistance  in 
the  vessels  of  the  collapsed  lung 
is  greater  than  that  in  the  sys- 
temic arteries,  and  hence  blood 
passes  from  the  pulmonary  artery 
to  the  aorta  through  the  ductus 
arteriosus  (Botalli). 

As  the  blood-pressure  in  young  in- 
fants is  80  mm.  Hg  (Trumpp),  it  must 
be  assumed  that  the  pulmonary  pressure 
is  somewhat  greater  than  this.  When 
the  area  of  lung  capillaries  widens  with 
the  first  inspiration,  the  resistance  in  the 
pulmonary  vessels  decreases  very  mark- 
edly. This  decrease  continues  during 
the  period  of  infancy  until  the  lung  is 
fully  expanded.  According  to  a  number 
of  observers  (Beutner,  Lichtheim,  Open- 
chowski,  Bradford  and  Dean,  Plumier), 
the  mean  pressure  in  the  pulmonary 
artery  of  rabbits,  cats,  and  dogs  varies 
from  6  to  35  mm.  Hg.  Wiggers  has 
found  that  the  maximal  pressure  in  the  pulmonary  artery  in  dogs  varies  between  36  and  48 
mm.  Hg,  the  minimal  between  5  and  12  mm.,  and  the  pulse-pressure  between  22  and  41  mm. 

Since  it  is  the  difference  of  pressure  between  pulmonary  artery  and 
pulmonary  vein  which  drives  blood  through  the  lungs  it  may  easily  be  seen 
how  a  slight  rise  of  pressure  in  the  latter  lessens  the  flow. 

Work  of  the  Right  Heart. — The  pressure  within  the  pulmonary  artery 
and  hence  the  work  of  the  right  heart  varies  within  wide  limits  under  experi- 
mental conditions.  (Wiggers  (Am.  J.  Physiol.,  1914,  xxxv,  124)  finds  13  to  20 
mm.  Hg  normal  in  dogs.) 

The  variations  are  in  part  passive,  due  to  passive  stasis,  and  in  part  due 
to  vasomotor  changes  in  the  pulmonary  vessels. 


Fig.  31. — Hooker  and  Eyster's  modification  of 
v.  Recklinghausen's  method  of  determining  the  venous 
pressure  in  man. 


52  DISEASES  OF  THE  HEART  AND  AORTA. 

The  conditions  in  which  the  changes  in  pulmonary  pressure  arise  pas- 
sively from  changes  in  the  left  Ventricle  are  the  most  common  and  are  clin- 
ically the  most  important. 

Increased  mean  pulmonary  pressure  may  arise  : 

1.  When  an  increased  amount  of  blood  enters  the  right  heart  from  the  veins  and  is 
expelled  into  the  pulmonary  artery. 

2.  The  pulmonary  blood-pressure  also  undergoes  rhythmic  variations,  falling  during 
inspiration  as  a  result  of  suction  (as  shown  by  de  Jager)  and  rising  during  expiration. 

3.  When  the  left  ventricle  fails  to  pump  an  equal  amount  onward  into  the  aorta, 
causing  blood  to  accumulate  in  the  pulmonary  capillaries  until  these  are  overfilled  and 
aid  in  increasing  the  resistance  in  this  circuit.  (The  left  ventricle  acts  upon  the  pulmonary 
circulation  as  a  suction  pump.) 

4.  Probably  from  constriction  of  the  pulmonary  arteries  under  the  influence  of  vaso- 
motor nerves. 

Pulmonary  Vasomotor  Nerves. — The  existence  of  vasomotor  nerves  in 
the  pulmonary  artery,  first  suggested  by  Brown-Sequard  (1870  to  1873)  and 
later  by  Badoud,  has  been  much  disputed,  but  seems  now  to  be  proved. 

Francois-Fran ck  has  shown  that  stimulation  of  the  lower  cervical  and  upper  five 
thoracic  ganglia  in  the  dog  uniformly  caused  a  rise  of  blood-pressure  in  the  pulmonary 
artery,  a  fall  of  pressure  in  the  left  auricle,  and  an  increase  in  the  volume  of  the  lungs, 
probably  due  to  accumulation  of  blood  on  the  arterial  side  of  the  capillaries.  This  rise  in 
pulmonary  pressure  bore  no  constant  relation  to  the  pressure  in  the  femoral  artery,  which 
sometimes  rose  and  sometimes  fell.  This  evidence  strongly  favors  the  existence  of  vasocon- 
strictor fibres.  Frangois-Franck  showed  further  that  these  same  changes  in  pulmonary 
arterial  pressure,  left  auricular  pressure,  and  lung  volume  occurred  reflexly  when  the  central 
end  of  the  femoral  nerve  or  a  proximal  branch  of  the  solar  plexus  was  stimulated.  This 
reflex,  as  he  shows  in  a  subsequent  paper,  may  have  important  bearings  in  the  production 
of  certain  cardiac  symptoms  and  in  influencing  the  course  of  cardiac  diseases. 

Action  of  Drugs  on  the  Pulmonary  Circulation. — Francois-Franck's  re- 
searches are  very  convincing.  They  have  been  confirmed  by  H.  C.  Wood,  Jr., 
and  others,  and  are  accepted  by  as  keen  a  critic  as  Tigerstedt;  but  Wood,  Jr., 
and  also  Petitjean  have  found  that  all  drugs  exert  a  much  less 
marked  effect  on  the  pulmonary  circulation  than  on 
the  systemic.  Wiggers  finds  that  adrenalin,  digitalis,  and  strophan- 
thin  increase  the  pulmonary  arterial  pressure  and  also  increase  both  arterial 
and  venous  hemorrhage  from  the  pulmonary  vessels.  The  nitrites  increase 
both  under  normal  conditions  but  diminish  both  in  the  last  stages  of  hemor- 
rhage. Ergotoxin  sometimes  raises  and  sometimes  lowers  pulmonary  arterial 
pressure  normally,  but  has  little  effect  during  hemorrhage.  Under  normal 
conditions  it  seems  to  diminish  the  pressure  in  the  pulmonary  veins.  Chloro- 
form always  diminishes  both  the  pressure  in  the  pulmonary  veins  and  arteries 
and  lessens  hemorrhage  from  the  lungs.  Pituitary  extract,  however,  according 
to  the  studies  of  Wiggers,  exerts  the  most  favorable  action  of  all,  for  the  in- 
flow of  blood  into  the  right  heart  is  diminished,  and  'pari  passu  with  this  a 
fall  in  pressure  in  the  pulmonary  vessels  and  a  diminution  of  hemorrhage 
from  the  latter  result,  which  is  particularly  marked  in  anaemic  conditions. 
Pituitary  extract  would  thus  appear  to  be  the  drug  indicated  for  the  relief  of 
pulmonary  hemorrhage,  especially  in  tuberculosis  and  congenital  heart  dis- 
ease. In  mitral  disease  its  use  is  more  questionable,  for  the  raising  of  the 
peripheral  resistance  in  the  systemic  circulation  may  increase  regurgitation 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  53 

or  stasis  in  the  pulmonary  circulation.  It  must  be  admitted  that  accept- 
ance is  not  universal.  The  clinical  importance  of  the  problem  renders  it  a 
matter  of  universal  interest. 

It  may  be  considered  proved  by  Francois-Franck's  work  that  sensory 
stimuli,  stimulation  of  the  sympathetic  nerves,  asphyxia,  etc.,  may  cause 
the  pulmonary  arterial  pressure  to  rise  to  about  double  its  original  height, 
and  hence  in  chronic  conditions  may  play  an  important  role  in  bringing 
about  hypertrophy  of  the  right  ventricle.  Moreover,  changes  of  pressure 
which  are  relatively  small  when  applied  to  the  left  ventricle  assume  much 
greater  proportions  when  applied  to  the  weaker  right  ventricle,  and  appar- 
ently slight  changes  in  the  strength  of  this  chamber  may  then  be  important 
factors  in  the  mechanism  of  the  circulation. 

Tonicity  of  the  Right  Ventricle. — More  important  than  the  changes  in 
pressure  in  the  pulmonary  artery  are  the  changes  in  tonus  of  the  right  ven- 
tricle. Owing  to  the  thinness  of  the  wall,  changes  in  tonicity  affect  this 
chamber  much  more  readily  than  they  do  the  left;  overstretching  of  the 
fibres  sets  in  more  readily,  and  weakening  of  the  right  ventricle  results  more 
readily.  These  changes  may  have  no  direct  relation  to  the  changes  in  pul- 
monary arterial  pressure. 

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Sampson,  J.  A.,  and  Pearce,  R.  M.:  A  Study  of  Experimental  Reduction  of  Kidney  Tissue 

with  Especial  Reference  to  the  Changes  in  that  Remaining,  J.  Exper.  Med.,  N.  Y. 

and  Lancaster,  1908,  x,  745. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  57 

Carrel,   A.:   Note  on   the   Production   of    Kidney   Insufficiency  by   Reduction   of   the 
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vi,  107. 
Janeway,  T.  C. :  A  Modification  of  the  Riva-Rocci  Method  of  Determining  Blood-pressure, 

for  Use  on  the  Dog,  ibid.,  1909,  vi,  108. 
Note  on  the  Blood-pressure  Changes  Following  Reduction  of  the  Renal  Arterial  Circula- 
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path.,  Par.,  1893,  v,  778. 
Tigerstedt,  R.,  and  Bergmann,  G.:  Niere  und  Kreislauf,  Skand.  Arch.  f.  Physiol.,  Leipz., 

1898,  viii,  223. 
Pearce,  R.  M.:  The  Theory  of  Chemical  Correlation  as  applied  to  the  Pathology  of  the 

Kidney,  Arch.  Int.  Med.,   Chicago,   1908,  ii,   77.   The  Problems  of  Experimental 

Nephritis,  ibid.,  1910,  v,  133. 
Fraenkel,  A.:  Ueber  den  Gehalt  des  Blutes  an  Adrenalin  bei  chronischer  Nephritis  und 

Morbus  Basedowii,  Arch,  f .  exper.  Path.  u.  Pharmakol.,  Leipz.,  1909,  Ix,  395. 
Rowntree,  L.  G.,  and  Geraghty,  J.  T.:   The  Phthalein  Test,  Arch.  Int.  Med.,  Chicago, 

1912,  ix,  284. 
Janeway,  T.  C:  Am.  J.  M.  Sc,  1906,  cxxxi,  772;  1907,  cxxxiii,  50. 
Matthews:  Quoted  on  page  257. 
Widal :  Quoted  on  page  224. 
Meyer,  E. :  Ueber  Diabetes  insipidus  und  andere  Polyurein,  Deutsches  Arch,  f .  klin.  Med., 

Leipz.,  1905,  lxxxiii,  1. 
Vaquez:  Hypertension  arterielle,  Bull.  soc.  med.  d.  hop.  de  Paris,  Feb.  5,  1904. 
Vaquez  and  Aubertin:  Sur  l'hyperplasie  surrenale  des  nephrites  hypertensives,  ibid.,  1905, 

xxii,  705. 
Wiesel:  Renale  Herzhypertrophie  und  chromaffines  System,  Wien.  med.  Wchnschr.,  1907, 

lvii,  673. 
Aschoff,  L. :  Bemerkungen  zur  Schur-Wiesel'sche  Lehre,  etc.  (nach  Untersuchungen  von- 

A.  E.  Cohn),  Verhandl.  d.  deutsch.  Path.  Gesellsch.,  Jena,  1908,  xix,  131. 
Schur,  H.,  and  Wiesel,  J.:  Beitrage  zur  Physiologie  und  Pathologie  des  chromaffinen ' Ge- 

webes,  Wien.  klin.  Wchnschr.,  1907,  xx,   1202.    Ueber  eine  der  Adrenalinwirkung 

analoge  Wirkung  des  Blutserums  von  Nephritikern  auf  das  Froschauge,  ibid.,  1907, 

xx,  699. 
Hasenfeld,  A.,  and  Fenevessy,  B.:  Ueber  die  Leistungsfahigkeit  des  fettigentarteten  Her- 

zens,  Berl.  klin.  Wchnschr.,  1899,  xxxvi,  80,  125,  150. 
Crile,  G.:  The  Blood-pressure  in  Surgery,  Phila.,  1903. 
Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough,  F.  P.  Chillingworth,  and 

J.  R.  Coffey) :  Acapnia  and  Shock.    I,  Carbon  Dioxide  as  a  Factor  in  the  Regulation 

of  the  Heart-rate,  Am.  Journ.  Physiol.,  Bost.,  1908,  xxi,  126;  Part  II,  ibid.,  1909, 

xxiii,  345,  and  Part  III,  ibid.,  1909,  xxiv,  66. 
Mosso,  A. :  Sui  rapporti  della  respirazione  abdominal  e  toracica,    Arch,  per  la  sci.  med., 

1878,  Fisiologia  dell'uomo  sulla  Alpi,  2d  ed.,  1888. 
Mosso,  A.:  La  respiration  periodique  (phenomene  de  Cheyne-Stokes)  telle  qu'elle  se  pro- 

duit  chez  l'homme  sur  les  Alpes  par  I'effet  de  Facapnie,  Arch.  ital.  de  biol.,  Turin, 

1905,  xliii,  81.    Differences  individuelles  dans  la  resistance  a  la  pression  partie  le  de 

1'oxygene,  ibid.,  1905,  lxiii,  197.     Demonstration  des  centres  respiratoires  spinaux 

au  moyen  de  Facapnie,  ibid.,  1905,  lxiii,  216. 
Barach,  J.  H.:  Blood-pressure  Studies  in  Typhoid,  N.  York  M.  J.,  1907,  Ixxvi,  348. 
Crile,  G. :  Diagnostic  Value  of  Blood-pressure  Determinations  in  the  Diagnosis  of  Typhoid 

Perforation,  Jour.  Am.  M.  Assoc,  Chicago,  1903,  xl,  1292. 
Briggs,  J.  W.,  and  Cook,  H.  W.:  Clinical  Observations  on  Blood-pressure,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1903,  xi,  451. 
Weigert,  K.:  Ueber  das  Verhalten  des  arteriellen  Blutdrucks  bei  den  akuten  Infections- 

krankheiten,  Samml.  klin.  Vortrage,  Leipz.,  1907,  Inn.  Med.,  No.  138. 
John,  M.:  Ueber  den  arteriellen  Blutdruck  bei  Phthisiker,  Ztschr.  f.  diat.  u.  physik.  Therap., 

Leipz.,  1901,  v,  275. 
Naumann:  Blutdruckmessungen  an  Lungenkranken,  Ztschr.  f.  Tuberkulose  u.  Heilstat- 

tenw.,  Leipz.,  1904,  v,  118. 


58  DISEASES  OF  THE  HEART  AND  AORTA. 

Stanton,  W.  B.:  The  Blood-pressure  in  Tuberculosis,  Internat.  Clin.,  Phila.,  1907,  17th 
Ser.,  60. 

Peters,  L.  S.:  Blood-pressure  in  100  Cases  of  Tuberculosis  at  High  Altitudes,  Arch.  iDt. 
Med.,  Chicago,  1908,  ii,  42. 

Goltz,  F.:  Vagus  und  Herz,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1863,  xxvi,  3,  and  1864,  xxix, 
394. 

Keen,  W.  W.,  Mitchell,  S.  Weir,  and  Morehouse,  G.  R.:  Circ.  No.  6,  Surg.  General's  Office, 
Washington,  1864. 

Brunton,  T.  Lauder:  On  the  Pathology  and  Treatment  of  Shock  and  Syncope,  Practi- 
tioner, Lond.,  1873,  xi,  246. 

Crile,  G.:  An  Experimental  Inquiry  into  Surgical  Shock,  Phila.,  1899;  Blood-pressure  in 
Surgery,  Phila.,  1903. 

Porter,  W.  T.:  The  Effect  of  Uniform  Afferent  Impulses  upon  the  Blood-pressure  at 
Different  Levels,  Am.  J.  Physiol.,  Bost.,  1907-8,  xx,  399. 

Porter,  W.  T.,  Marks,  H.  K.,  and  Swift,  J.  B. :  The  Relation  of  Afferent  Impulses  to  Fatigue 
of  the  Vasomotor  Centre,  ibid.,  1907-8,  xx,  444. 

Porter,  W.  T.,  and  Quinby,  W.  C:  Further  Data  Regarding  the  Condition  of  the  Vaso- 
motor Neurons  in  Shock,  ibid.,  1907-8,  xx,  500. 

Seelig,  M.  G.,  and  Lyon,  E.  P.:  The  Condition  of  the  Peripheral  Blood-vessels  in  Shock, 
J.  Am.  M.  Assoc,  Chicago,  1909,  Hi,  45. 

Malcolm,  J.  D.:  A  Lecture  on  the  Condition  of  the  Blood-vessels  during  Shock,  Lancet, 
Lond.,  1905,  i,  573,  618,  737,  922. 

Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough,  F.  P.  Chillingworth,  and 
Caffey):  Acapnia  and  Shock,  Am.  J.  Physiol.,  Bost.,  1908,  xxi,  126;  1909,  xxiii,  345; 
1909,  xxiv,  66;  1910,  xxv,  310;  1910,  xxv,  385;  1910,  xxvi,  260. 

Gatch,  W.  D.:  Nitrous-Oxid-Oxygen  Anesthesia  by  the  Method  of  Rebreathing,  with 
Especial  Reference  to  the  Prevention  of  Shock,  J.  Am.  M.  Assoc,  Chicago,  1910, 
liv,  775. 

Crile,  G.,  and  Dolley,  D.  H.:  A  Method  of  Treatment  of  Hemorrhage,  Jour.  Am.  M.  Assoc, 
Chicago,  1906,  xlvii,  189. 

V.  Recklinghausen,  H. :  Unblutige  Blutdruckmessung,  Arch.  f.  exper.  Path.  u.  Pharmakol., 
Leipz.,  1906,  lv. 

Hooker,  D.  R.,  and  Eyster,  J.  A.  E. :  An  Instrument  for  the  Determination  of  Venous  Pres- 
sure in  Man,  Johns  Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  274. 

Pulmonary  Circulation. 

Trumpp,  J.:  Blutdruckmessungen  an  gesunden  und  kranken  Sauglingen,  Jahrb.  f.  Kinder- 
heilk.,  Berl.,  1906,  lxiii,  43. 

Beutner,  Lichtheim,  Openchowski,  Bradford  and  Dean,  Plumier,  quoted  from  Tigerstedt, 
R.:  Der  kleine  Kreislauf,  Ergeb.  d.  Physiologie,  Wiesb.,  1903,  ii,  52  (in  which  a  com- 
plete summary  of  the  literature  to  that  date  is  to  be  found,  with  excellent  resume 
of  the  facts). 

De  Jager,  S.:  Ueber  den  Blutstrom  in  den  Lungen,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1879, 
xxi,  426. 

Francois-Franck,  Ch.  A.:  Nouvelles  recherches  sur  Taction  vaso-constrictive  pulmonaire 
du  grand  sympathique,  Arch,  de  physiol.  nor.  et  path.,  Par.,  1895,  5  Ser.,  vii,  744,  816. 
Etude  critique  et  experimentale  de  la  vasoconstriction  pulmonaire  reflexe,  ibid.,  1896, 
5  Ser.,  viii,  178,  193. 

Wood,  H.  C,  Jr. :  A  Physiological  Study  of  the  Pulmonary  Circulation,  Am.  Jour.  Physiol., 
Bost.,  1902,  vi,  283. 

Petitjean,  G. :  Action  de  quelques  medicaments  vasomoteurs  (nitrite  d'amyle,  adrenaline, 
ergot  de  seigle)  sur  la  circulation  pulmonaire,  J.  de  physiol.  et  de  path,  gen.,  Par., 
1908,  x,  403. 

Wiggers,  C.  J.:  An  Improved  Outflow-recording  Apparatus,  Am.  J.  Physiol.,  Bost.,  1908-9, 
xxiii,  23.  The  Action  of  Adrenalin  on  the  Pulmonary  Circulation,  J.  Pharmacol, 
and  Exper.  Therap.,  Bait.,  1909,  i,  341.  A  Physiological  Investigation  of  the  Treat- 
ment of  Haemoptysis,  Arch.  Int.  Med.,  Chicago,  1911,  viii,  17. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY. 


59 


VISCOSITY  OF  THE  BLOOD. 

One  of  the  most  important  factors  in  determining  the  work  of  the  heart 
and  the  nutriment  of  the  tissues  is  the  viscosity  of  the  blood, — that  is,  the 
friction  which  its  molecules  exert  upon  each  other  and  upon  the  walls  of  the 
blood-vessels. 

Poisseuille  and  later  Arrhenius  introduced  a  method  for  determining  viscosity  quan- 
titatively for  indifferent  fluids  by  observing  the  time  taken  for  a  given  volume  of  fluid  to 
flow  vertically  down  a  given  length  of  capillary  tube.  The  time  taken  by  water  to  flow 
under  the  same  conditions  was  used  as  the  unit.    Poisseuille  found 

Quantity  of  blood  flowing  in  given  time  =  viscosity  coefficient  X  (diameter  of  capil- 
lary)4 X  height  of  pressure:  length  of  tube  for  distance  of  flow. 

Huerthle  found  that  Poisseuille's  law  also  held  for  pulsating  fluids  and  measured  the 
viscosity  of  the  blood  in  the  living  animal  by  comparing  the  outflow  of  blood  from  a  capil- 
lary tube  introduced  into  the  aorta  to  the  outflow  of  water  under  the  same  conditions. 

Viscosity  coefficient  (water)  =4700 
Dog's  blood  =  1045 

Water        4700 

=  4.5     Coefficient  of  viscosity. 


Dog's  blood     1045 

Apparatus  for  Clinical  Determination  of  Viscosity. — Various  forms  of 
apparatus  have  been  devised  for  determining  the  viscosity  clinically,  most 
of  them  depending  upon  the  time  taken  for  a  column  of  blood  in  a  given 

capillary  to  traverse  a  given  distance 
a  or  to  flow  out  of  a  given  orifice  when 

subjected  to  the  pressure  exerted  by 
a  constant  column  of  water. 


WATCfiJACKET 


Fig.  32. — Determann's  apparatus  for  determining  the  viscosity  of  the  blood.  (After  Brugsch  and 
8chittenhelm.)  A.  Apparatus  at  rest  on  its  stand,  pivoted  on  the  thermometer  and  the  handle  as  an  axis. 
In  the  blood-receiving  tube  within  the  water-jacket  ae  =  df,  ab  =  cd.  B.  Method  of  application.  (After 
Brugsch  and  Schittenhelm.) 


Such  apparatus  has  been  described  by  Huerthle,  Burton-Opitz,  Hirsch  and  Beck, 
Determann.  Hess  and  also  McCaskey  have  devised  very  simple  forms  of  apparatus  in 
which  suction  from  a  rubber  bulb  is  used  instead  of  positive  pressure.  C.  R.  Austrian  in  the 
Johns  Hopkins  Medical  Clinic  has  found  that  the  Hess  apparatus  gives  results  with  normal 
blood  which  tally  well  with  the  blood  count,  and  which  therefore  seem  quite  satisfactory. 


60  DISEASES  OF  THE  HEART  AND  AORTA. 

Determann's  newer  apparatus  (Fig.  32),  however,  combines  clinical 
convenience  with  accuracy  and  is  probably  the  most  satisfactory  now  in  use.  It  consists 
of  a  capillary  tube  surrounded  by  a  small  condenser- jacket  of  glass  containing  water  at 
38°.  The  jacket  bears  two  side  arms  which  rest  in  the  forks  of  two  uprights  so  that  the 
jackets  always  assume  a  vertical  position.  The  apparatus  is  taken  up  as  a  whole  and  the 
blood  sucked  up  to  a  mark  on  the  capillary.  The  apparatus  is  then  placed  back  on  the 
forks  and  the  time  taken  for  the  blood  to  flow  out  until  it  reaches  a  second  (lower)  mark 
is  noted.  (This  should  require  30-40  seconds.)  A  similar  determination  is  made  with  water 
(6-8  seconds). 

In  order  to  keep  the  blood  from  clotting,  a  little  hirudin  may  be  placed  upon  the  ear 
before  stabbing  it.  This  does  not  alter  the  viscosity  as  do  adding  sodium  oxalate,  laking, 
and  defibrination;  and  keeps  the  blood  from  clotting  for  20-30  minutes. 

Determann  obtains  a  few  drops  of  blood  quickly  by  having  the  patient  exert  a  forced 
expiration  with  the  glottis  closed  (Valsalva's  experiment). 

Factors  Influencing  Viscosity. — Heubner,  Determann,  and  others  have 
found  that  the  chief  factor  in  determining  the  viscosity  is  the  viscosity  of 
the  red  corpuscles,  to  which  about  two-thirds  of  the  viscosity  of  the  blood  is 
due.  Indeed,  in  many  cases  these  observers,  and  also  Austrian,  have  found 
that  the  blood-count  and  the  viscosity  furnish  accurate  controls  of  one  an- 
other,— though  there  are  exceptions  under  pathological  conditions  (leukaemia, 
etc.).  There  is  little  if  any  difference  between  the  viscosity  of  the  normal 
blood  in  the  arteries,  capillaries,  and  veins.  But  in  venous  stasis  the  vis- 
cosity increases  tremendously. 

In  a  polycythaemica  with  11,000,000  red  corpuscles  the  v  i  s- 
cosity  may  be  three  or  more  times  the  normal   (Stern) . 

On  the  other  hand,  in  anaemias,  fever,  the  hydraemia 
which  is  associated  with  anasarca  in  broken  compensation  or  exudates  the 
viscosity  is  uniformly  greatly  diminished. 

Burton-Opitz  found  that  diet  exerted  a  considerable  effect,  meat 
raising  the  viscosity,  carbohydrates  and  fats  lowering  it. 
He  also  found  that  hot  baths  lowered  viscosity,  while  cold  baths  increased  it. 
Hot-air  baths  seem  to  have  little  effect. 

In  compensated  heart  disease  the  water  content  of  the  blood  does  not 
change  (Askanazy),  nor  does  the  viscosity,  but  the  water  is  increased  and 
the  viscosity  diminished  (3.74  to  4.21)  when  compensation  is  broken  (Deter- 
mann).   In  bronchitis  and  diabetes  it  is  high  (5.5). 

Determann  cannot  confirm  the  findings  of  Otfried  Miiller  and  Inada 
that  potassium  iodide  lowers  viscosity;  and  indeed  the  changes  which  they 
obtained  were  less  than  1.0  per  cent.,  well  within  the  limits  of  experimental 
error.  Their  paper,  as  well  as  those  of  Hirsch  and  Beck,  illustrates  the  ten- 
dency of  workers  in  the  field  to  draw  too  definite  conclusions  from  too  small 
variations. 

BIBLIOGRAPHY. 

Viscosity. 

Poisseuille:  Ann.  de  chim.  et  de  phys.,  Par.,  1847,  3  ser.,  i,  21  (quoted  from  Hirsch  and 

Beck). 
Arrhenius,  S.:  Innere  Reibung  wasseriger  Losungen,  Ztschr.  f .  physik.  Chem.,  Leipz.,  1887, 

i,  289. 
Huerthle,  K.:  Widerstand  der  Blutbahn,  Deutsch.  med.  Wochenschr.,  Leipz.,  1897,  809. 

Ueber  eine  Methode  zur  Bestimmung  der  Viskositat  des  lebenden  Blutes  und  ihre 

Ergebnisse,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1900,  lxxxii,  415. 


BLOOD-PRESSURE  AND  BLOOD  VISCOSITY.  61 

Burton-Opitz,  R.:  Ueber  die  Veranderung  der  Viskositat  des  Blutes  unter  dem  Einfluss 
verschiedener  Ernahrung  und  experimenteller  Eingriffe,  Arch.  f.  d.  ges.  Physiol., 
Bonn,  1900,  lxxxii,  447.  Vergleich  der  Viskositat  des  normalen  mit  der  des  Oxalat- 
blutes  und  des  defibrinirten  Blutes  und  des  Blutserums  bei  verschiedener  Tempera- 
ture, ibid.,  1900,  lxxxii,  464.  Weitere  Studien  ueber  die  Viskositat  des  Blutes,  ibid., 
1906,  cxii,  189;  also  Am.  Med.,  1900,  vii,  111.  The  Effect  of  Changes  in  Tempera- 
ture upon  the  Viscosity  of  the  Living  Blood,  J.  Exper.  Med.,  N.  York,  1906,  viii,  59. 
The  Effect  of  Intravenous  Injections  of  Solutions  of  Dextrose  upon  the  Viscosity  of 
the  Blood,  ibid.,  viii,  240. 

Hirsch,  C,  and  Beck,  C:  Studien  zur  Lehre  von  der  Viscositat  (innere  Reibung)  des  leben- 
den  menschlichen  Blutes,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1900,  lxix,  503:  and 
1902,  lxxii,  560. 

Determann:  Klinische  Untersuchungen  ueber  die  Viskositat  des  menschlichen  Blutes, 
Ztschr.  f .  klin.  Med.,  Berl.,  1906,  lix,  283.  Discussion  upon  this  paper  in  the  Zentralbl. 
f.  inn.  Med.,  1906,  xxvii,  519.  Die  Beinflussung  der  Viskositat  des  menschlichen 
Blutes  durch  Kaltereize,  Warmeentziehung,  Warmezufuhr,  und  Warmestauung,  Berl. 
klin.  Wochnschr.,  1907,  xliv,  687,  723. 

Hess,  W. :  Ein  neuer  Apparat  zur  Bestimmung  der  Viscositat  des  Blutes,  Cor.-Bl.  f .  schweiz. 
Aerzte,  Basel,  1907,  xxxvii,  73. 

McCaskey,  G.  W.:  The  Viscosity  of  the  Blood;  Its  Value  in  Clinical  Medicine,  J.  Am.  M. 
Assoc,  Chicago,  1908,  li,  1653. 

Determann:  Ein  einfaches,  stets  gebrauchfertiges  Blutviskosimeter,  Muenchen.  med. 
Wochnschr.,  1907,  liv,  1130. 

Heubner,  W.:  Die  Viskositat  des  Blutes,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz., 
1905,  liii,  280. 

Stern:  Discussion  of  Determann's  paper. 

Askanasy,  S. :  Ueber  den  Wassergehalt  des  Blutes  und  des  Blutserums  bei  Kreislaufstorung, 
u.  s.  w.,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1897,  lix,  385. 

DETERMINATION  OF  THE  VOLUME  OF  THE  BLOOD  PLASMA  AND  THE 
TOTAL  VOLUME  OF  THE  BLOOD. 

The  older  studies  of  Welker  placed  the  volume  of  the  blood  at  one  thir- 
teenth of  the  body  weight.  More  recently  Haldane  and  Smith  have  given 
one  twenty-first  and  Plesch  has  given  one-nineteenth  as  the  figure,  but  their 
methods  are  both  complicated,  fraught  with  discomfort  or  danger  to  the 
patient,  and  full  of  inherent  technical  errors.  A  simple  practical  clinical 
method  has  recently  been  introduced  by  Keith,  Rowntree  and  Geraghty 
which  has  given  valuable  clinical  and  experimental  data,  and  has  opened  up 
new  lines  of  investigation. 

In  carrying  out  this  determination  they  inject  intravenously  a  dye  (vital 
red)  which  does  not  diffuse  out  of  the  arteries,  capillaries  and  veins  for  quite 


NaS03l     X     JS03Na  I     )    NaSO.L     I     JS03Na 


a  while  after  its  injection.  The  blood  plasma  therefore  remains  stained  with 
the  dye.  A  small  quantity  (10  cc.)  of  blood  is  removed  within  ten  minutes 
after  the  injection,  sodium  oxalate  added  to  prevent  coagulation,  and  the 
corpuscles  are  centrifugalized  off  with  a  high  power  centrifuge  (3000  revolu- 
tions per  minute)  for  twenty  minutes  in  a  graduated  centrifuge  tube.  The 
ratio  of  blood  corpuscle  volume  to  plasma  is  noted.  The  plasma  thus  ob- 
tained is  colored  by  the  dye.  Experiments  have  shown  that  this  dye  is  not 
absorbed  by  the  corpuscles.  The  amount  of  dye  contained  in  the  plasma  can 
readily  be  determined  by  comparison  with  a  standard  solution  of  vital  red 


62  DISEASES  OF  THE  HEART  AND  AORTA. 

in  a  colorimeter.  From  the  proportion  between  the  amount  of  dye  injected 
and  the  amount  found  in  a  known  amount  of  blood  plasma,  the  total  volume 
of  blood  plasma  can  be  calculated.  The  total  volume  of  the  blood  can  be 
calculated  from  the  ratio  of  corpuscles  to  plasma  obtained  in  the  graduated 

centrifuge  tube. 

Total  volume  of  blood       Corpuscles + Plasma 
Total  volume  of  plasma  Plasma 

Keith,  Rowntree,  and  Geraghty  have  found  that  in  normal  subjects  the 
volume  of  blood  plasma  varied  from  42  to  56  cc.  per  kilogram  of  body  weight 
(^_  to  |f  total  body  weight  average  j^l)  so  that  a  man  of  140  lbs.  weight 
would  have  three  litres  of  plasma. 

The  average  volume  of  total  blood  is  5350  cc.  or  85  cc.  per  Kg.  (yy^  of 
body  weight,  the  variations  being  from  yV  to  1^75). 

They  found  normal  values  in  emaciation,  chronic  hypertension,  several 
cases  of  myocardial  insufficiency,  aneurism  and  in  some  cases  of  anaemia,  high 
values  were  encountered  in  pregnancy,  anaemia,  polycythaemia,  and  in  one 
case  of  general  anasarca.  In  obesity  and  diabetes  the  blood  volume  is  rela- 
tively low. 

Marked  variations  of  blood-pressure  in  animals  produced  by  the  injec- 
tion of  adrenalin  caused  no  change  in  the  total  volume  of  the  blood. 

BIBLIOGRAPHY 

Welcker,  H.:  Bestimmungen  der  Menge  des  Korperblutes,  etc.,  Prager  Vrtljahresschr.. 

1854,  iv,  11;  Ztschr.  f.  Prat.  Med.,  1858,  iv,  145. 
Haldane  J.,  and  Smith,  J.  Lorrain :    The  Mass  and  Oxygen  Capacity  of  the  Blood  in  Man, 

J.  Physiol.,  1899-1900,  xxv,  331. 
Smith,  J.  Lorrain:  Discussion  on  the  Blood  in  Disease,  Trans.  Path.  Soc,  Lond.,  1900,  li, 

311. 
Plesch,  J.:  Haemodynamische  Studien,  Ztschr.  f.  exper.  Path.  u.  Therap.,  1909,  vi,  380. 
Keith,  N.  M.,  Rowntree,  L.  G.,  and  Geraghty,  J.  T. :  A  Method  for  the  Determination  of 

Plasma  and  Blood  Volume,  Arch.  Int.  Med.,  1915,  xvi,  547. 


III. 

THE    ARTERIAL    PULSE. 

Historical. — Observation  of  the  arterial  pulse  began  almost  synchronously  with  the 
accurate  observation  of  disease  in  general.  Hippocrates  (B.  C.  500)  noted  the  marked 
pulsation  (a^vyfiog)  of  the  arteries  in  certain  diseases,  but  did  not  associate  it  with  the  beat 
of  the  heart.  Herophilus  (B.  C.  300)  observed  the  relative  synchronism  of  these  two  events 
and  speaks  of  the  quiet  pulse  in  health  (acpvy/iog)  in  contrast  to  the  marked  pulsation  in 
disease  (the  iral/idg  of  Hippocrates).  Eristratus  (B.  C.  280)  showed  that  the  arteries  near 
the  heart  beat  before  the  arteries  more  distant  from  it.  Aristotle  and  later  Archigenes 
(first  century  after  the  Christian  era)  made  numerous  observations  upon  the  pulse  in  various 
diseases,  and  the  latter  described  and  gave  the  name  to  the  dicrotic  type  in  cases 
of  fever,  although  he  still  believed  that  the  arteries  were  filled  with  air.  Galen  (A.  D.  131- 
202)  demonstrated  that  the  arteries  were  filled  with  blood  and  studied  the  influence  of  sex, 
'  age,  climate,  sleep,  hot  and  cold  baths  upon  the  rhythm  of  the  pulse. 

The  old  Chinese  physicians  also  described  the  pulse  and  even  made  drawings  to 
illustrate  their  sensory  impressions — a  practice  which  did  not  begin  in  Europe  until  the 
time  of  Henri  Fouquet  in  1767.  After  Harvey's  demonstration  of  the  circulation  of  the 
blood  (1628),  the  study  of  the  pulse  was  resumed  with  renewed  vigor  and  has  continued 
to  the  present  day. 

Examination  of  the  Pulse. — The  characteristics  of  the  pulse-wave  are, 
as  a  rule,  determined  upon  the  radial  artery,  in  which  the  arterial  tension 
may  be  estimated  as  described  on  page  26,  the  wall  of  the  artery  being  also 
rolled  under  the  ringer  while  the  artery  is  empty,  and  thus  the  presence  or 
absence  of  arteriosclerosis  noted.  The  walls  of  a  normal  artery  are  barely, 
if  at  all,  palpable;  an  atheromatous  artery  may  feel  like  the  trachea  of  a 
small  animal  (goose-neck) ;  a  diffusely  sclerotic  artery  feels  like  a  piece  of 
thick-walled  rubber  tube. 

It  is  important  to  note  the  palpability  of  several  arteries,  since  one 
of  them  may  escape  a  sclerotic  process.  All  the  blood  must  have  been 
pressed  out  of  their  lumina  and  of  the  venae  comites  that  accompany  them 
before  palpation  is  begun,  or  else  normal  arteries  may  appear  to  be 
sclerotic.  The  pressure  is  then  relieved,  and  the  tips  of  two  or  three  fingers 
are  pressed  upon  the  artery  until  the  pulse  appears  maximal  (at  about 
the  minimal  pressure),  when  the  following  characteristics  are  noted:  (1) 
whether  the  artery  (hence  the  pulse)  feels  large  and  dilated  (pulsus  m  a  g  - 
nu s)  or  small  and  constricted  (pulsus  parvus);  (2)  whether  the 
pulse  is  hard  (pulsus  durus)  or  soft  (pulsus  mollis),— i.e.,  whether 
the  minimal  pressure  is  low  or  high;  (3)  whether  the  onset  of  the  wave  is 
sudden  (pulsus  celer)or  gradual  ( p  u  Is  u  s  tardus);  (4)  whether 
the  wave  is  sustained  (anacrotic)  or  subsides  suddenly  under  the 
finger  (collapsing,  water-hammer,  or  Corrigan  pulse) ;  (5)  the 
rate  of  the  heart  per  minute  (counted  continuously  during  at  least  a  half 
minute) ;  (6)  whether  the  rhythm  is  regular  (pulsus  regularis)or 
irregular   (pulsus    irregularis). 

Clinical  Sphygmographs.  —  An  instrument  (sphygmograph)  to 
record  the  pulse-wave  graphically  was  first  devised  by  K.  Vierordt  (1855), 

63 


64 


DISEASES  OF  THE  HEART  AND  AORTA. 


but  it  was  not  until  1860  that  E.  J.  Marey  devised  a  thoroughly  practical 
and  accurate  form,  almost  devoid  of  error,  which  is  still  in  use. 

Marey's  sphygmograph  consists  of  a  button  (pelote)  pressed  against  the  skin  over 
the  artery  by  means  of  a  spring  so  as  to  receive  the  pulsations  from  the  artery.  It  is  held 
in  place  by  a  leather  cuff,  and  it  is  most  important  that  the  pelote  remain  exactly  over  and 
not  to  one  side  of  the  artery.  The  pelote  is  surmounted  by  a  vertical  rod  or  screw  which 
articulates  by  a  movable  joint  with  a  long  writing  lever.  The  writing  lever  records  the 
magnified  pulse  movements  upon  a  surface  of  smoked  paper  held  in  vertical  position  by  a 
brass  upright  and  driven  by  a  small  piece  of  clock-work. 

A  more  compact  and  convenient  form  of  sphygmograph  is  that  of  Dudgeon,  in  which 
the  straight  lever  is  supplanted  by  a  double-jointed  one  which  writes  on  a  horizontal  instead 
of  a  vertical  strip  of  smoked  paper.  The  tension  of  the  spring  pressing  down  the  pelote 
is  roughly  adjustable,  which  allows  some  variation  in  the  pressure  over  the  artery. 
V  .  J  a  q  u  e  t  has  improved  Dudgeon's  apparatus  by  adding  to  it  a  small  time  marker 
recording  fifths  of  a  second. 

O.  Frank  has  introduced  a  method  for  recording  the  form  of  the  pulse-wave  by  photo- 
graphing the  movement  of  a  beam  of  light  thrown  from  an  arc  light  on  to  a  small  mirror 
made  of  mercury-coated  cover-glass  fixed  upon  a  very  small  vertically  placed  tambour, 
and  thence  reflected  upon  a  moving  surface  of  photographic  film.  C.  J.  Wiggers  has  per- 
fected this  apparatus  and  adapted  it  to  clinical  purposes,  using  a  delicate  rubber  membrane 
made  by  dipping  a  piece  of  half-inch  brass  tube  into  liquid  rubber  cement.  The  bit  of 
mirrored  cover-glass  is  fixed  upon  the  membrane  before  it  is  dry. 


mte 


Fig.  33a. — Diagram  showing  principle  of  apparatus.  G,  piece  of 
celluloid;  M,  mirror.    (After  Wiggers,  Jour.  Amer.  Med.  Assoc.) 


IHIIHllllllllllllH  A 
Fig.  336. — Mounting  of  capsules. 


Errors  in  Sphygmography. — In  spite  of  the  existence  of  these  fairly 
satisfactory  sphygmographs  and  of  their  wide  use,  discrepancies  between 
the  clinical  observations  and  the  tracings  obtained  are  so  great  that  Cabot 
refers  to  the  sphygmograph  as  "  an  interesting  little  toy."  The  reason  that 
it  is  not  of  value  must  be  either  that  the  apparatus  itself  is  subject  to 
inherent  errors,  or  that,  as  Mackenzie  states,  "it  was  expected  to  give  in- 
formation of  a  kind  that  it  was  incapable  of  supplying.''  Unfortunately, 
both  are  the  case. 

Athanasiu,  in  investigating  the  accuracy  of  graphic  recording  devices,  found  that  all 
sphygmographs  which  magnified  the  movement  more  than  twenty  times  introduced  a 
large  inherent  error,  that  of  all  the  forms  in  use  Marey's  introduced  the  least  error,  while 
the  Dudgeon  apparatus  and  the  Jaquet  magnified  it  130  times,  introducing  tremendous 
distortion  from  flinging  large  pulsations. 

On  the  other  hand,  the  writer,  D.  Gerhardt,  and  Stewart  have  been  able  to  show 
that  not  only  the  size  but  also  the  entire  type  of  the  pulse-curve  obtained  depends  upon 
the  pressure  exerted  upon  the  artery  and  other  similar  factors;  the  true  form  of  the  pulse- 
wave  being  obtained  only  when  the  pressure  exerted  by  the  sphygmograph  is  exactly  equal 


PLATE  II. 


,  V  ^  h* 

life:  ,\'7\  ,^.™Vk.! 

Fig.   1. — Two  segments  of  radial  and  carotid  pulse:    A,  under  normal  conditions  and  B,  after  irthakt 
tion  of  amyl  nitrite  (low  peripheral  resistance).     (After  Wiggers,  Amer.  Med.  Assoc.) 


/ 


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y 

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1 

51 

I 

>/. 

'    W 

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^x 

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N'3.fc 

A  B 

Fig.  2. — Volume  pulse  curve  superposed.  A.  I,  Normal  pulse  curve;  II,  curve  showing  the  effect  of 
nitroglycerine  (predicrotic  reflux) ;  III,  tracing  from  a  case  of  aortic  insufficiency  (showing  an  intense  degree 
of  predicrotic  reflux).  B.  Heavy  line,  volume  pulse  curve  before  exercise.  Broken  line,  curve  from  same 
person  after  exercise.  The  numbers  indicate  cubic  centimetres  of  blood-flow  per  100  Gm.  arm  per  minute. 
(Modified  from  Hewlett's  curves.) 


THE  ARTERIAL  PULSE. 


65 


NORMAL 


AORTIC 
INSUFFICIENCY 


to  the  pressure  within  the  artery.  Fortunately,  this  is  the  point  at  which  the  pulse  excur- 
sion is  maximal,  and  as  all  observers  strive  for  the  largest  excursion,  it  is  probable  that 
most  sphygmographic  records  are  taken  at  about  this  pressure.     The  ideal  apparatus  is 

the  one  in  which  it  is  not  merely  probable  but  certain,  and 
hence  that  of  Roy  and  Adami  is  the  only  one  which  abso- 
lutely fulfils  the  requirements. 

The  Absolute  Sphygmogram.  —  A  very  con- 
venient and  instructive  method  of  recording  pulse 
tracings  has  been  introduced  by  Sahli.  Sahli 
transfers  the  pulse -curve  to  coordinate  paper 
upon  which  the  ordinates  represent  millimetres 
of  mercury  and  the  abscissae  represent  fractions 
of  a  second.  The  lowest  point  of  the  pulse-curve 
he  marks  at  the  level  corresponding  to  the  mini- 
mal blood-pressure,  determined  at  the  time  with 
the  sphygmomanometer;  the  highest  point  at  the 
level  corresponding  to  the  maximal  pressure;  and 
maps  out  besides  this  the  other  main  points  of 
the  pulse-curve  (predicrotic  fall  and  wave,  dicrotic 
notch,  summit  of  dicrotic  wave,  etc.)  at  heights 
and  distances  proportional  to  their  occurrence  upon 
the  sphygmogram,  but  translated  to  this  new 
sphygmogramsraii  of  which    scale  of  pressure  and  time.     This  curve  he  terms 

correspond  to  the  radial  trac-  file    absolute     Sphy^HlOgram. 

ing  above.   The  figures  to  the 

left    indicate    pressures    in  _,,         ,       .  , 

mm.  Hg.  Ine  absolute  sphygmogram  can  also  be  read  off  from 

the  ordinary  sphygmogram  by  using  the  lowest  point  on 
the  tracing  as  the  ordinate  of  minimal  pressure  and  as  a  base  line  for  determining 
the  pressure  at  other  points,  and  calculating  these  from  the  proportion 

Ordinate    of    point  :    Total   height  of   pulse-wave  = 
Pressure  at  that  instant  (above  minimal  arterial  pressure)   :  Pulse-pressure. 

Discrepancies  between  Feeling  and  Recording  the  Pulse. — Not  all  the 

discrepancies  between  sensory  impression  and  sphygmogram  are  the  fault 
of  the  instrument.  In  the  first  place,  there  is  no  absolute  uniformity  in 
the  minds  of  physicians  as  the  standard  to  be  applied  to  the  individual 
pulse.  Thus,  the  writer  has  seen  one  eminent  clinician  dictate  a  note, 
"pulse  not  collapsing,"  and  another  a  few  minutes  later  state  that  the 
same  "pulse  is  collapsing  in  quality."  The  pulse  had  not  changed,  but 
the  subjective  criteria  of  the  two  men  were  slightly  different. 

Again,  between  pulse  palpation  and  sphygmogram  there  is  a  difference.  It  is  very 
difficult,  almost  impossible,  to  determine  just  how  long  a  pulse  is  sustained  and  how  quickly 
it  falls,  since  these  judgments  are  based  upon  a  sequence  of  events  lasting  for  an  interval 
of  about  one-tenth  of  a  second,  and  changes  both  in  time  and  in  pressure  must  be  con- 
sidered without  the  presence  of  any  simultaneous  standard  for  comparison.  Psychologic- 
ally, such  comparisons  must  be  very  fallible.  Practically  they  are  not  as  fallible  as  they 
appear,  for  the  judgment  is  based  not  upon  form  or  duration,  unless  the  abnormalities  are 
marked,  as  much  as  upon  changes  of  pressure.  What  one  really  appreciates  most  in  feel- 
ing the  pulse  is  the  amount  of  minimal  pressure  ("hardness"  of  the  pulse)  and  the  amount 
of  the  pulse-pressure  (size  of  pulse),  and  only  to  a  lesser  extent  the  duration  of  the  pulse- 
wave.  Hence,  the  sensation  due  to  a  high  pulse-pressure  with  a  moderate  diastolic 
pressure  is  often  mistaken  for  that  due  to  a  collapsing  pulse,  though  the  form  of  the  pulse- 

5 


66 


DISEASES  OF  THE  HEART  AND  AORTA. 


-¥^*o 


Fig.  35. — Significance  of  the  pulse-curve. 
J,  inflow  into  the  artery  from  heart;  O,  outflow 
from  the  artery  toward  the  periphery,  or  actual 
reflux  toward  the  aorta. 


wave  may  show  that  it  is  quite  well  sustained.  In  comparing  the  pulse  sensation  with  the 
sphygmogram,  one  is  therefore  comparing  two  somewhat  different  standards,  and  this 
inherent  difference  must  be  taken  into  account. 

Significance  of  the  Pulse=curve. — Assuming,  however,  that  one  has  ob- 
tained a  correct  tracing  from  the  artery,  what  deductions  are  allowable?  It 
is  evident  that  the  artery  expands  somewhat  under  an  increase  in  pressure 

(causing  a  rise  in  the  pulse-wave)  and 
contracts  when  pressure  decreases 
(causing  a  fall  in  the  pulse-wave,. 
Further,  the  pressure  in  the  artery  in- 
creases or  decreases,  depending  upon 
whether  more  blood  enters  it  than  can 
leave  it  at  that  instant  (Fig.  35,  I>0) 
or  whether  the  reverse  is  the  case 
(I <0).  When  the  inflow  exactly 
equals  the  outflow  (1=  0),  no  change 
of  pressure  occurs  and  a  plateau 
results.  The  pulse  tracing  is  merely  the  record  of  these  events — but,  as  Hew- 
lett has  shown,  the  emptying  of  the  radial  artery  may  occur  either  onward 
to  the  arterioles  or  as  an  ebbing  back  into  the  brachial  and  subclavian. 

The  normal  pulse-wave  has  the 
following  forms:  an  upstroke  more 
or  less  steep  (percussion  wave;,  a 
rather  acute  summit,  and  sudden  fall 
(predicrotic)  followed  by  a  very  small 
rebounding  wave  (predicrotic  wave), 
then  another  more  gradual  fall  termi- 
nating in  a  small  notch  (dicrotic  notch) 
which  marks  the  end  of  systole 
(Marey,  Huerthle) ,  then  a  gradual  fall 
during  diastole.  In  the  aorta  the  fall 
in  waves  is  not  as  steep  as  in  the 
radial  artery,  which  indicates  that 
the  former  reflects  the  conditions 
near  the  heart,  the  latter  shows  the 
conditions  at  the  periphery  (Marey) 
Relation  of  Pulse  Form  to  Peri= 
pheral  Resistance. — There  are  three 
general  types  of  pulse  (Marey,  Hirsch- 
felder)  which  may  occur  without  any 
heart  lesion  whatever,  and  even  in  the  same  individual  at  the  same  maxi- 
mal and  minimal  pressures,  though  usually  the  maximal  and  minimal  pres- 
sures vary  with  these  conditions.     (Fig.  36.) 

Type  I  corresponds  to  marked  peripheral  dilata- 
tion, as  after  exercise,  after  meals,  in  shock,  fevers,  or  in  some  nervous 
individuals  with  vasomotor  instability.  This  is  the  collapsing  type  of  pulse, 
rapid  rise  and  rapid  fall  sometimes  followed  by  a  large  dicrotic  wave  (see 
page  68).  The  rise  is,  however,  about  two  hundredths  of  a  second  slower 
than  normal,  but  this  difference  is  not  within  the  limits  of  perception.     It 


Fig.  36.— Diagram  showing  the  time  rela- 
tions of  ventricular  volume  and  pressure  curves 
to  pulse  tracings  from  the  aorta,  carotid  and 
radial  arteries.  Time  divisions  in  one-tenth  sec- 
onds. (Schematic.)  Dotted  lines  represent  curves 
taken  with  high  peripheral  resistance. 


THE  ARTERIAL  PULSE. 


67 


feels  more  sudden  because  it  is  sharply  followed  by  the  sudden  fall.  The 
fall  in  this  type  of  pulse  is  almost  complete  before  the  end  of  systole,  i.e., 
before  the  dicrotic  notch  which  marks  that  point  (Marey,  Huerthle). 


no 


~7&~^ — =" 


Fig.  37. — Three  types  of  arterial  pulse-curve  corresponding  to  the  same  pulse-pressure  and  same  pulse- 
rate.     (Johns  Hopkins  Hosp.  Bull,  xviii.)     I,  vasodilation;    II,  normal;    III,  vasoconstriction. 

In  T  y  p  e  II  only  about  half  the  fall  occurs  during  systole.  This 
corresponds  to  moderate  degree  of  dilatation  and  is 
the  type  present  in  normal  individuals. 

In  Type  III  the  wave  soon  rises  to  the  summit  and  remains  there, 
forming  a  sustained  plateau  (outflow  =  inflow)  until  the  end  of  systole,  when 

it  gradually  falls.  This  corresponds 
to  peripheral  constriction, 
preventing  the  outflow  from  the  aorta 
from  exceeding  the  inflow  into  it, 
as  is  the  case  where  a  normal  degree 
of  dilatation  is  present.  The  normal 
pulse  in  man  may  be  converted  into 
this  type  by  compression  of  both 
femoral  arteries  (Marey)  or  of  the  ab- 
dominal aorta  (Stewart).  The  mere 
increase  of  the  blood-pressure  is  not 
a  cause,  because  after  exercise  the 
blood-pressure  is  increased  and  yet 
the  pulse  becomes  more  collapsing 
than  before. 


Fig.  38. — Effect  of  inhalation  of  amyl  nitrite 
upon  the  pulse-form.  (After  v.  Kries.)  Curves 
taken  in  succession.  Vasodilation  reaches  its 
maximum  at  c  and  diminishes  at  d  and  e.  Well- 
marked  dicrotism  at  d.  /3  and  a  indicate  second- 
ary waves  due  to  elasticity  of  the  artery. 


These  general  outlines  of  the  pulse- 
waves  are  further  modified  by  smaller  wave- 
lets due  to  the  elastic  vibrations  of  the  artery 
wall,  or  to  the  rebound  of  the  percussion 
wave  at  the  periphery  (v.  Kries).  The  most  important  of  these  is  the  dicrotic  wave 
following  immediately  upon  the  closure  of  the  aortic  valves  and  due  either  to 
a  centrifugal  wave  from  the  blood  impinging  against  them,  or  to 
a  reflected  centripetal  wave  from  the  periphery  toward  the 
heart  (y.  Kries).  Whichever  theory  may  be  correct,  the  essential  fact  remains  that 
the  dicrotic  wave  is  a  secondary  one  and  is  dependent  upon  arterial  elasticity.  V.  Kries 
has  shown  that  the  dicrotic  wave  is  most  marked  when  the  peripheral  vessels  are  consider- 
ably dilated,  but  not  when  they  are  dilated  to  their  fullest  extent  (Fig.  38). 

The  other  waves  may  occur  upon  either  upstroke  (anacrotic)  or  upon  the  downstroke 
(Jsatacrotic,  Fig.  38,  a,  b)  and  are  designated  accordingly.     Small  secondary  waves  of  this 


68 


DISEASES  OF  THE  HEART  AND  AORTA. 


type  are  most  marked  when  the  pressure  is  high  and  the  heart  action  strong  {e.g.,  pulsus 
bisferiens),  but  their  occurrence  is  often  due  to  twitching  of  the  tendons  near  the  pelote 
of  the  sphygmograph,  and  too  great  weight  must  not  be  attached  to  them. 


•h     _ 


Fig.  39. — Mercury  manometer  tracing  from  the  carotid  artery  of  a  dog,  showing  rhythmic  varia- 
tions in  blood-pressure  and  rhythmic  increase  in  dicrotism.  (Kindness  of  Prof.  Abel  and  Dr.  Rowntree.) 
The  dicrotic  wave  increases  at  the  points  (D  + )  at  which  the  blood-pressure  is  lowest  ( — )  and  the  peripheral 
arteries  are  dilated.     Time  in  seconds. 

Volume  Pulse  and  Pressure  Pulse. — A  totally  new  viewpoint  for  the 
interpretation  of  the  pulse-wave  has  been  introduced  by  the  investigations 
of  Hewlett  and  van  Zwalwenberg  upon  the  velocity  of  blood  flow  in  the  arm 
at  each  portion  of  the  cardiac  cycle.  Hewlett  made  use  of  the  same  apparatus 
as  had  been  used  by  him  for  the  study  of  velocity  of  blood  flow  in  the  arm 

except  that  in  order  to  obtain  the  indi- 
vidual waves  more  accurately  he  re- 
corded them  with  a  Frank  capsule 
instead  of  an  ordinary  tambour.  Using 
this  apparatus  Hewlett  has  found  that 
when  there  is  relaxation  of  the  periph- 
eral arteries  accompanied  by  a  great 
increase  in  the  velocity  of  blood  flow 
through  the  arm,  such  as  is  met  with 
after  exercise  or  exposure  to  heat  or 
in  exophthalmic  goitre,  the  collapsing 
type  maybe  present  and  the  collapse  ac- 
companied by  an  acceleration  of  blood 
flow  through  the  arterioles.  Under 
other  circumstances,  however,  a  totally 
different  condition  may  be  accom- 
panied by  a  collapsing  pulse  of  ex- 
actly the  same  quality  and  possessed 
of  exactly  the  same  form  of  sphygmo- 
gram.  This  was  well  typified  by  the 
collapsing  pulse  obtained  after  nitro- 
glycerine. Hewlett's  blood  flow  curves 
showed  that  in  spite  of  the  onset  of 
peripheral  dilatation,  a  larger  pulse 
wave  and  a  collapsing  type  of  pulse  the  velocity  of  blood  flow  per 
minute  was  not  increased  after  nitroglycerine,  but  was  unchanged  or 
even  slightly  diminished.  Here  the  form  of  the  collapsing  pulse  is  met 
in  the  plethysmograph  curve  after  compression  of  the  veins  as  well  as 
in  the  pulse  curve,  and  this  shows  that  during  the  period  of  collapse 
less  blood  is  present  in  the  arm  than  had  been  present  at  the  crest  of 
the  wave — in  ottfer  words,  since  no  blood  could  pass  out  through  the  veins 


Fig.  40. — Diagram  showing  various  forms 
of  pulse-curve  encountered  clinically.  Systolic 
portions  of  the  curve  are  underlined.  HYPER- 
DICROT,  hyperdicrotic. 


TYPES    OF    PULSE    IN    VARIOUS    DISEASES. 

The  following  types  of  pulse  are  associated  with  various  pathological 
conditions  and  corresponding  states  of  the  heart  and  vessels. 


60 

s 

a 

Clinical  condi- 

Blood-pressure associated  with  it. 

Type 
of  pulse.1 

Characteristics. 

tions  in  which  it 
is  most  fre- 

Vascular 
condition. 

Pulse- 

o 

quently  observed. 

Maximum. 

Minimum. 

pressure. 

Normal .... 

40 

Sudden  rise,  sharp 
apex,  slight  pre- 
dicrotic  fall;  then 

Normal     individ- 
uals 

Normal  . . 

Normal. 

slow    fall,    small 

Some  cases  of  aor- 

High  

Normal . . . 

Increased . 

Dilated. 

dicrotic    wave, 

tic  insufficiency 

gradual  fall  in  di- 

astole 

A  few  cases   of 
fever 

Normal  or 

dimin- 
ished 

Pulse -rate 
qui  c  k- 
ened 

Dilated- 

Anacrotic . 

40 

Sudden     rise      or 

Arteriosclerosis  ; 

High 

High...    , 

Slightlyin- 

Va  socon- 

slightly  rounded 

chronic  nephritis 

creased 

striction. 

plateau  top  last- 

or   u  n  - 

ing  almost  to  di- 

Some  cases  of  aor- 

changed 

crotic    notch 

tic  insufficiency 

which    is    small; 

gradual  diastolic 

Some  normal  indi- 

Normal. . . 

High 

Slightly  di- 

Vasocon- 

fall 

viduals 

minished 

striction. 

Bisferiens  . 

40 

Resembling     ana- 
crotic        except 
that     the    small 
predicrotic  fall  is 
followed   by  rise 
equal    or    above 
that  of  the  per- 
cussion  wave, 
making  the  sum- 
mit bifurcate 

Arteriosclerosis; 
chronic  nephritis 

Hypertrophied 
heart  acting 
strongly 

High 

High 

Increased 

Va  socon- 
btriction. 

Tardus. .  . . 

40 

Gradual  slow  rise, 

Aortic  stenosis  . . . 

Slightly  or 

Elevated. . 

Increased 

Vasocon- 

percussion  wave 

greatly 

or   nor- 

striction. 

oblique,   summit 

elevated 

mal 

round,      gradual 
fall 

Collapsing. 

40 

Steep    rise,    apex 

Aortic  insufficien- 

Low    or 

Increased 

sharp,    sudden 

cy     (water-ham- 

normal 

Dilata- 

steep fall,  di- 

mer or  Corrigan 

tion    of 

crotic    notch    in 

pulse) 

the  larger 

lower   half   of 

arteries 

curve  often  level 

Fevers 

Normal  or 

Normal  or 

Normal  or 

(not  nec- 

after  the   predi- 

low 

low 

increased 

essarily 

crotic  wave 

of  the  ar- 

Normal     individ- 

Normal or 

Normal  or 

Normal  or 

terioles). 

uals,   neuras- 

low 

low 

increased 

thenics 

Some  cases  of 

Increased 

Slightly  in- 

Increased. 

Vasodila- 

Basedow's     dis- 

creased 

tion. 

ease 

Dicrotic.  .  . 

40 

Collapsing  in  qual- 

Fevers,   especially 

Normal  or 

Normal  or 

Normal  or 

Vasodila- 

ity  but   dicrotic 

typhoid 

subnor- 

subnor- 

increased 

tion. 

wave   very    pro- 

mal 

mal 

nounced  and  pal- 

pable, as  a  small 

Normal  individ- 

Increased 

Normal  or 

Increased 

Vasodila- 

wave     regularly 

uals     during     or 

increased 

tion. 

following     soon 

after    exercise 

after  the  percus- 

sion wave 

Neurasthenics, 
after     amyl     ni- 
trite    or     nitro- 
glycerin 

Normal  or 
increased 

Normal.  . . 

Increased 

Vasodila- 
tion. 

Hyper- 

40 

Dicrotic  wave  oc- 

Any of  the  condi- 

Normal or 

Normal.. . 

Increased 

Vasodila- 

dicrotic 

curs  at  the  foot 
of    the     ascend- 
ing    instead     of 
descending   limb 

tions     in     which 
dicrotism     may 
occur,   but    with 
more  rapid  pulse- 
rate. 

increased 

tion. 

*For  forms  of  ii  regular  pulse  see  page  99. 


THE  ARTERIAL  PULSE.  69 

there  must  have  been  a  regurgitation  of  blood  from  the  arm  back  into  the  sub- 
clavian artery  and  the  aorta.  This  condition  occurs  also  with  the  collapsing 
pulse  of  aortic  insufficiency  and  with  the  monocrotic  pulse  of  shock  and  col- 
lapse, as  well  as  during  the  predicrotic  fall  of  the  pulse-wave  in  the  dicrotic 
pulse  of  typhoid  fever.  With  the  onset  of  the  dicrotic  wave,  however,  the  blood 
flows  on  again  into  the  arm  only  to  ebb  back  again  into  the  subclavian  after 
the  crest  of  the  wave  is  reached.  Similar  ebbs  and  flows  may  occur  with  the 
bifurcated  pulsus  bisferiens  and  other  atypical  reflected  wavelets  upon  the 
pulse.  Hewlett  has  shown  that  they  represent  true  movements  of  fluid  as 
well  as  waves  of  pressure.  His  studies  explain  the  feeling  of  ultimate  tense- 
ness and  relaxation  that  accompanies  a  throbbing  pulse  as  well  as  many  other 
features  of  the  pulse-wave  which  had  been  hitherto  obscure. 


THE  PULSE-RATE. 

The  normal  pulse  varies  considerably  in  different  individuals,  being 
in  general  more  rapid  in  those  of  small  stature  and  slower  in  persons 
of  large  stature,  hence,  more  rapid  in  women  than  in  men.  It  also 
varies  considerably  according  to  age,  being  dependent  upon  the  relative 
tone  of  vagi  and  accelerators.  The  pulse-rate  is  also  more  rapid  (tachy- 
cardia) in  fevers,  varying  in  general  according  to  the  temperature — each 
degree  Fahrenheit  increase  corresponds  to  an  acceleration  of  about  four  to  five 
beats  per  minute.  C.  D.  Snyder,  as  the  result  of  a  long  series  of  experi- 
ments upon  the  heart-rate  in  different  vertebrates,  finds  that  the  rate  is 
influenced  by  temperature  in  the  same  degree  as  is  the  velocity  of  simple 
chemical  reactions  and  follows  the  logarithmic  formula 


Coefficient    of   differ-  _  /Rate  at  higher  temperature  \      higher      _      lower 
ence  of  rate  for  10°  C.     Uate  at  lower  temperature  jtemPerature    temperature 

In  typhoid  fever  there  is  often  an  exception,  a  temperature  of  103°  to  105°  being 
accompanied  by  a  pulse-rate  of  about  90  per  minute,  owing  to  a  toxic  stimulation  of  the 
vagus;  while  in  meningitis  the  high  intracranial  pressure  may  bring  the  rate  down  to  a 
great  deal  lower  (50  to  60)  and  may  cause  irregularity.  In  tuberculosis  the  pulse  is  rapid 
even  in  the  early  stages.  The  pulse-rate  is  also  accelerated  in  the  anaemias,  in  neuras- 
thenia, Graves's  disease,  hysteria,  shock  and  collapse,  abdominal  distention,  peritonitis 
and  other  diseases  of  the  abdominal  viscera,  and  in  numerous  cardiac  diseases.  In  fevers 
and  in  many  other  conditions  of  acceleration  the  pulse  becomes  extremely  small  and 
barely  palpable,  on  the  one  hand,  and  extremely  rapid,  barely  countable,  on  the  other — a 
small  and  "running"  pulse.  Pulse-rates  of  over  160  per  minute  are  not  uncommon  in 
fevers,  while  200  or  even  300  is  reached  in  paroxysmal  tachycardia.  At  these  great  rates 
the  duration  of  systole  is  markedly  shortened,  as  well  as  that  of  diastole  (the  period  of 
systolic  output  falling  from  0.26  sec.  to  0.2  or  even  less). 

Slow  pulse  (bradycardia)  (below  60  per  minute)  is  observed  especially  in  conditions 
with  intracranial  tension,  in  meningitis,  in  digitalis  poisoning,  chronic  nephritis,  chronic 
myocarditis,  in  convalescence  from  some  fevers,  especially  diphtheria  and  influenza,  and 
in  Adams-Stokes  disease.  In  the  latter  condition  the  auricles  and  ventricles  are  beating 
independently  (see  chapter  on  Adams-Stokes  disease). 


70  DISEASES  OF  THE  HEART  AND  AORTA. 

BIBLIOGRAPHY. 

Pulse. 

Harvey,  W.:  Exercitationes  anatomicae  de  motu  cordis  et  sanguinis  circulatione,  Rotero- 

dami,  1671. 
For  historical  resume"  cf.   Morrow,  W.  S.:  "The  Pulse,"  Reference  Hand-book  of    the 

Medical  Sciences,  Phila.,  1903,  vi,  797. 
Vierordt,  K. :  Die  Lehre  vom  Arterienpuls,  Braunschweig,  1855. 
Marey,  C.  J.:  Recherches  sur  l'etat  de  la   circulation  d'apres  les  caracteres  du  pouls 

fournis  par  un   nouveau  sphygmographe,  Journal  de  la  physiol.  de  l'homme,  Par., 

1860,  iii,  241. 
V.  Jaquet,  A.:    Studien  ueber  graphische  Zeitregistrirung,  Ztschr.  f.  Biol.,  Muenchen  u. 

Leipz.,  1891,  xxviii,  N.  F.  x.,  1. 
Roy,  C.  S.,  and  Adami,  J.  G.:    Heart-beat  and  Pulse-wave,  Practitioner,  Lond.,  1890, 

xliv,  81,  161,  241,  347,  412,  xlv,  20. 
Athanasiu,  J. :    Methode  graphique,  Trav.  Assoc,  de  l'lnstitut  Marey,  Paris,  1905,  p.  29. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of    Cardiac  Diseases,  Am.  Jour.  M. 

Sci.,  Phila.,  1906,  cxxxii,  378. 
Gerhardt,  D. :   Beitrage  zur  Lehre  vom  Blutdruck,  Rindfleisch  Festschrift,  Leipz.,  1907. 
Stewart,  H.  A. :  An  Experimental  and  Clinical  Study  of  the  Blood-pressure  and  Pulse  in 

Aortic  Insufficiency,  Thesis,  Edinb.,  1907;  also  Arch.  Int.  Med.,  Chicago,  1908,  i,  102. 
Sahli,  H.:  Ueber  das  absolute  Sphygmogram  und  seine  klinische  Bedeutung  nebst  kriti- 

schen  Bemerkungen  ueber  einige  neuere  sphygmographische  Arbeiten,  Deutsch.  Arch. 

f.  klin.  Med.,  Leipz.,  1904,  lxxxi,  493. 
Marey,  E.  J. :  La  circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Par.,  1881. 
Huerthle,  K.:  Beitrage  zur  Haemodynamik,  Arch.  f.  d.  ges.  Physiol,  Bonn,  1891,  xlix,  29. 
Hirschfelder,  A.  D. :  Some  Observations  upon  Blood-pressure  and  Pulse  Form,  Bull.  Johns 

Hopkins  Hosp.,  Baltimore,  1907,  xviii,  262. 
V.  Kries,  J. :  Studien  zur  Pulslehre,  Freiburg,  1892. 
Snyder,  C.  D.:  The   Influence  of  Temperature  upon    the   Rate  of    the  Heart-beat   in 

the  Light  of  the  Law  for  Chemical   Reaction  Velocity,  Am.  J.  Physiol.,  Bost.,  1906, 

xvii,  350. 


IV. 

THE    VENOUS    PULSE    AND    ELECTROCARDIOGRAM 
IN    HEALTH   AND    DISEASE. 

THE  NORMAL  VENOUS  PULSE. 

As  has  been  seen,  the  study  of  the  blood-pressure  and  of  the  arterial 
pulse  conveys  information  regarding  the  strength  of  the  heart-beat,  the 
condition  of  the  peripheral  arteries,  and  the  velocity  which  the  heart  is 
imparting  to  the  blood  stream.  But  it  reveals  the  action  of  the  left  ven- 
tricle only,  and  what  occurs  in  the  other  chambers  of  the  heart  must  be 
sought  for  elsewhere. 

In  studying  the  heart  from  the  four  stand-points  of  Engelmann, 
rhythmicity,  irritability,  conductivity,  and  contractility, 
it  is  necessary  to  obtain  a  knowledge  of  the  origination  of  the  impulses 
in  or  above  the  right  auricle  (atrium),  of  whether  impulses  other  than 
those  causing  the  normal  rhythm  are  acting  upon  that  chamber,  of  whether 
the  right  auricle  (atrium)  is  itself  contracting,  and  of  whether  all  the 
impulses  are  being  properly  conducted  to  the  ventricle.  Our  knowledge 
upon  these  points  has  been  derived  almost  entirely  from  the  study  of  the 
pulsation  in  the  jugular  vein. 

Inspection  of  the  Pulsation  in  the  Veins. — As  Hewlett  has  shown,  a  pul- 
sation is  visible  over  the  jugular  vein  in  the  supraclavicular  fossa  in  over  80 
per  cent,  of  normal  individuals.  Morrow  has  also  observed  it  in  all  the  large 
veins  of  dogs,  and  Friedreich  mentions  its  presence  in  the  arm  veins  of  man. 
This  pulsation  is  not  a  positive  beat  like  the  arterial  pulse,  but  is  a  collapse 
of  the  vein  due  to  the  suction-pump  and  not  to  the  force-pump  action  of  the 
heart.  It  is  the  collapse  rather  than  the  pulsation 
which  is  visible.  Since  the  vein  collapses  only  when  the  venous  pres- 
sure is  less  than  the  atmospheric  pressure  (i.e.,  zero),  it  is  evident  that  the 
pulsation  will  be  seen  best  when  the  pressure  within 
the  vein  is  alternating  between  a  positive  pressure 
which  fills  the  vein  and  a  negative  pressure  which 
collapses  it.  In  persons  with  a  high  venous  pressure  this  condition 
can  be  elicited  best  on  sitting  up  and  lowering  the  feet  or  on  standing ,  in 
those  with  a  low  venous  pressure  the  pulsation  can  be  brought  out  by  laying 
the  patient  horizontal  or  even  by  elevating  his  feet. 

It  is  also  possible  to  emphasize  the  pulsation  so  that  it  can  be  seen  and 
timed  more  easily  by  the  simple  procedure  of  holding  the  edge  of  a  visiting 
card  parallel  to  the  skin  over  the  sternocleidomastoid  and  about  1  mm.  away 
from  it  (Plate  XIII).  The  to  and  fro  movement  of  the  vein  can  thus  be  seen 
as  an  alternate  widening  and  narrowing  of  the  slit  between  skin  and  card, 
which  appears  as  a  dark  band  of  shadow,  widening  with  the  collapses  of  the 
vein,  narrowing  with  the  filling.  The  visual  impression  made  by  this  move- 
ment is  enhanced  by  the  juxtaposition  of  the  card  or  similar  object,  owing 
to  two  psychological  factors: 

71 


72  DISEASES  OF  THE  HEART  AND  AORTA. 

1.  The  movement  of  a  moving  surface  is  exaggerated  by  contrast  with 
the  fixity  of  a  fixed  line  in  close  approximation  to  it. 

2.  The  intensity  of  a  visual  impression  depends  upon  the  relation  be- 
tween the  amount  of  the  total  impression  and  the  increment  of  change.  If 
the  card  is  so  held  that  the  slit  between  the  card  and  skin  is  two  millimetres, 
a  collapse  of  only  two  millimetres  doubles  the  diameter  of  the  slit  between 
them  and  the  visual  impression  thus  alternately  doubles  and  halves. 

3.  The  contrast  between  the  white  surfaces  of  card  and  skin  and  the  dark 
shadow  cast  by  the  card  gives  a  contrast  of  light  and  shadow. 

The  pulsation  can  also  be  exaggerated  in  another  way — by  holding  a  pencil 
near  the  skin  and  turning  the  patient  so  that  the  light  is  falling  almost  parallel 
to  the  pulsating  skin  surface  and  almost  perpendicular  to  the  direction  of 
pulsation.  If  the  room  is  darkened  this  can  be  accomplished  most  easily  by 
using  a  pocket  electric  light  or  a  drop-light  as  the  source  of  light  and  moving 
it  about  until  suitable  shadows  are  obtained.  The  movement  of  the  shadow 
may  be  four  or  five  times  as  great  as  that  of  the  pulsation  itself. 

Another  very  ingenious  method  of  exaggerating  a  shadow  has  been  de- 
vised by  Henry  Sewall.  It  is  performed  by  fixing  a  strip  of  card  about  2  mm. 
wide  to  the  skin  over  the  pulsating  area  by  means  of  adhesive  or  by  a  drop 
of  collodion  and  allowing  this  bit  of  card  to  move  like  the  lever  of  a  tambour; 
so  that  the  end  of  the  lever  exaggerates  the  pulsation. 

It  is  equally  necessary,  however,  that  the  pulsations  in  the  veins  should 
be  compared  with  the  beats  in  the  carotid  artery  as  a  standard  of  time  and 
rate.  During  every  observation  of  the  venous  pulse  the  observer  should  keep 
one  finger  tightly  pressed  on  the  carotid  and  should  note  carefully  whether 
the  pulsations  seen  over  the  jugular  precede,  accompany,  or  follow  the  ar- 
terial pulsation,  as  well  as  the  number  of  pulsations  accompanying  each  beat 
of  the  carotid,  the  number  of  each  in  ten  seconds,  and  the  number  of  jugular 
pulsations  occurring  between  successive  pairs  of  carotid  beats. 

Auscultation  of  the  Veins. — Josue  has  found  that  each  pulsation  of  the 
vein  in  the  supraclavicular  fossa  often  gives  rise  to  an  audible  sound  when  a 
stethoscope  is  held  over  it,  one  sound  corresponding  to  each  filling  or  positive 
wave  in  the  vein.    This  method  also  is  a  great  help  in  diagnosis. 

GRAPHIC  RECORDS  OF  VENOUS  PULSATIONS. 

A  far  more  exact  idea  of  the  nature  of  the  jugular  pulsation  can  be 
obtained  by  recording  it  graphically  than  by  mere  inspection.  With  proper 
apparatus  this  is  not  accompanied  by  any  difficulty,  and  a  satisfactory 
record  of  both  venous  and  carotid  pulsations  can  be  obtained  in  about  the 
same  time  as  a  radial  sphygmogram.  For  the  interpretation  of  the  venous 
tracing  it  is  necessary  to  compare  it  with  the  other  events  of  the  cardiac 
cycle,  to  record  simultaneously  the  venous  pulse  and  either  the  arterial  pulse 
or  the  cardiogram,  and  to  see  at  which  point  in  the  cardiac  cycle  each  event 
will  fall.  Accordingly,  all  forms  of  apparatus  (polygraph)  for  obtaining 
such  records  are  arranged  for  taking  at  least  two  records  simultaneously. 

Application  of  the  Receivers. — -The  pulsation  in  the  jugular  vein  is  recorded  by 
holding  over  the  skin  above  it  a  small  glass  funnel  on  special  receiver  (Fig.  41,  c),  which  is 
connected  with  a  Marey  recording  kymograph  tambour.    The  movements  of  the  skin  are 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.         73 

transmitted  at  once  to  the  kymograph  tambour  and  recorded  by  the  lever.  As  a  rule,  the 
most  favorable  conditions  are  obtained  when  the  patient  is  lying  with  head  and  neck 
supported  on  a  single  pillow  that  extends  down  just  to  the  shoulders,  with  his  head  turned 
wel!  to  the  right  and  the  neck  definitely  flexed.  In  this  way  the  right  sternocleidomastoid 
is  relaxed  and  a  tracing  over  the  pulsation  from  base  of  the  internal  jugular  vein  is  trans- 
mitted to  the  skin.  When  this  is  not  obtainable  the  junction  of  the  external  jugular  vein 
with  the  subclavian  should  be  tried  in  the  same  way.     The  funnel  should  be  pressed  against 

the  skin  just  enough  to  make  the  contact  air- 
tight without  affecting  the  pulsation,  but  this 
is  effected  without  any  great  dexterity,  and 
oscillations  due  to  the  holding  of  the  re- 
ceiver rarely  appear  upon  the  tracing.  When 
they  do  so  it  is  in  the  form  of  fine  oscillations 
bearing  no  relation  to  the  cardiac  cycle  and 
having  a  rate  of  from  four  to  eight  per 
second,  in  contrast  to  the  much  slower  and 
larger  movements  in  the  veins.  Such 
tracings  should  be  discarded. 

In  many  cases  the  simple  glass  funnel 
is  not  as  satisfactory  as  a  receiving  device 
introduced  by  Mackenzie  (Fig.  41,  c),  con- 
sisting of  a  shallow  metal  pan  3  cm.  in 
diameter  with  a  tube  leading  off  from  it  in 
the  form  shown  in  Fig.  41,  one  portion  of 
the  circumference  being  flattened  instead 
of  round  in  order  to  fit  closely  above  the 
clavicle.  It  is  convenient  to  have  a  small 
hole  in  the  top  of  the  pan  so  that  it  may 
be  adjusted  to  the  skin  without  moving 
the  recording  lever,  and  after  adjustment 
is  complete  the  hole  is  closed  by  placing 
the  finger  over  it. 

The  tracing  from  the  carotid  artery  is 
obtained  in  a  similar  way,  using  for  a 
receiver  a  small  tambour  surmounted  by  a 
button  to  fit  over  the  artery  (Fig.  41,  d). 
A  small  hole  in  the  top  of  this  tambour 
serves  the  same  purpose  as  before  and  is 
The  carotid  artery  is  next  to  the  skin  just 
head    is    turned    toward   the    corresponding 


RECEIVER  FOR  VEIN 


RECEIVER  FOR  ARTERY 


Fig.  41. — Sites  for  recording  the  jugular  and 
carotid  pulsations.  A,  distribution  of  the  veins 
(shaded  in  black),  showing  the  sites  for  applying  the 
jugular  receiver  (truncated)  and  the  carotid  receiver 
(concentric  circles);  B,  appearance  of  the  valves 
within  the  jugular  vein  when  closed  by  back  pres- 
sure; C,  receiver  for  jugular  vein;  D,  spring  tambour 
for  recording  the  pulsation  over  the  carotid  artery. 


also  stopped  by  covering  with  the  finger. 

inside   the    sternocleidomastoid   when    the 

side,  the  pulsation  being  most  marked  when  the  receiver  is  pressed  heavily  upon  it 


Comparison  of  Carotid  and  Jugular  Pulsation. — Since  the  jugular  vein 
and  the  carotid  artery  are  at  about  the  same  distance  from  the  heart,  the 
tracings  from  the  latter  must  always  be  compared 
with  the  former  in  order  to  exclude  waves  which  might  have  been 
transmitted  to  it  from  the  artery,  and  also  to  indicate  the  relations  of  the 
venous  waves  to  the  cardiac  cycle.1 

This  comparison  may  be  made  by  taking  the  jugular  and  the  carotid  tracings  simul- 
taneously and  comparing  them  with  each  other  directly,2  or,  for  the  sake  of  convenience, 


1  Where  great  accuracy  is  necessary  the  onset  of  the  c  wave  must  be  compared  with 
that  of  the  apex  beat. 

2  It  is  not  necessary  that  the  levers  be  exactly  superposed,  but  it  is  preferable  to 
measure  off  the  distance  of  the  given  point  horizontally  from  the  arc  described  by  the 
lever  at  the  beginning  of  the  tracing  {e.g.,  Fig.  44).  This  distance  is  then  laid  off  upon  the 
other  curve  in  the  same  manner.  Wherever  the  curve  may  begin  the  paper  traverses  the 
same  distance  upon  both  curves  in  the  same  time. 


74 


DISEASES  OF  THE  HEART  AND  AORTA. 


Fig.  42. — Apparatus  for  recording  the  respiration. 
RUB,  rubber  tube;  GL,  glass  tube 


a  carotid  and  a  brachial  or  radial  tracing  may  be  made  simultaneously,  and  the  point  at 
which  the  carotid  wave  begins  marked  off  upon  the  latter.  Then  a  jugular  and  a  brachial 
tracing  may  be  made,  and  the  time  that  the  carotid  wave  occurs  before  the  brachial  marked 
off  before  each  brachial  wave  in  this  tracing,  and  these  points  then  measured  off  upon  the 
jugular  tracing.    This  is  often  the  simplest  and  quickest  procedure. 

Respiration  Recorder. — It  is  often  of  importance  to  determine  the 
relation  of  an  arrhythmia  to  the  phases  of  respiration.  The  simplest  device 
for  recording  the  latter  consists  of  a  piece  of  rubber  tube  (Fig.  42,  rub) 
connected  with  the  tube  to  the  recording  tambours  by  a  short  L-shaped 
piece  of  glass  tubing  (gl).  Apiece 
of  string  or  tape  is  attached  to  the 
rubber  tube,  another  to  the  glass 
tube.  The  apparatus  is  then  put 
on  so  as  to  encircle  the  level  of  the 
nipples.  The  strings  are  tied  tightly 
enough  to  just  stretch  the  rubber 

tube  during  expiration.    Inspiration      \    Y5!F££**§~IH    /  ^      \¥  \ 
then   causes  a  downstroke  of   the 
levers,  expiration  an  upstroke. 

Forms  of  Polygraph. — Several  forms 
of  polygraph  for  clinical  purposes  have 
been  devised  to  record  these  curves.  Their 
relative  value  depends  largely  upon  the 

delicacy  of  the  tambours.  The  oldest  form  is  the  polygraph  of  Marey,  consisting  of  an  ordi- 
nary kymograph  drum  arranged  to  rotate  horizontally  with  two  Marey  tambours  to  write 
upon  it,  so  as  to  record  simultaneously  the  curve  from  the  jugular  and  carotid  or  jugular  and 

cardiogram.  This  is  fairly  satisfactory,  but 
in  mechanical  perfection  some  others  are 
superior.  Mackenzie  has  devised  two  forms 
of  polygraph.  The  first,  a  simple  Jaquet 
sphygmograph  upon  which  a  Marey  tam- 
bour is  mounted  in  addition  so  as  to  record 
the  radial  pulse  and  jugular  or  carotid,  etc., 
simultaneously,  the  time  being  marked  off 
in  \  seconds  by  a  small  clock-work  as  well. 
In  the  improved  form  of  Mackenzie  poly- 
graph, the  levers  bear  ink  pens  and  write 
upon  an  endless  roll  of  white  paper,  so  that 
a  very  long  series  can  be  obtained.  The 
radial  pulse  is  obtained  by  air  transmission, 
which  is  a  decided  advantage.  V.  Jaquet's 
cardiosphygmograph  differs  from  the  simple 
sphygmograph  only  in  bearing  in  addition 
two  Marey  tambours  whose  double-jointed 
levers  wrice  just  above  the  lever  attached  to 
the  radial  pelotte.  One  great  objection  to 
the  Jaquet  instrument  is  the  inconvenience  of  adjusting  the  sphygmograph  to  the  radial 
artery  and  keeping  it  adjusted  during  the  entire  observation,  a  factor  which  is  very  dis- 
concerting to  both  patient  and  physician  and  which  prevents  many  important  observations 
from  being  taken  on  restless  patients. 

This  difficulty  is  obviated  in  the  writer's  modification  of  the  E  r  - 
langer  blood-pressure  apparatus  (Fig.  22,  page  27),  in  which  two  small 
Marey  tambours  and  a  time-marker  are  arranged  to  write  above  the  lever  of  the  blood- 
pressure  apparatus.  When  the  bag  is  inflated  upon  the  arm,  the  brachial  pulse  is  recorded 
by  the  lever  of  the  blood-pressure  apparatus  and  used  as  the  standard  instead  of  the  radial 


Fig.  43. — V.  Jaquet's  cardiosphygmograph. 
(Kindness  of  A.  H.  Thomas  Co.)  a,  time  marker 
(s  sec);  b,  c,  levers  of  tambours  for  recording 
venous  tracing,  carotid  pulse,  or  cardiogram;  d, 
lever  recording  radial  pulse-wave. 


PLATE  III. 


Uskoff  sphygmotonograph.     (Kindness  of  A.  H.  Thomas  Company.) 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


75 


pulse.  This  entails  no  trouble  and  no  expenditure  of  time,  thereby  saving  much  of  the 
trouble  given  by  the  other  methods,  and  permits  a  set  of  records  to  be  obtained  very  quickly. 
It  is  also  possible  for  the  operator  to  work  with  one  hand  free  and  thus  save  the  necessity 
of  an  assistant.  The  curve  thus  obtained  from  the  jugular  vein  is  shown  in  Fig.  44  and 
its  relation  to  the  other  events  in  the  cardiac  cycle  shown  in  Fig.  45. 

Recently,  Uskoff  has  constructed  a  very  compact  form  of  this  apparatus,  bearing  an 
Erlanger  blood-pressure  apparatus,  a  tambour  for  recording  the  height  of  the  blood- 


SLOW 


FAST 


CAROTID 


JUGULAR 


Fig.  44. — Normal  venous  tracings,  a,  wave  due  to  auricular  contraction;  c,  wave  at  onset  of 
ventricular  contraction  (the  vertical  line  c  representing  the  beginning  of  the  carotid  pulse-wave);  x,  the 
bottom  of  the  mesosystolic  collapse;  d  time  of  dicrotic  notch  in  the  carotid;  v,  wave  at  end  of  systole; 
y,  hollow  at  tiie  end  of  the  postsystolic  collapse;  t,  d  (Bard),  telesystolic  and  protodiastolic  waves 
described  by  Bard.      (The  x  and  y  depressions  are  not  lettered  on  all  tracings.) 


pressure  objectively,  a  tambour  for  apex  or  venous  or  carotid  tracings,  and  an  excellent 
time-marker.  This  seems  to  be  a  very  good  instrument  of  wide  applicability,  suitable 
to  all  the  needs  of  the  practitioner. 

A  slight  modification  of  the 
original  Marey  polygraph  is  still 
manufactured  by  the  French  instru- 
ment-makers, and,  as  the  tambours 
which  write  horizontally  are  unex- 
celled for  delicacy,  this  form  is  to 
be  highly  recommended. 

A.  G.  Gibson  has  devised  an 
upright  polygraph  for  taking  a  con- 
tinuous record  in  ink  upon  an  end- 
less roll  of  paper.  It  is  not  much 
larger  than  the  Mackenzie  poly- 
graph, and  the  fact  that  the  tam- 
bours are  upright  increases  their 
delicacy  considerably.  This  instru- 
ment is  also  provided  with  a  time- 
marker  and  with  excellent  receivers 
which  may  be  applied  with  straps 
and  adjustable  screws  so  that  the 
receivers  remain  in  place  perma- 
nently and  need  not  be  held  with 
the  hands.  These  receivers,  it  may 
be  added,  may  be  purchased  sepa- 
rately, and  are  a  great  addition  to 
any  form  of  polygraph. 


TRICUSPID 
AORTIC 
PULMONIC 


Fig.   45. 


-Shaded  portion  of  the   cardiac   cycle  represents 
systole  of  the  ventricles. 


Photographic  Record  of  the  Venous  Pulse. — The  photographic  sphygmo- 
graph  devised  by  0.  Frank  (see  page  64)  may  be  used  for  the  venous  as  well 
as  for  the  arterial  pulse  and  has  the  advantage  of  freedom  from  artefact  and 
fling.     In  order  to  obtain  both  the  venous  and  the  arterial  pulse  simultane- 


76  DISEASES    OF   THE   HEART   AND   AORTA. 

ously  the  light  from  the  two  mirrors  of  the  two  Frank  capsules  must  be  kept 
from  interfering,  but  this  may  be  accomplished  by  means  of  a  suitable  screen. 
Phlebograms  obtained  in  this  way  are  almost  free  from  criticism  and  will  prob- 
ably occupy  much  of  the  foreground  in  the  future. 

THE   MICROGRAPH. 

Crehore  and  Meara  have  employed  for  the  registration  of  both  pulsa- 
tions and  heart  sounds  an  instrument  devised  by  the  former  and  termed  the 
micrograph.  The  pulsation  is  received  upon  an  ordinary  receiving  tambour 
and  transmitted  by  a  rubber  tube  to  the  micrograph  proper.  This  instru- 
ment consists  essentially  of  a  small  pressure  chamber  surmounted  by  a  more 
or  less  elastic  diaphragm  similar  to  that  of  a  telephone.  At  the  centre  of  the 
disk  there  is  a  small  reflector,  above  which,  and  separated  from  it  by  a  small 
air  space,  is  placed  a  planocylindrical  lens,  convexity  downward.  This 
micrograph  is  placed  upon  the  stage  of  a  microscope  and  illuminated  from 
above  with  monochromatic  light,  which  gives  rise  to  a  series  of  light  and 
dark  concentric  circles  (interference  rings)  when  looked  at  through  the  micro- 
scope. When  a  vibration  is  communicated  to  the  diaphragm  and  the  mirror 
moves  toward  or  away  from  the  lens,  the  movement  of  these  interference 
rings  greatly  magnifies  the  movement  of  the  diaphragm,  and  when  these  in 
turn  are  viewed  under  a  magnification  of  2000  diameters,  the  original  move- 
ment is  seen  to  be  magnified  50,000  times.  As  the  distance  between  two  bands 
of  light  is  readily  determined  in  wave-lengths  of  the  light  used  for  illumina- 
tion, the  amount  of  this  movement  can  be  readily  calculated.  The  move- 
ments of  the  rings  are  recorded  photographically  by  throwing  them  upon  a 
slit  in  front  of  a  rapidly  moving  photographic  film.  In  order  to  obtain  the 
correct  curve,  however,  the  curve  obtained  photographically  must  be  plotted 
out  upon  coordinate  paper  with  considerable  labor,  the  ordinates  represent- 
ing the  amplitude  of  vibration,  the  abscissa  the  time.  Laborious  as  this  method 
may  seem,  it  is  extremely  delicate,  and  it  is  possible  that  it  may  reveal  many 
facts  undiscovered  by  ordinary  means. 

INTERPRETATION   OF   WAVES   UPON   THE    VENOUS  TRACING. 

The  curve  of  venous  pressure  obtained  clinically  and  in  animals  (Fred- 
ericq,  Morrow,  Hering,  Theopold)  corresponds  exactly  to  those  obtained 
within  the  auricles  (Chauveau  and  Marey,  Fredericq,  Porter).  The  first 
wave  (a)1  in  the  venous  pulse  is  due  to  the  contraction  of  the 
right  auricle,  and  disappears  when  the  auricle  is  paralyzed.  It  occurs 
about  one-fifth  second  before  the  contraction  of  the  ventricle.  The  onset  of 
the  ventricular  contraction  is  marked  on  the  venous  tracing 
by  a  small'  wave  (c),  caused  in  part  by  the  pushing  up  of  the  tricuspid 
valve  when  the  intraventricular  pressure  rises  (Hirschfelder,  1.  c,  Bard,  1.  c, 
Morrow,  Cushny  and  Grosh),  and  in  part  by  the  flow  of  blood  from  the  coro- 
nary veins,  which,  as  Porter  has  shown,  are  forcibly  emptied  into  the  auricle 
at  this  instant  (Sewall  and  Hirschfelder).     Mackenzie  thinks  that  it  is  due 

1  Since  Mackenzie's  first  nomenclature  and  lettering  of  the  waves  was  introduced,  a 
great  variety  of  lettering  and  of  designation  by  numerals  has  been  used  by  different  authors; 
but  these  serve  to  complicate  rather  than  to  simplify  the  question.  The  letters  or  numbers- 
are  merely  symbols,  and  a  single  uniform  system  would  be  better  than  a  Babel  of  terms. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


77 


JUG. 


CAR. 


only  to  the  carotid  pulsation  transmitted  to  the  vein,  but  Morrow  has  obtained 
it  after  ligature  of  the  carotid  in  animals.  Besides  the  wave  appears  about 
2V  second  before  the  carotid  wave  in  many  cases  (Hirschf elder,  Bard).  When 
the  tracings  are  taken  from  the  left  jugular  and  right  carotid,  the  c  wave  in 
the  vein  may  be  later  than  that  in  the  artery,  owing  to  longer  time  of  trans- 
mission. The  c  wave  is  almost  always 
present;  but,  as  Bard  has  shown,  it 
may  be  very  small  or  entirely  absent 
in  hearts  whose  ventricles  are  failing 
(Fig.  46).  The  rise  of  the  c  wave  is 
followed  by  a  large  fall  (x) ,  which 
may  be  the  largest  fall  of  pressure  in 
the  whole  cardiac  cycle.  The  exact 
mechanism  by  which  this  fall  of  pres- 
sure in  the  veins  (and  also  in  the 
auricles)  is  produced,  and  especially 
why  it  should  sometimes  represent  the 
largest  fall  of  pressure,  is  not  clear. 
It  is  evident  at  this  period  of  the  cycle  that  several  events  are  taking 
place:  (1)  relaxation  of  the  auricle;  (2)  a  certain  amount  of  downward 
pull  which  the  papillary  muscles  exert  upon  the  tricuspid  and  mitral 
valves;  (3)  at  each  systole,  as  can  be  seen  when  the  heart  is  exposed,  the 
movements  of  the  latter  within  the  chest  are  exerting  a  pull  upon  the 
venae  cavse,  thus  pumping  their  contents  into  the  auricles;  (4)  the  outflow 
of  blood  and  the  decrease  in  size  of  the  heart  during  systole  cause  a  slight 
increase  in  the  negative  pressure  within  the  thorax  which  may  be  trans- 
mitted to  the  thin-walled  veins.    It  is  probable  that  neither  of  these  factors 


Fig.  46. — Venous  tracing  showing  ab- 
sence of  the  c  wave  in  a  case  of  heart  fail- 
ure. The  tracing  is  otherwise  normal. 
JUG.,  right  jugular  vein;  CAR.,  left  ca- 
rotid artery.    Time  in  J  seconds. 


Fig.  47. — A.  Venous  tracing  showing  auricular  paralysis  (absence  of  a  wave)  with  large  (x)  depression 
during  ventricular  systole  between  c  and  v.     B.  Same  tracing,  faster  speed. 


alone  is  responsible  for  the  fall  (x  depression),  but  that  each  is  active.  Cer- 
tain it  is  that  auricular  relaxation  is  not  the  sole  cause,  for  as  shown  in  Fig. 
47  it  may  still  be  the  largest  depression  in  cases  in  which  the  auricle  is  par- 
alyzed. 

Dr.  Peabody  has  called  the  writer's  attention  to  a  small  wave  which  is  frequently 
seen  during  midsystole,  especially  in  tracings  from  vigorous  hearts,  occurring  just  at  the 
base  of  the  x  depression,  and  which  in  many  cases  cannot  be  due  to  fling  of  the  lever.  The 
origin  and  significance  of  this  wave  are  extremely  uncertain.  It  may  be  really  transmitted 
from  the  artery;  or,  as  Dr.  Peabody  suggests,  may  be  due  to  slight  insufficiency  of  the 
papillary  muscles  studied  by  Sewall. 


78 


DISEASES  OF  THE  HEART  AND  AORTA. 


The  fall  which  leads  to  the  x  depression  usually  lasts  until  about  the 
end  of  ventricular  systole,  d  (instant  of  the  dicrotic  notch),  after  which  it 
is  followed  by  a  large  rise  (diastolic  wave  of  Porter;  v  or  ventricular  wave 
of  Mackenzie;  vs,  ventricular  stagnation  (Ventrikelstauungswelle),  Hering; 
telesystolic  wave,  t,  Bard).  This  wave  is  very  constant  in  its  occurrence 
and  is  usually  supposed  to  represent  stagnation  within  the  ventricle,  lasting 
from  the  end  of  systole  until  the  tricuspid  valve  opens;  the  fall  v-y  indicates 
the  opening  of    the  tricuspid  valve. 

As  Bard  has  shown,  two  undulations  are  occasionally  found  (t,  d,  t,  telesystolic,  occur- 
ring at  the  end  of  systole;  and  d,  protodiastolic,  occurring  at  the  very  beginning  of  diastole). 
Bard  states  that  the  wave  t  is  coincident  with  the  first  secondary  (predicrotic)  wave  of  the 
arterial  pulse,  the  second  with  the  vibration  of  the  ventricles  due  to  the  closure  of  the 
aortic  valves,  and  Eyster  has  shown  recently  that  the  notch  between  the  t  and  d  waves 
upon  the  venous  pulse  indicates  exactly  the  end  of  ventricular  systole. 


Fig.  48. — Venous  tracing  from  a  very  slow  heart,  with  loud  third  heart  sound,  showing  the  presence 
of  the  h  wave.    Max,  maximal  blood-pressure:  Min,  minimal  blood-pressure. 


Sewall  believes  that  the  stagnation  at  the  end  of  systole  (when  the  upstroke  of  the 
v  or  t  wave  occurs  before  the  end  of  systole)  is  due  to  a  fatiguing  or  stretching  of  the  papil- 
lary muscles,  causing  a  slight  tricuspid  regurgitation  at  that  instant;  but  in  cases  with  no 
murmur  in  the  tricuspid  region  this  explanation  needs  confirmation. 

The  rise  upon  the  v  wave  outlasts  the  end  of  systole  by  about  tV  sec, 
which  probably  represents  the  time  required  to  transmit  this  change  of  pres- 
sure to  the  veins. 

Most  writers  follow  Mackenzie  in  believing  that  the  upstroke  of  the  v  wave  repre- 
sents stasis  within  the  ventricle  lasting  until  the  tricuspid  valve  opens,  but  cardiometer 

tracings  show  that  filling  of  the  ventricles, 
or,  at  least,  dilatation,  begins  at  the  instant 
systole  ends.  Chauveau's  tracings  of  the 
movements  of  the  heart  valves  also  show 
that  the  tricuspid  valve  opens  before  the  time 
at  which  the  crest  of  the  v  wave  appears,  so 
that  it  is  probable  that  this  wave  does  not 
represent  the  very  instant  at  which  the  tri- 
cuspid valve  opens,  but  that  when  the  period 
x-v  exceeds  the  transmission  time  the  interval 
represents  a  period  during  which  the  venous 
pressure  remains  greater  than  atmospheric 
pressure.  Or  it  may  last  until  a  sufficient  amount  of  blood  has  entered  the  ventricle  to 
have  relieved  the  venous  engorgement  which  followed  the  cessation  of  the  factors  which 
had  produced  the  x  depression. 

The  descending  limb  of  the  v  wave  continues  as  long  as  blood  is  rushing 
in  to  fill  the  ventricle  (Henderson's  period  of  diastolic  filling),  after  which 


Fig.  49. — Tracing  from  the  same  person 
one  hour  later,  after  giving  atropine  and  quick- 
ening the  pulse.     The  h  wave  is  absent. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.    79 

there  is  a  gradual  filling  of  the  vein  and  a  rise  until  the  next  auricular  systole. 
In  slow  hearts  Hirschfelder  and  A.  G.  Gibson  have  shown  that  the  inflow 
into  the  auricles  and  the  filling  of  the  veins  is  no  longer  uniform  but  is  inter- 
rupted by  a  well-defined  wavelet  (h,  Hirschfelder;  b,  Gibson)  which  follows 
the  v  wave  by  a  definite  interval  (Fig.  48,  h).  Both  these  writers  indepen- 
dently ascribed  this  wave  to  the  snapping  together  of  the 
auricula  ventricular  cusps  at  the  end  of  ventricu- 
lar f  i  1 1  i  n  g  in  mid-diastole,  and  the  former  called  attention  to  its  corre- 
spondence with  the  onset  of  Henderson's  period  of  diastasis.  This  fact  is 
further  borne  out  by  the  presence  of  a  corresponding  wave  upon  the  tracing 
from  the  oesophagus  (Fig.  54,  h),  and  it  can  be  reproduced  on  a  mechanical 
model.  This  wave  disappears  when  the  pulse-rate  becomes  more  rapid  (Fig.  49) . 

A.  G.  Gibson,  Eyster,  and  the  writer  have  occasionally  seen  a  wave  w  in  late  diastole 
of  slow  pulse  preceding  the  wave  of  auricular  contraction  (a  wave)  by  a  rather  definite 


Fig  50  — Showing  a  wave  w  occurring  shortly  before  the  a  wave.     (From  a  tracing  made  in  collaboration 

with  Prof.  L.  F.  Barker.) 

interval  (Fig.  50).  The  distance  from  the  h  wave  varies.  This  wave  is  assumed  by 
the  former  writer  to  represent  a  contraction  originating  in  the  sinus  region  of  the  heart. 
However,  Hirschfelder  has  recently  produced  similar  waves  upon  a  mechanical 
model  and  proved  that  they  are  merely  waves  of  elastic  recoil  like  the  accessory  waves  on 
the  arterial  pulse. 

VISUAL   EXAMINATION    OF   THE    VENOUS   PULSE. 

Some  of  these  events  in  the  cardiac  cycle  may  be  clearly  distinguished 
with  the  naked  eye  by  the  methods  described  on  page  72.  The  vein  will  be 
seen  to  fill  twice  (a  wave  and  v  wave)  and  to  collapse  twice  (x  depression  and 
y  depression)  for  each  beat  felt  in  the  carotid  artery  ("presystolic-diastolic," 
"physiological,"  "negative,"  "double"  venous  pulse  (Hirschfelder)  ).  Josue" 
can,  over  a  normal  vein,  hear  three  sounds  in  gallop  rhythm,  corresponding 
to  the  a,  c,  and  v  waves.  These  waves  may  be  timed  less  accurately  with 
the  eye,  but  although,  as  Mackenzie  states,  visual  examination  may  save 
the  examiner  many  unnecessary  tracings,  it  should  not  be  relied  upon  in 
doubtful  cases.  For  example,  a  simple  mesosystolic  collapse  (like  that  shown 
in  Fig.  44)  with  fibrillation  of  paralysis  of  the  auricles  may  simulate  a  normal 
venous  pulse. 

ABNORMAL  TYPES  OF  VENOUS  PULSE. 

Auricular  Paralysis. — Besides  this  normal  (negative  or  double  venous) 
pulse  several  other  types  of  venous  pulse  are  seen.  In  venous  stasis  and 
cardiac  failure  the  auricles  may  soon  become  weakened  and  the  a  wave,  due 
to  their  contraction,  may  disappear  entirely  (Figs.  47  and  51).  V.  Frey  and 
Krehl  demonstrated  that  this  takes  place  in  animals  when  the  venous  pres- 


80 


DISEASES  OF  THE  HEART  AND  AORTA. 


sure  reaches  20  mm.  Hg,  and  it  may  occur  in  man  even  when  the  electro- 
cardiogram shows  an  auricular  wave  (Lewis). 

Positive  Venous  Pulse. — The  ventricular  type  of  venous  pulse  is  met 
with  when  the  heart-rate  is  regular  in  cases  of  tricuspid  insufficiency  and 
paroxysmal  tachycardia,  but  is  most  frequently  seen  accompanying  the 
absolute  irregularity  due  to  auricular  fibrillation.  In  the  latter  case,  as  The- 
opold,  Cushny  and  Edmunds,  and  Rihl  have  shown,  the  tricuspid  valves 


Fig.  51. — Positive  or  ventricular  type  of  venous  pulse  in  tricuspid  insufficiency,  showing  absence  of  the 
a  wave.     VJD,  right  jugular  vein;  ACS,  left  carotid  artery. 


JUG 


probably  close  perfectly,  but  the  ventricular  form  is  due  to  stasis  and  the 
effect  of  small  auricular  movements.    On  the  other  hand,  as  Rihl  has  shown, 
tricuspid  insufficiency  may  be  present  without  a  positive  venous  pulse. 
pv  pv  pv  Information  furnished  by  the 

Venous  Pulse. — It  is  apparent 
from  the  above  description  that 
the  following  facts  are  to  be 
learned  from  the  normal  venous 
pulse-curve:  (1)  whether  the  au- 
ricle (atrium)  is  contracting,  and 
whether  each  auricular  (atrial) 
contraction  is  followed  by  a 
ventricular  contraction;  (2)  the 
time  required  for  the  conduc- 
tion of  the  impulse  from  auricle 
(atrium)  to  ventricle  (the  inter- 
val a-c  on  the  tracing,  about  i 
second  in  normal  individuals — 
conduction  time) ;  (3)  whether  or 
not  the  tricuspid  valve  is  closing 
perfectly  (shown  by  the  fall  or 
pressure  during  systole  and  the  subsequent  v  wave).1  In  irregular  pulses 
many  more  important  facts  are  to  be  learned  from  the  venous  pulse,  which 
will  be  discussed  in  connection  with  this  disturbance  of  function. 


BRACH 


Fig.  52. — Positive  or  ventricular  type  of  venous  pulse 
in  tricuspid  insufficiency,  showing  absence  of  the  a  wave. 
JUG,  right  jugular  vein;  BRACH,  right  brachial  artery. 


(ESOPHAGEAL  TRACINGS. 

The  venous  pulse  tracing  reveals  the  conditions  prevailing  in  the  right  auricle  (atrium) 
and  the  state  of  the  tricuspid  valve.  A  corresponding  investigation  of  the  state  of  the 
left  auricle  (atrium)  and  of  the  mitral  valve  was  made  possible  by  a  method  used  in  ani- 
mals by  Fredericq  and  in  man  by  Sarolea  (1890),  Minkowski  (1906),  Rautenberg  (1907), 


This,  as  has  been  shown  by  Mackenzie  and  by  Rihl,  is  not  absolute. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


81 


Hewlett  (1907),  Joachim  (1907),  Lian  (1909),  Clerc  and  Esmein  (1910).  Minkowski  calls 
attention  to  the  fact  that  at  the  level  of  the  seventh  to  the  ninth  thoracic  vertebrae  (about 
35  to  37  cm.  from  the  teeth)  the  left  auricle  is  in  contact  with  the  oesophagus,  and  when  one 
introduces  a  stomach-tube  to  this  level  it  receives  impulses  from  the  left  auricle  alone. 
Accordingly,  an  ordinary  stomach-tube  is 
capped  with  a  thin  rubber  finger  cot,  and  the 
latter  secured  by  winding  a  silk  ligature  sev- 
eral times  around  it.  The  stomach-tube  is 
then  swallowed  by  the  patient  until  it  extends 
down  35  to  37  cm.  from  the  teeth.  It  is  then 
connected  with  a  Marey  tambour  whose  oscil- 
lations record  the  contraction  of  the  auricle 
and  ventricle  (Figs.  53  and  54).  The  fall  in 
the  wave  occurs  when  the  auricle  moves  away 
from  the  oesophagus,  the  rise  when  it  is  pressed 
against  the  latter  by  filling  with  blood.  Under 
ordinary  circumstances  ventricular  as  well  as 
auricular  systole  draws  the  auricle  away  from 
the  oesophagus  so  that  the  falls  and  rises  cor- 
respond to  auricular  and  ventricular  systole 
respectively. 

(Esophageal  Tracing  in  'Mitral]  Insuffi- 
ciency.— When  the  mitral  valve  does  not  close 
(mitral  insufficiency),  blood  is  forced  back  into 
the  auricle  during  ventricular  systole,  and, 
instead  of  a  fall,  there  is  a  rise  during  systole.  Minkowski's  method  furnishes  the  means  for 
obtaining  the  missing  link  in  our  knowledge  of  the  cardiac  impulse  and  the  meaning  of 
functional  murmurs,  but  unfortunately  the  swallowing  of  the  stomach-tube  is  so  disagree- 
able to  the  ordinary  patient  and  so  dangerous  in  all  very  severe  cases  as  to  preclude  its 


Fig.  53. — Method  of  taking  tracing  from 
the  oesophagus  to  show  the  contractions  of 
the  left  auricle.  The  arrow  points  to  the  thin 
rubber  bulb  at  the  end  of  the  oesophageal  tube. 
ST.,  stomach. 


CAROT. 


CESOPH. 


Fig.  54. — (Esophageal  and  carotid  tracings  from  a  normal  man. 

adoption  into  general  use.  Patients  can,  however,  often  be  trained  to  swallow  the  stomach- 
tube  without  difficulty,  or  a  rubber  tube  of  small  bore  may  be  substituted,  and  then  very 
satisfactory  results  may  be  obtained. 

INTRANASAL  TRACINGS. 

Mosso  and  also  the  writer  have  obtained  very  satisfactory  cardiographic  curves  from 
the  changes  of  air  pressure  within  the  thorax.  These  may  be  obtained  by  placing  in  one 
nostril  a  cork  perforated  by  a  glass  tube  which  is  connected  with  the  recording  lever.  The 
lips  are  closed  and  the  other  nostril  is  closed  by  pressure.  Or,  the  tube  may  be  placed  in 
the  mouth  and  both  nostrils  closed  by  pressure.  The  glottis  must  be  open  and  the  breath 
held.  Curves  thus  obtained  closely  resemble  the  oesophageal  tracings  in  normal  indivi- 
duals, though  the  waves  are  smaller. 


THE  ELECTROCARDIOGRAPH. 

In  recent  years  another  method  for  the  observation  of  cardiac  function, 
the  study  of  the  electrical  variations  accompanying  the  heart-beat,  has  at- 
tracted much  attention,  and  has  yielded  so  many  results  of  both  theoretical 
6 


82 


DISEASES  OF  THE  HEART  AND  AORTA. 


and  practical  importance  that  it  has  come  almost  to  supplant  the  venous 
pulse  tracing  for  the  analysis  of  the  arrhythmias.1 

Historical. — The  study  of  the  electrical  variations  of  the  heart-beat  is  not  new- 
Kolliker  and  Miiller  in  1855  found  that  each  beat  of  the  frog's  heart  was  accompanied  by  a 
definite  electric  current,  and  numerous  subsequent  observers  verified  their  findings.  In 
1887  Ludwig  and  his  pupil  Waller  applied  these  findings  to  man,  and  discovered  that  the 
currents  accompanying  the  beat  of  the  human  heart  could  be  recorded  by  means  of  the 
capillary  electrometer  when  electrodes  were  placed  upon  the  precordial  region.  Their 
studies  were  extended  by  Einthoven  of  Leyden  in  1895,  but  he  soon  found  that,  although 
electrical  curves  (electrocardiograms)  could  be  obtained  in  this  way,  the  inertia  of  the  cap- 
illary electrometer  was  too  great  to  respond  satisfactorily  to  the  changes  of  1/10000  to 
1/3000  of  a  volt  which  are  concerned  in  the  heart-beat  and  that  a  more  delicate  method 
must  be  resorted  to.  In  1897  Ader  invented  a  new  type  of  galvanometer,  now  known  as 
the  string  galvanometer  or  thread  galvanometer,  whose  delicacy  was  almost  sufficient  for 
the  purpose.  This  galvanometer  depends  upon  the  well-known  fact  that  a  current  gen- 
erates a.  magnetic  field  acting  at  right  angles  to  its  course,  which  varies  with  the  strength 
of  the  current,  and  which  may  thus  exert  a  varying  attraction  or  repulsion  upon  a  second 
magnetic  field  in  its  vicinity.     In  Ader's  instrument,  which  was  designed  for  receiving 


Fig.  55. — Photograph  of   the   electrocardiograph   laboratory  or 

Hospital. 


'heart   station"  of  the   Johns  Hopkins 


transatlantic  dispatches,  a  copper  or  aluminum  wire  100  cm.  long  and  0.2  mm.  thick  was 
used  to  carry  the  current. 

Einthoven  (1903)  constructed  a  much  more  delicate  modification  of  this,  in  which 
the  current  from  the  body,  which  is  thus  varying  in  intensity,  is  carried  upon  a  silver- 
coated  quartz  or  a  platinum  filament  about  3M  (.003  mm.)  thick.  This  wire  is  so  light 
that  its  weight  is  negligible,  for  it  cannot  be  weighed  with  the  most  delicate  balances.    It 


*The  entire  literature  of  this  subject  up  to  1910  has  been  collected  and  reviewed  by 
Lewellys  F.  Barker:  Electrocardiography  and  Phonocardiography,  Johns  Hopkins  Hosp. 

Bull.,  Baltimore.  1910,  xxi,  359,  and  Fr.  Kraus  and  Ge.  Fr.  Nicolai:  Das  Elektro- 

kardiogramm  des  gesunden  und  Kranken  Menschen,  Leipz.,  1910;  other  reviews  of 

the  literature  are  to  be  found  in 
T.  Lewis:  Chapter  on  the  Electrocardiograph  in  Mackenzie  s  Diseases  of  the  Heart,  2d 

edition.  .  .     ,,,,..        .        T   ,, 

W  B.  James  and  H.  B.  Williams:  The  Electrocardiogram  m  Clinical  Medicine,  Am.  J.  M. 

Sc,  Phila.  and  N.  Y.,  1910,  cxl,  644.  _  .    ,, 

A   D.  Hirschf elder:  Recent  Studies  upon  the  Electrocardiogram  and  upon  Change  in  the 

Volume  of  the  Heart,  Interstate  M.  J.,  St.  Louis,  1911,  xvm. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.    83 

is  suspended  between  the  poles  of  a  very  powerful  electro-magnet  with  large  cast-iron 
armatures.  The  movements  of  the  thread  are  recorded  by  projecting  its  shadow  under  the 
magnification  of  a  high-power  microscope  upon  the  slit  of  a  specially  devised  camera,  about 
six  feet  away.  The  film  of  this  camera  moves  rapidly  past  the  slit,  and  the  oscillations  of 
the  thread  are  recorded  as  a  curve.  The  time  is  indicated  by  the  shadow  of  a  time-marker 
placed  in  front  of  the  slit. 

The  current  is  led  off  from  the  body  from  German  silver  or  zinc  electrodes,  covering 
the  forearm  placed  over  a  felt  soaked  in  physiological  salt  solution  (Fig.  58).  Thus  obtained 
it  represents  the  difference  of  potential  between  the  skin  under  two  electrodes,  and  is  gen- 
erated by  two  elements.  1.  The  permanent  difference  of  potential  between  these  two  differ- 
ent parts  of  the  body,  which  is  dependent  upon  local  conditions  of  the  skin  and  tissues 
and  is  quite  independent  of  the  cardiac  cycle.  This  is  known  as  the  current  of  rest. 
2.  The  oscillations  due  to  the  action-current  of  the  heart  itself,  the  electrocardiogram 
proper.  Since  we  are  interested  only  in  the  latter,  the  current  of  rest  is  neutralized  by  pass- 
ing through  the  galvanometer  a  battery  current  exactly  equal  to  it,  but  opposite  in  direc- 
tion, after  which  compensation  the  only  current  acting  upon  the  galvanometer  is  that 
which  accompanies  the  contraction  of  muscles.    When  the  patient  is  quiet,  the  tonic  con- 


Fig.   56. — Cambridge  modification  of  Einthoven's  string  galvanometer.     A,   the  galvanometer  with  its 
magnets  and  microscope.     B,  the  holder  for  the  filament. 

tractions  of  the  skeletal  muscles  play  but  a  little  role,  and  the  action-current  that  is  ob- 
served is  seen  to  accompany  cardiac  contractions  (Fig.  59).  Contraction  of  the  hand  or 
foot  muscles  exerts  a  definite  effect,  which  is  much  slower  than  the  cardiac  impulse;  and  the 
same  is  true  of  the  wave  accompanying  deep  inspiration. 

Einthoven  has  shown  that  it  is  by  no  means  necessary  that  the  patient  be  kept  in 
the  same  room  with  the  instrument,  but  that,  on  the  contrary,  the  wards  of  the  hospital 
may  be  connected  by  wires  with  the  electrocardiographic  laboratory  and  the  patient  thus 
examined  without  leaving  his  bed  or  even  changing  his  position.  The  wiring  in  this  case 
cannot  be  done  on  a  grounded  circuit,  but  requires  double  wires  placed  underground  and 
very  completely  insulated.  If  this  is  done  the  electrocardiographic  variations  are  com- 
municated very  well  to  a  great  distance,  Einthoven's  own  laboratory,  in  which  the  original 
work  was  done,  having  been  located  1.5  kilometres  (one  mile)  from  the  hospital  in  which  the 
patients  lay.  With  proper  care  even  greater  distances  are  feasible.  In  the  short  space 
between  the  wards  and  the  laboratory  of  the  Johns  Hopkins  Hospital  no  difficulties  were 
encountered. 

In  practice,  the  setting  construction  and  setting  up  of  an  electrocardiographic  outfit 
or  "heart  station"  is  a  very  laborious  matter.  The  instruments  themselves  may  be  bought 
ready  made  at  a  considerable  cost,  but  much  labor  must  still  be  spent  in  installing  them. 


84 


DISEASES  OF  THE  HEART  AND  AORTA. 


Installation  of  the  Electrocardiograph. — Except  the  photo-registration  apparatus,  all 
the  apparatus  should  be  mounted  on  a  heavy  table  3x5  feet  in  size,  which  must  be  very 
steady  to  avoid  mechanical  vibrations  of  the  string.  A  concrete  pillar  may  also  be  used, 
especially  if  the  laboratory  is  in  the  basement;  but,  best  of  all,  'according  to  James  and 
Williams,  who  worked  in  a  laboratory  subject  to  great  vibrations,  is  to  allow  the  table  to 
rest  in  a  box  of  sand,  which  damps  all  the  small  vibrations. 

The  use  of  the  string  galvanometer  requires  three  separate  electrical  circuits, — a 
circuit  for  the  electric-light  current  for  illuminating  the  filament,  the  circuit  for  charging 


®    oo  1000    ®     100  10     ® 


(&y£&. 


Kindness  of  A.  II.  Thomas  &  Co. 

Fig.  57. — Edelmann'3  convenient  switchboard  and  short-circuiting  keys. 


the  electromagnets  of  the  galvanometer,  and  the  main  circuit  connecting  the  galvanometer 
and  the  patient. 

1.  The  electric  light-circuit  must  be  capable  of  carrying  over  ten  amperes  of  110  or 
220  volts  for  supplying  a  large  arc  lamp.  For  the  installation  of  two  galvanometers  wires 
must  be  used  which  are  capable  of  carrying  between  20  and  30  amperes,  or  a  double  circuit 
installed. 

Arc  lamps,  such  as  are  used  for  stereopticons  or  moving  pictures,  suffice  for  all  purposes, 
and  an  automatic  feed  for  the  carbons,  though  very  convenient,  is  not  indispensable. 

Just  as  for  magic-lantern  work,  the  lamp  must  be  provided  with  a  cooling  chamber  for 
water,  having  parallel  glass  walls  at  least  two  inches  apart.    By  staining  the  water  in  this 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.    85 

cooler  with  methylene  blue  or  some  other  fluid,  it  is  possible  to  obtain  an  almost  mono- 
chromatic light,  which  gives  much  sharper  outlines  to  the  shadows  upon  the  film  and  greater 
contrasts  than  are  otherwise  attainable. 

THE   STRING   GALVANOMETER. 

A  slight  modification  of  Einthoven's  original  model  may  be  obtained  from  the  firm 
of  Edelmann  of  Munich,  the  Cambridge  Scientific  Apparatus  Co.,  of  Cambridge,  England, 
and  Wertheim-Solamonson  of  Amsterdam.  As  stated  above,  it  consists  essentially  of  a 
fine  filament  of  platinum  or  silvered  quartz  which  is  suspended  between  the  two  poles  of 
a  large  electromagnet.    The  Cambridge  apparatus  is  the  most  convenient. 

The  two  poles  of  the  electromagnets  consist  of  large  wire-wound  soft-iron  cores  capa- 
ble of  generating  a  field  of  20,000  electromagnetic  units  (C.  G.  S.)  per  q.  cm.    Each  core  is 


Fig.  58. — Diagram  showing  the  main  connections  for  the  electrocardiograph.  The  heaviest  lines 
(110-220  V)  mark  the  electric  light  connections;  the  medium  lines  indicate  the  main  circuit  from  right 
hand  (RH),  left  hand  (LH)  or  left  foot  (LF)  of  the  patient  through  the  galvanometer,  showing  the 
shunt  through  the  rheostat  (RHEOST).  The  galvanometer  is  shown  between  the  two  poles  of  the 
MAGNET,  which  is  charged  by  the  storage  battery  circuit  (10  7).  The  connections  for  the  compensating 
current,  shown  in  the  darkly  shaded  area;  those  for  the  standardizing  current  are  shown  in  the  lightly 
shaded  area.    The  construction  of  the  photo-registration  apparatus  is  shown  upon  the  right  of  the  figure. 


penetrated  by  a  large  hole  to  accommodate  a  microscope  to  condense  the  light  upon  the 
filament  and  to  magnify  the  image  of  the  latter.  The  electromagnets  are  charged  with  a 
current  from  a  ten-volt  storage  battery,  which  is  provided  with  connections  for  recharg- 
ing, preferably  from  a  direct  street  current. 

Between  the  electromagnets  there  is  a  framework  for  holding  the  thread-carrier. 
The  latter  is  a  small  separate  holder  consisting  of  an  upright  frame  with  binding  posts  at 
each  end.  The  upper  binding  post  is  provided  with  a  micrometer  screw  for  adjusting  the 
tightness  of  the  filament  and  binder;  thus  each  binding  post  is  provided  with  two  laterally 
acting  micrometer  screws  for  centring  the  filament  between  the  lenses  of  the  microscopes 
after  its  tautness  has  been  adjusted. 

The  Galvanometer  Thread. — The  thread  or  filament  which  constitutes  the  main  part 
of  the  galvanometer  may  be  either  of  platinum  or  of  quartz  coated  with  silver,  but  in 
neither  case  should  its  diameter  be  greater  than  three  microns  (3^). 


86  DISEASES  OF  THE  HEART  AND  AORTA. 

Platinum  Filaments. — The  platinum  filaments  can  be  prepared  from  ordinary  Wollas- 
ton  wire,  platinum  wire  coated  with  silver  and  then  drawn  out  as  fine  as  possible,  by  simply 
dissolving  off  the  silver  with  dilute  acid. 

This  procedure,  which  at  first  blush  appears  extremely  simple,  is  a  matter  of  a  good 
deal  of  technical  difficulty:  first,  because  the  platinum  core  of  the  Wollaston  wire  is  by  no 
means  uniform,  and  many  samples  may  be  used  up  before  a  piece  ten  centimetres  in  length 
can  be  secured;  and,  secondly,  because  the  surface  tension  of  the  acid  is  strong  enough  to 
break  many  filaments  as  they  are  being  lifted  out  of  it.  Indeed  twenty  or  more  bits  of 
Wollaston  wire  may  be  used  up  before  a  single  filament  is  obtained  in  this  way, — at  least 
until  one  has  acquired  some  degree  of  skill  in  the  technique. 

The  filaments  are  then  s  o  1  d  e  r  e  d  on  to  the  ends  of  the  thread-holder,  which  are  first 
carefully  coated  with  ordinary  soft  solder  or  Woods'  metal,  using  acid-free  zinc  chloride 
solution  or  a  solder  paste  as  the  flux.  The  solder  coat  is  then  softened  once  more  and  the 
end  of  the  filament  caught  in  it  without  allowing  the  latter  to  touch  the  soldering  iron. 

Preparation  of  Quartz  Filaments. — Filaments  of  silver-coated  quartz  are,  however, 
six  or  seven  times  more  sensitive  and  are  capable  of  being  made  much  more  tense  than 
those  of  platinum.  According  to  Wertheim-Solamonson,  quartz  filaments  may  be  pre- 
pared in  the  following  way:  The  operator  sits  with  his  back  to  the  light,  facing  a  screen 
of  black  silk.  This  silk  curtain  is  hung  a  couple  of  feet  above  the  head  of  the  operator 
and  passes  obliquely  downward  to  a  horizontal  bar  above  the  opposite  edge  of  the  table, 
so  as  to  catch  all  the  fine  filaments  that  may  be  blown  off  the  quartz.  By  means  of  an 
oxygen-illuminating-gas  burner  he  fuses  a  stick  of  quartz  in  the  middle,  draws  it  out 
rapidly,  cuts  it  at  its  thinnest  point,  and  bends  the  tapering  portion  in  the  flame  to  a  right 
angle  about  5  cm.  from  the  end.  The  shaft  of  this  L  is  then  placed  in  the  axis  of  the  blast 
flame  and  in  fusing  it  fine  filaments  will  be  found  to  be  blown  off  onto  the  silk  screen,  es- 
pecially its  upper  portion.  These  filaments  are  taken  up  on  a  ,— !  shaped  bow  of  glass  rod, 
to  which  they  are  sealed  with  melted  rubber.  The  holder  and  thread  are  then  immersed  in 
a  5  per  cent,  solution  of  the  double  cyanide  of  silver  and  potassium  and  plated  with  a  10-20 
micro-ampere  current  using  a  high  graphite  resistance  (the  current  strength  must  be  con- 
trolled with  a  very  fine  ammeter),  gradually  sinking  them  lower  and  lower  in  the  fluid. 
They  are  then  carefully  removed  and  washed  several  times  by  dipping  in  distilled  water. 
After  this  procedure,  the  ends  of  the  filament  are  copper-plated  by  clamping  a  fine  copper 
wire  (cathode)  against  them  and  then  immersing  the  other  end  in  a  very  dilute  CuSO* 
solution  in  a  bath  containing  a  copper  strip  (anode)  also  connected  with  the  battery. 

When  the  ends  are  copper-plated,  the  filaments  are  soldered  into  the  holders,  as 
described  above. 

Wertheim-Solamonson  states  that  in  this  way  he  has  been  able  to  obtain  excellent 
filaments  with  a  thickness  (including  coating)  of  not  more  than  1.7  n  (.0017  mm.)  and  a 
resistance  of  only  440  ohms. 

Inserting  the  String. — The  filament  is  then  placed  loosely  in  a  temporary  holder  with 
which  it  can  be  carried  to  the  holder  of  the  galvanometer. 

Before  doing  so  it  must  bs  stretched  sufficiently  taut  in  the  holder  by  means  of  a  mi- 
crometer screw.  The  filament  is  so  thin  that  this  is  a  matter  of  some  delicacy.  The  fila- 
ment itself  can  barely  be  seen  even  in  a  strong  light  against  a  dark  background,  and  when 
it  is  loose  it  can  easily  be  broken  by  the  breathing  of  the  observer.  When  sufficiently  tight 
for  placing  in  the  galvanometer,  it  will  be  moved  only  2-3  mm.  by  a  gentle  zephyr,  or  by 
gentle  breathing  of  a  person  about  a  foot  away.  It  is  then  placed  in  the  holder  of  the  gal- 
vanometer and  transferred  to  its  place  between  the  electrodes  and  just  in  front  of  the  lenses 
of  the  two  microscopes.  This  must  be  done  with  great  care  and  all  draughts  or  currents  of 
air  must  be  avoided.  Care  must  be  taken  that  no  current  is  passing  through  the  electromag- 
nets while  the  thread  is  being  adjusted.  Even  if  these  are  free  from  current,  the  adjustment 
must  be  carried  out  slowly,  gradually  tightening  the  screws  and  gradually  sliding  the  holder 
in  between  the  lenses  to  keep  the  filament  from  touching  the  latter  and  adhering  to  them. 

When  the  filament  is  brought  between  the  lenses,  it  must  be  accurately  centred.  The 
light  is  turned  on,  the  microscope  lenses  are  focused  so  as  to  throw  a  sharp  shadow  of  the 
thread  on  a  screen,  and  the  filament  is  adjusted  by  means  of  the  centring  screws  to  bring  it 
to  the  exact  centre  of  the  magnetic  field.  This  is  attained  when  the  thread  is  no  longer 
pulled  out  to  focus  by  making  or  breaking  the  circuit  through  the  electromagnet,  but  the 
thread  must  be  centred  again  whenever  the  degree  of  tautness  is  changed. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.    87 

Edelmann  has  also  constructed  a  much  smaller  thread  galvanometer,  which  may  be 
used  with  either  a  permanent  magnet  or  an  electromagnet. 

The  former  was  given  an  extended  trial  by  the  writer  in  collaboration  with  Prof. 
Barker  and  Dr.  Bond,  but,  though  it  can  be  made  to  show  all  the  waves  of  the  normal 
electrocardiogram,  the  excursions  are  quite  small,  and  even  then  the  filament  must  be 
loosened  to  such  a  degree  that  it  fails  to  record  the  fine  wavelets  of  auricular  fibrillation; 
and  it  cannot  be  recommended  for  clinical  work.  With  the  electromagnet,  however,  a 
field  of  10,000  C.  G.  S.  (of  half  the  strength  of  that  in  the  large  galvanometer)  may  be 
obtained,  and  this  is  sufficient  for  most  clinical  purposes.  The  small  galvanometer  with 
electromagnet  may  still  be  used  for  clinical  purposes  in  case  expense  precludes  the  pur- 
chase of  the  larger  form;  but  the  loss  in  delicacy  must  always  be  borne  in  mind. 

Electrical  Connections  in  the  Galvanometer  Circuit. — The  essential  portions  of  the  con- 
nections with  the  galvanometer  are  made  up  of  three  distinct  circuits, — 

1.  The  circuit  from  the  electrodes  on  the  patient  through  the  galvanometer. 

2.  The  compensating  current  through  a  cell  and  the  galvanometer  in  the  reverse 

direction. 

3.  The  standardizing  circuit  to  determine  the  excursion  of  the  galvanometer. 
Electrodes. — Einthoven  originally  immersed  the  hands  or  feet  of  the  patient  in  large 

jars  of  physiological  sodium  chloride  solution  in  which  electrodes  of  zinc  were  placed,  and 
these  in  turn  connected  with  the  galvanometer  circuit. 

Later  investigators,  however,  have  found  it  more  convenient  to  use  large  plates  of 
German  silver,  about  15  x  25  cm.,  applied  to  the  skin  by  tying  about  the  limb  over  flannel 
pads  soaked  in  0.9  per  cent,  sodium  chloride  solution. 

Standardizing  the  Thread. — For  most  purposes  it  has  become  conventional  usage  to 
employ  strings  of  excursions  standardized  so  that  1  millivolt  gives  an  excursion  of  1 
centimetre.  This  adjustment  is  made  before  the  electrocardiogram  is  taken,  by  throwing 
in  a  current  of  exactly  1  millivolt  from  the  standardizing  circuit  and  then  adjusting  the 
tightness  of  the  thread  until  each  make  or  break  of  this  current  gives  an  excursion  of 
exactly  1  cm.  After  doing  so  the  thread  must  be  readjusted  to  the  exact  centre  of  the 
magnetic  field. 

Procedure  for  Taking  an  Electrocardiogram. — In  proceeding  to  take  an  electrocardio- 
gram, the  operator  immerses  the  pads  in  salt  solution,  applies  them  to  the  right  and  left 
forearm  and  left  shin  of  the  patient,  and  then  connects  two  of  them  with  the  binding  posts 
of  the  galvanometer  circuit. 

The  electric  lights  are  turned  on  and  the  shadow  of  the  thread  focussed  upon  the 
recording  apparatus.  The  double  connection  is  then  made,  which  first  throws  the  current 
into  the  electromagnet,  and  an  instant 

later  throws  the  galvanometer  circuit,  in  .1.  1 .  I .  .L  JJ-LJL 
which  the  current  is  temporarily  prevented  (uncompe  nsatc  t) 
from  passing  through  the  thread  by  keep- 
ing the  short-circuiting  key  (0  resistance) 
in  the  rheostat.  This  and  from  one  to  ten 
others  are  then  removed  in  order  to  see 
in  which  direction  the  body  current  (rest 
current,  zero  current,  Nullstrom)  is  pass- ' Ur»«IU  «1o-eLwJL.  ° 


ing ;  after  which  the  compensating  current      _      ,_     _.  ,      .     x.       ,  .;      .    , '        .. 

.    °.\  .  ,    ,  r   f.  Fig.  59. — Diagram  showing  the  relation  between  the 

IS  thrown  in   and    by  means   OI    the  com-  compensated  and  uncompensated  currents. 

mutator  sent  in  the  opposite  direction. 
The  resistance  plugs  are  removed  grad- 
ually from  the  rheostat  in  the  compensating  circuit  until  the  shadow  of  the  thread  is 
brought  back  to  its  original  position,  after  which  more  and  more  of  the  body  current  is 
shunted  in  by  removing  plugs  from  the  rheostat  on  the  main  circuit,  and  the  shadow  of 
the  thread  brought  back  to  centre  as  before.  These  oscillations  of  the  thread  now  corre- 
spond to  each  heart-beat,  and  the  wavelets  P,  R,  and  T  can  usually  be  seen  plainly.  The 
arc  light  is  once  more  adjusted  carefully,  the  shadows  focused,  and  the  movement  of 
the  thread  photographed. 

Photo  Registration. — The  oscillations  of  the  thread  are  recorded  in  the  usual  way 
by  photographing  its  shadow  upon  a  moving  film  at  a  distance  of  1-2  metres  from 
the  galvanometer;  but  the  great  magnification  of  this  shadow  and  the  shortness  of  the 


88  DISEASES  OF  THE  HEART  AND  AORTA. 

exposure  (less  than  T^o  second)  give  rise  to  certain  technical  difficulties.  In  the  first  place, 
as  has  been  stated  above,  it  is  necessary  to  have  an  arc  light  of  sufficient  power,  and 
small  lights,  such  as  are  used  for  photomicrography  or  dark-field  illumination,  are  inade- 
quate. An  arc  light  with  half  inch  or  f  inch  carbons,  such  as  is  used  for  magic  lanterns, 
represents  the  minimum  illumination. 

In  addition,  it  is  necessary  to  obtain  the  sharpest  possible  shadow,  for  which  the  light 
must  be  focused  sharply  upon  the  thread  with  the  condensing  microscope  and  the  image 
of  the  thread  in  turn  focused  upon  the  screen.  Chromatic  aberration,  which,  owing  to 
long  distance  from  the  lens  to  screen  is  considerable,  may  be  greatly  reduced  by  using  the 
methylene-blue  color  screen  described  above,  which  allows  most  of  the  blue  and  ultra- 
violet rays  to  pass  through,  and  this  gives  a  sharper  and  blacker  shadow  by  limiting  the 
refraction  to  the  waves  of  shorter  wave-length,  with  very  little  loss  in  photochemical  power. 

The  essential  part  of  the  photographic  apparatus  itself  is  a  light-tight  box  with  a 
slit,  past  which  a  film  or  strip  of  highly  sensitized  paper  is  rotated  by  means  of  a  horizon- 
tally moving  drum,  a  clock-work,  or  a  motor. 

In  the  very  elaborate  apparatus  which  usually  accompanies  the  electrocardiograph 
a  film  or  roll  of  highly  sensitized  paper  75  metres  long  is  held  in  a  light-tight  metal  box 
and  driven  at  any  desired  speed  by  an  electric  motor.  A  special  lever  is  arranged  so  that 
the  motor  may  attain  a  uniform  speed  before  starting  the  film,  and  this  in  turn  may  be 
started  before  the  exposure  is  made.  The  latter  is  accomplished  by  raising  the  shutter 
which  covers  a  horizontal  slit  in  the  box. 

In  order  to  concentrate  all  the  light  possible  upon  the  slit,  the  latter  is  covered  with 
a  plano-convex  cylindrical  lens  whose  axis  is  horizontal,  so  that  all  the  possible  illumina- 
tion is  obtained  but  the  side-to-side  movement  is  not  altered. 

After  passing  the  slit  the  film  travels  through  a  slit  in  the  bottom  of  the  box,  to  curl 
up  in  a  second  light-tight  box  below,  where  a  plane-like  blade  running  in  a  partition  be- 
tween the  two  boxes  cuts  off  the  exposed  from  the  unexposed  film.  Just  before  being 
moved,  each  film  may  be  numbered,  either  by  means  of  a  disk  perforated  with  holes  to 
show  the  numbers,  or  else  with  a  notched  line  made  by  signalling  upon  a  telegraph  key; 
these  may  be  indicated  by  the  number  of  movements  made  by  the  shadow  of  a  signal  mag- 
net, connected  with  a  telegraph  (make-and-break)  key. 

A  time-marking  lever  should  also  be  placed  in  front  of  the  slit.  The  time-marker 
may  be  an  ordinary  Jaquet  chronograph  recording  fifths  of  a  second  or  a  signal  magnet 
connected  with  an  electrically-driven  spring  interrupter  recording  \  or  T£g-  seconds.  For 
very  fast  speeds  a  convenient  time-marker  recording  t|q  seconds  can  be  secured  by  simply 
attaching  a  signal  magnet  in  series  with  a  32-candle-power  electric-light  bulb  attached  to 
the  ordinary  alternating  (60  cycle  per  second)  street  current. 

Carotid  and  Venous  Tracings. — It  is  also  important  to  obtain  some  other  curve  of 
the  cardiac  cycle  besides  the  electrocardiogram,  especially  the  venous  or  the  carotid  trac- 
ing. If  the  patient  is  brought  to  the  electrocardiograph  laboratory,  this  may  be  done  in 
the  usual  manner,  allowing  the  recording  lever  to  move  across  the  slit  instead  of  writing 
upon  a  smoked  surface. 

When  the  patient  is  at  a  distance,  however,  this  cannot  be  done  directly.  The  sim- 
plest method  then  consists  of  recording  merely  the  upstroke  of  the  carotid  wave  by  allow- 
ing the  tambour  to  make  and  break  an  electrical  circuit  as  the  lever  rises  and  falls,  and 
transferring  these  movements  to  a  signal  magnet  in  the  circuit  in  front  of  the  slit.  This 
suffices  for  many  purposes. 

Quite  perfect  curves  may  be  recorded,  however,  even  from  a  distance,  when  two  string 
galvanometers  are  used,  for  in  this  case  a  variety  of  means  for  securing  tracings  may  be 
employed. 

1.  The  lever  of  the  receiving  tambour  may  be  allowed  to  move  over  a  surface  of  tin 
or  aluminum  foil,  the  lever  and  one  margin  of  the  foil  being  connected  with  a  shunt  on 
the  second  galvanometer  circuit,  and  the  latter  activated  by  a  dry  cell.  The  movements 
of  the  lever  across  the  foil  cause  varying  resistances  in  the  circuit  and  corresponding  fluctu- 
ations of  the  galvanometer. 

2.  The  rubber  drum  of  the  tambour  may  be  provided  with  a  metal  armature  connected 
by  means  of  very  light  wire  in  the  primary  circuit  of  an  induction  coil.  The  movements 
to  and  fro  of  the  armature  cause  changes  in  the  secondary  current  of  the  induction  coil, 
and  these  variations  in  turn  can,  after  proper  shunting  down,  be  recorded  with  the  second 
galvanometer. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM. 


89 


Developing  and  Printing  the  Films. — After  the  exposures  are  made,  the  receiving  boxes 
covered  and  taken  from  the  instrument,  the  films  should  be  cut  as  long  as  possible  and  trans- 
ferred to  long  trays  or  else  passed  up  and  down  through  the  developer  by  holding  each 
end.  The  developer  should  have  a  composition  calculated  to  give  the  greatest  possible  con- 
trast, and  for  this  purpose  the  following  formula  has  been  found  satisfactory  by  Dr.  Bond : 

Solution    I.  Grams.  Ounces. 

Sodium  sulphite  crystals 3  : xii 

Hydrochinon |  ii 

Potassium  bromide \  i 

Water 25  c 

Solution   II. 

Potassium  carbonate  crystals. ...    6      xxiv 

Water 25     c 

Use  equal  parts  of  I  and  II  for  developer. 

Leads  or  Derivations. — It  has  become  conventional  to  obtain  tracings  in  man  with  the 
electrodes  in  three  sites : 
1st  lead  or  derivation  (D  1),  right  hand 

and  left  hand; 
2d  lead  or   derivation  (D  2),  right   hand 

and  left  foot; 
3d  lead  or  derivation    (D  3),  left  hand 

and  left  foot ; 
but  for  special  purposes  Kraus  and  Nicolal 
use  the  right  hand  to  right  foot,  left  hand 
to  right  foot,  right  foot  to  left  foot. 
Thomas  Lewis  has  found  that  he  could 
study  the  contractions  of  the  auricles  more 
closely  by  using  the  electrodes  over  the  pre- 
cordium  and  back. 

Fig.  60. — Distribution  of  the  electromotive  force 
Form  of  the  Electrocardiogram.       ln  tae  body  in  the  three  principal  leads  or  deriva- 
A  ,.         .i  i       ,.     ",         tions   (Z>  J,   D  II,   D  III).2    The  areas    shaded  in 
A  CUrve  representing  the  electrical        black  are  opposite  in  sign  to  those  left  white. 

variations  due  to  the  heart-beat  is 

known  as  an  electrocardiogram,  and  that  of  a  normal  heart-beat  is  shown  in 

Plate  IV. 

The  first  part  of  the  curve  is  represented  by  a  small  wave,  which  Eintho- 
ven  designates  by  P  (presystolic  wave),1  equivalent  to  a  variation  of  .0002  to 
.0004  volt,  coincident  with  the  onset  of  auricular  systole.  This  is  followed 
by  a  small  depression,  Q,  below  the  base-line  just  before  the  electrical  wave 
of  the  ventricle.  The  ventricular  wave  (R)  is  the  largest  wave  of  the  curve 
and  represents  about  .003-004  volt.  It  sets  in  and  subsides  within  .02  second, 
and  then  falls  below  the  base-line  to  form  a  depression,  S,  just  before  the 
mechanical  contraction  of  the  left  ventricle  sets  in.  This  is  followed  by  an 
instant  during  which  the  curve  remains  near  the  base-line,  and  then  gradually 
ascends  to  form  a  wave,  T,  lasting  about  .1  second  in  midsystole. 


1  Nicolai  designates  the  auricular  P  wave  by  A  (auricular  oscillation),  the  large  ven- 
tricular wave  R  by  I  (initial  oscillation),  the  T  wave  by/  (final  oscillation).  When  either 
of  these  waves  are  split,  they  designate  the  wavelets  as  A1,  A2,  I,  I2,  etc.  They  also  desig- 
nate the  horizontal  stretches  by  the  letters  h,  t,  p,  respectively,  h  representing  the  period 
of  conduction  in  the  His  bundle. 

2  A.  D.  Waller  (Jour.  Physiol.,  1913,  xlvi,  p.  lix)  gives  a  method  for  determining  the 
electrical  axis  of  the  heart. 


90 


DISEASES  OF  THE  HEART  AND  AORTA. 


Eyster  has  recently  called  attention  to  the  significant  fact  that  when 
very  loose  strings  are  used  there  is  no  period  of  zero  potential,  but  that  the 
T  wave,  which  is  then  relatively  much  larger  than  in  tracings  taken  with  the 
string  of  standard  tightness,  begins  immediately  after  the  S  wave  and  con- 
tinues until  the  exact  end  of  ventricular  systole.  There  are  no  waves  at  the 
end  of  systole  or  in  the  diastolic  period  until  the  beginning  of  auricular  con- 
traction. 

In  the  perfectly  normal  curve,  the  tracings  taken  with  the  different 
leads  are  quite  similar  (Plate  III),  except  that  the  R  wave  is  largest  in  the 
second  derivation  (D  2,  right  hand  to  left  foot). 

Although  the  forms  of  the  waves  of  the  electrocardiogram  are  very 
definite,  there  is  little  that  is  certain  about  the  causation  of  the  individual 
waves. 

According  to  Kraus  and  Nicolai,  the  cardiac  cycle  may  be  divided  into  the  following 
periods : 


AorP 

h  (P-Q  Interval)  . 

J  or  R 

t 

For  T 

V 


Auricular  activity. 

Conduction  time  in 
His  bundle. 

Activity  of  the  papil- 
lary muscles. 

Activity  of  the 
"Treibwerk"  of 
ventricular  fibres. 

Activity  of  the  conus 
arteriosus. 

Rest  of  the  entire 
heart. 


Presystole . 


Intersystole 


Systole 


Diastole . 


Filling  of  ventricles. 


Presphygmic     period 
(Anspannungszeit) 


Period  of  outflow. 


Filling  of  ventricles. 


This  division  of  the  cardiac  cycle  is  in  many  ways  an  arbitrary  one.  It  is  by  no  means 
certain  that  the  waves  (especially  J  and  F)  correspond  to  the  events  assigned  to  them  by 
Nicolai,  and  indeed  many  physiological  facts  point  to  the  contrary.  On  the  other  hand, 
it  seems  probable  that  at  least  the  ventricular  waves  are  composite  in  character. 

Cause  of  Waves  upon  the  Electrocardiogram. — As  Judin  and  Nicolai  have  pointed  out, 
some  of  the  waves  present  certain  analogies  to  those  produced  in  skeletal  muscle  where  the 
electrodes  are  placed  near  the  two  ends  of  the  muscle.  In  this  case  there  occurs  a  diphasic 
variation,  a  large  wave  which  is  followed  by  a  period  of  zero  potential,  and  this  in  turn  by 
a  similar  large  wave  opposite  in  sign  to  the  first.  Such  a  diphasic  variation 
(Fig.  61)  is  shown  almost  exactly  by  the  auricular  (P)  wave  of  the 
electrocardiogram,  with  its  period  of  A  potential  and  its  subsequent  (Q)  depres- 
sion, and  also  by  the  curves  obtained  with  extra  systoles. 

The  waves  (R,  S,  T)  of  ventricular  systole  are,  on  the  other  hand,  more  difficult  to 
explain,  but  Judin  has  obtained  from  a  normal  skeletal  muscle 
(frog's  gastrocnemius)  electrographic  tracings  showing 
waves  which  closely  resemble  the  R ,  S ,  and  T  waves  of  the 
v  ntricular  impulse.  Somewhat  similar  curves  have  been  obtained  by  Nicolai 
from  skeletal  muscle  systems  in  which  two  muscles  were  simultaneously  conducting  im- 
pulses in  opposite  directions,  and  represent,  more  or  less,  the  algebraic  sum  of  the  two 
impulses.  The  double  spiral  of  ventricular  muscle  (see  p.  6  and  Fig.  11)  represent  a 
somewhat  similar  double  system  of  contracting  muscle  fibres,  and  perhaps  on  this  account 
the  electrocardiogram  somewhat  resembles  the  wave  thus  elicited. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.  91 

PLATE  IV. 


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R 

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T 

s 

:^^ 

jm'-nflm 

R 

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Q 

ma^^^^mmmm"*"'iiitm-W'*m-i 

*             *---—*■-■ *mtmmA             AAA              *  .  ■      f             S             *             A              I 

Kindness  of  Interstate  Medical  Journal. 

Plate  IV. — Electrocardiograms  from  a  normal  man.  A,  Tracing  taken  with  the  electrodes  upon 
the  right  arm  and  left  arm  (Dl).  B,  Tracing  taken  with  the  electrodes  upon  the  right  arm  and  left  leg  (D2)- 
C,  Tracing  taken  with  the  electrodes  upon  the  left  arm  and  left  leg  (D3).  The  lowest  line  and  the  third  line 
from  the  bottom  represent  signals,  the  second  line  from  the  bottom  represents  time  in  J  seconds. 


92 


DISEASES  OF  THE  HEART  AND  AORTA. 


iiiiiiiiiiiiiiNiiiiiiiiiiiiiriiiiiiiiiHiiiiiiiiiiiifimiiiii 

ttt] 

Fig.  61. — Normal  electrocardiogram  showing 
the  time  relations  to  the  venous  and  carotid  pulse- 
wave.      (After  Einthoven.) 


It  must  be  remembered,  as  Gotch  and  Florence  Buchanan  have  pointed  out,  that 
these  waves  represent  the  difference  of  potential  between  the  skin  under  the  two  electrodes. 
If  both  electrodes  remain  entirely  free  from  charge,  the  curve  remains  at  the  base-line. 
But  if  both  electrodes  receive  an  electric  charge  of  the  same  intensity  (say,  four  milli- 
volts), the  difference  of  potential  between  them  remains  zero,  and  the  curve  remains  at 
the  base-line  (Fig.  62).  It  is  a  matter  of  empirical  fact,  shown  by  Kraus  and  Nicolai,  that 
the  contraction  originating  at  the  base  of  the  right  ventricle  causes  a  wave  exactly  oppo- 
site in  sign  to  that  accompanying  a  contraction  originating  at  the  left  apex,  and  it  has  been 
assumed  by  these  writers  that  the  ventricular  part  of  the  normal  elec- 
trocardiogram represents  the  algebraic  sum  of  two  such 
almost  equal  and  opposite  currents,  but  that  the  R  S  wave,  which 
occurs  before  the  onset  of  the  mechanical  contraction,  is  caused  by  the  impulse  passing 

down  the  cells  of  the  atrioventricular  conduc- 
tion system.  In  conformity  with  this  hypoth- 
esis, Nicolai  found  all  the  waves  inverted  in  a 
patient  with  dextrocardia  (see  page  550) ;  but, 
on  the  other  hand,  Gotch,  Buchanan,  Straub, 
and  Samojloff  found  electrocardiograms  simi- 
lar to  those  of  mammals  in  frogs,  snakes,  and 
tortoises,  in  spite  of  the  fact  that  these  ani- 
mals possess  but  one  ventricle. 

Florence  Buchanan  suggests  that  it  may 
not  be  the  separate  ventricles,  but  the  sepa- 
rate layers  of  muscle-fibres  which  arise  in  each 
papillary  muscle.  She  suggests,  moreover, 
that  the  R  wave  is  produced  by  a  slight  asyn- 
chronism  between  the  two  ventricles,  so  that 
one  ventricle  only  is  acting  during  the  instant  in  which  the  R  wave  occurs.  This  view  is 
shared  by  Rothberger  and  Winterberg.  Such  an  asynchronism  has  indeed  been  shown  by 
Knoll,  Fredericq,  Stassen,  Barker  and  Hirschfelder  during  vagus  stimulation,  and  it  is 
possible  that  even  under  normal  conditions  it  may  exist  for  a  period  long  enough  to  just 
give  rise  to  the  deflection  of  the  R  wave. 

As  a  matter  of  fact,  one  occasionally 
meets  with  definite  bifurcations  of  the  R  wave 
which  seem  to  furnish  support  to  this  theory, 
but  H.  B.  Williams  (Am.  J.  Physiol.,  1914, 
xxxv,  292)  finds  on  simultaneous  tracings  from 
different  leads  that  homonymous  peaks  are 
not  always  in  the  same  phase.  And  still 
further  evidence  is  furnished  by  the  electro- 
cardiograms of  Eppinger  and  Rothberger  from 
dogs,  in  which  one  branch  of  the  His  bundle 
was  injured  in  which  usually  broad  R  waves 
were  recorded.  On  the  other  hand,  the  R 
wave  is  not  broadened  by  stimulation  of  the 
vagi  nor  in  persons  with  slow  hearts,  as  might 
be  expected  from  the  results  of  the  above- 
mentioned  observers. 

The  validity  of  these  hypotheses  is,  how- 
ever, rendered  questionable  by  the  fact  that 

Eyster  has  obtained  the  R  and  T  waves  in  typical  form  from 
isolatedstripsof  terrapin's  ventricleashas  also  W.  A.  Jolly  (J.  Physiol, 
1913-1914,  xlvii,  p.  xxx).  The  latter  observer  found,  however,  that,  though  such  a  wave  was 
obtained  when  both  electrodes  were  applied  to  the  ends  of  the  strip,  a  plateau-like  curve 
was  obtained  when  only  one  electrode  was  applied  to  the  edge  of  the  strip.  He  concludes 
that  this  is  definite  evidence  in  favor  of  algebraic  summation. 

Extracardiac  Vibrations  of  the  String.— Although  these  waves  and  other 
waves  to  be  discussed  later  are  produced  by  the  electrical  variations  of  the 


Fig.  62. — Factors  involved  in  the  normal 
electrocardiogram,  according  to  the  theories.  (7) 
Ordinary  diphasic  variation  in  skeletal  muscle 
of  algebraic  summation.  The  white  and  black 
areas  (77  and  777)  indicate  electrical  changes  going 
on  in  each  of  the  ventricles  or  in  different  layers 
of  ventricular  muscle.  The  small  diagram  (7)  at 
the  left  shows  the  connections  of  the  electrodes 
in  obtaining  the  tracing  from  skeletal  muscle. 


PLATE  V. 


Typical  electrocardiograms.  (Kindness  of  Dr.  R.  E.  Morris.)  A,  electrocardiogram,  showing  split  P 
wave.  B,  electrocardiogram,  showing  split  R  wave  and  inverted  T  wave.  C,  e  echocardiogram  showing 
the  P  wave  encroaching  upon  the  R  wave  (atrioventricular  rhythm).  The  wavelets  between  the  last  three 
R  waves  suggest  momentary  auricular  flutter. 


THE  VENOUS  PULSE  AND  ELECTROCARDIOGRAM.         93 

heart,  irregular  and  rapid  vibrations  are  sometimes  encountered  which  are 
superposed  upon  the  main  waves,  and  may  be  due  to  the  following  causes 
(James  and  Williams) : 

I.  Induction  from   outside   sources. 

1.  Neighboring  strong  electrical  vibrations,  such  as  the  passage  of  elec- 
tric cars,  etc. 

2.  Defective  insulation. 

3.  Induction  caused  by  hissing  of  the  arc  lamp. 

II.  Muscular  contractions. 

1.  Tenseness  of  the  patient's  muscles,  which  gives  rise  to  a  vibration  of 
the  string  (Einthoven)  at  a  rate  of  about  50  per  second  (Piper).  This  is 
especially  common  in  persons  who  work  with  their  hands  (Strubell) . 

2.  Gross  muscular  movements,  such  as  coughing,  sneezing,  movements 
of  the  hand,  etc.,  which  cause  large  irregular  movements  of  the  string,  which 
can  be  readily  distinguished  from  those  due  to  the  heart's  action. 

The  latter  are  easily  recognized,  but  the  finer  vibrations  might  some- 
times be  confused  with  those  due  to  fibrillation  of  the  auricles,  except  for  the 
fact  that  they  are  merely  superposed  upon  the  other  waves  of  the  electro- 
cardiogram, whereas  in  fibrillation  the  P  wave  disappears  entirely.  The 
nonmuscular  extraneous  vibrations  may,  moreover,  be  recognized  by  taking 
a  short  control  without  connecting  the  galvanometer  with  the  patient. 

Exaggerated  P  Wave  in  Mitral  Stenosis. — Although  the  P  (or  A)  wave 
may  diminish  or  disappear  under  the  influence  of  vagus  stimulation  even 
when  the  auricles  are  still  contracting  actively,  under  other  circumstances 
it  may  be  markedly  increased  in  size  (Plates  XVI  and  XVIII).  This,  as 
Samojloff  has  shown,  is  especially  the  case  in  compensated  mitral  stenosis, 
in  which,  accompanying  the  hypertrophy  and  increased  force  of  the  auricles, 
the  auricular  (P)  wave  may  become  definitely  in- 
creased in  height,  though  this  is  scarcely  characteristic  enough  to 
warrant  the  diagnosis  of  mitral  stenosis  from  the  form  of  the  electrocardio- 
gram alone. 

Change  in  Form  of  the  Electrocardiogram  Accompanying  Change  of 
Position  of  the  Body. — E  inthoven  and  August  Hoffmann 
have  shown  that  alterations  in  the  position  of  the 
heart  within  the  body,  from  change  in  position  of 
the  body,  inflation  of  the  stomach,  displacement 
of  the  heart  from  pleural  effusion,  etc.,  cause 
changes  to  take  place  in  the  electrocardiogram, 
the  R  wave  to  become  smaller  and  the  S  larger;  and  Waller1  has  found 
great  effect  from  deep  inspiration. 

Also  somewhat  arbitrary  is  the  claim  of  Kraus  and  Nicolai  that  the 
size  of  the  T  wave  is  in  some  way  an  index  of  the  vigor  of  the  contraction. 

1  Waller,  A.  D.  :  Effect  of  Respiration  on  the  Electrocardiogram  and  upon  the  Elec- 
trical Axis  of  the  Heart,  J.  Physiol.,  1913,  xlvi,  p,  bcii. 


94  DISEASES  OF  THE  HEART  AND  AORTA. 

True,  they  found  that  in  many,  though  by  no  means  all,  cases  of  feeble 
heart  action,  this  wave  is  small,  absent,  or  inverted,  and,  on  the  other 
hand,  that  it  may  be  large  in  hypertrophic  hearts  and  in  overacting  hearts, 
in  Basedow's  disease,  after  exercise,  etc.,  but  many  failing  hearts  retain  a 
high  T  wave  to  the  end,  and  in  many  otherwise  vigorous  persons  the  T  wave 
may  be  small  or  even  inverted. 

In  hypertrophy  of  the  right  ventricle  and  also  after  stimulation  of  the 
vagus,  the  R  wave  becomes  higher;  in  hypertrophy  of  the  left  ventricle  it 
becomes  inverted. 

Kraus  and  Nicolai  have  called  attention  to  the  fact  that  in  nervous 
people,  as  well  as  in  patients  with  mitral  insufficiency,  the  S  depression  is 
very  deep,  so  that  they  have  termed  it  the  Neurasthenikerzacke  (neurasthenic 
notch) ;  but  Strubell  has  encountered  this  form  in  so  many  vigorous,  athletic 
persons  that  this  designation  seems  entirely  too  arbitrary.  A  very  marked 
S  depression  has  been  obtained  by  Rothberger  and  Winterberg  from  stimu- 
lation of  the  right  acceleratory  nerve.  And  it  is,  of  course,  possible  that  in  all 
these  persons,  whether  from  nervous  excitement  or  exercise,  the  right  accelera- 
tor may  be  stimulated,  though  by  no  means  all  have  rapid  pulse-rates. 

An  exceptionally  high  T  wave  may  also  be  obtained  when  the  galvanom- 
eter thread  is  loose. 

Rothberger  and  Winterberg  have  also  obtained  peculiar  deformations 
of  the  electrocardiogram  by  stimulating  the  various  branches  of  the  cervical 
sympathetic  (accelerator)  nerves,  and  have  found  a  different  form  of  electro- 
cardiogram for  each  branch  of  the  ganglia  stimulated,  corresponding  probably 
to  an  exaggerated  effect  localized  in  each  case  to  a  certain  region  of  the  heart 
wall. 

In  general,  stimulation  of  the  right  accelerator  branches  produced  effects 
somewhat  resembling  those  of  the  right  ventricular  hypertrophy,  and  those 
of  the  left  suggested  more  or  less  hypertrophy  of  the  left  ventricle.     (Fig.  78.) 

Stimulation  of  the  vagi,  on  the  other  hand,  as  has  been  stated,  usually 
causes  a  large  R  wave  with  diminution  or  disappearance  of  P  and  T. 

The  inversions  and  changes  in  form  due  to  hypertrophy  of  the  two 
ventricles  and  to  situs  inversus  will  be  discussed  under  these  heads  (pages 
297  and  560). 

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Barker,  L.  F  ,  and  Hirschfelder,  A.  D. :  The  Effects  of  Cutting  the  Branch  of  the  His  Bundle 

Going  to  the  Left  Ventricle,  Arch.  Int.  Med.,  Chicago,  1909,  iv,  193. 
Barker,  L.  F.,  Hirschfelder,  A.  D.,  and  Bond,  G.  S.:  The  Electrocardiogram  in  Clinical 

Diagnosis,  J.  Am.  M.  Assoc,  Chicago,  1910,  Iv,  1350. 
Buchanan,  F. :  Note  on  the  Electrocardiogram,  Frequency  of  the  Heart-beat  and  Respira- 
tory Exchange  in  Reptiles,  J.  Physiol.,  Camb.,  1909-10,  xxxix,  Proc.  Physiol.  Soc, 

p.  xxv. 
Einthoven,  W.:  Ueber  die  Form  des  menschlichen  Elektrocardiogramms,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1895,  lx,  101. 

—  Ein  neues  Galvanometer,  Ann.  d.  Physik,  1903,  iv,  Ser.  xii,  1059. 

—  Ueber  einige  Anwendungen  der  Saitengalvanometers,  ibid.,  1904,  xiv,  182. 
— ■  Le  Telecardiogramme,  Arch,  internat.  de  physiol.,  Liege,  1906,  iv,  132. 

Einthoven,  W.,  and  Vaandrager:  Weiteres  ueber  das  Elektrocardiogramm,  Arch.  f.  d. 
ges.  Physiol.,  Bonn,  1908,  cxxii,  517. 

Eppinger,  J.,  and  Rothberger,  J.:  Ueber  die  Folgen  der  Durchschneidung  der  Tawara's- 
schen  Schenkel  des  Reizleitungssystems,  Ztschr.  f.  klin.  Med.,  Berl.,  1910,  Ixx,  i. 

Fredericq,  L.:  La  pulsation  du  cceur  du  chien  est  une  contraction,  etc.,  Arch,  internat.  de 
physiol.,  Liege,  1906,  iv,  60. 

Gotch,  F. :  The  Succession  of  Events  in  the  Contracting  Ventricle  as  shown  by  Electrom- 
eter Records,  Heart,  Lond.,  1909-10,  i,  235. 

Hoffmann,  A.:  Zur  Kritik  des  Elektrokardiogramms,  Verhandl.  d.  Kong.  f.  innere  Med., 
Wiesbaden,  1909,  xxvi,  614. 

Kolliker,  A.,  and  M  tiller,  H.:  Nachweis  der  negativen  Schwankung  am  naturlich 
sich  kontrahierenden  Muskel,  Verh.  d.  physikmed.  Gesellsch.,  Wiirzburg,  1855, 
vi,  528. 

Knoll,  P. :  Ueber  Incongruenz  in  der  Thatigkeit  der  beiden  Herzhalften,  Sitzungsber.  d. 
K.  Akad.  d.  Wissensch.,  Math,  naturw.  Kl.,  Vienna,  1890,  xcix,  31. 

Kraus,  F.,  and  Nicolai,  G.  F.:  Ueber  das  Elektrokardiogramm  unter  normalen  und  path- 
ologischen  Verhaltnissen,  Berl.  klin.  Wchnschr.,  1907,  765,  811;  Das  Elektrokardio- 
gramm des  gesunden  und  kranken  Menschen,  Leipz.,  1910. 

Piper:  Ueber  den  willkurlichen  Muskeltetanus,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907, 
cxix,  301;  Ztschr.  f.  Biol.,  Muenchen,  1908,  1,  393. 

Rothberger,  J.,  and  Winterberg,  H. :  Ueber  die  Beziehungen  der  Herznerven  zur  i<  orm  des 
Elektrokardiogramms,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1910,  cxxxv,  506. 

Samojloff,  A.:  Ueber  die  Vorhoferhebung  des  Elektrokardiogramms  bie  Mitralstenose, 
Muenchen.  med.  Wchnschr.,  1909,  lvi,  1942. 

Stassen,  A. :  De  l'ordre  de  succession  des  diff erentes  phases  de  la  pulsation  cardiaque  chez 
le  chien,  Arch,  internat.  de  physiol.,  Liege,  1907,  v,  600. 

Strubell,  A.:  Zur  Klinik  des  Elektrokardiogramms,  Verhandl.  d.  Kong.  f.  innere  Med., 
Wiesbaden,  1909,  xxiv,  623. 

Waller,  A.  D.J  A  Demonstration  on  Man  of  Electromotive  Changes  Accompanying  the 
Heart's  Beat,  J.  Physiol.,  Camb.,  1887,  viii,  229.  Introductory  Address  on  the  Elec- 
tromotive Properties  of  the  Human  Heart,  Brit.  M.  J.,  Lond.,  1888.  ii,  751.  On  the 
Electromotive  Changes  Connected  with  the  Beat  of  the  Mammalian  Heart,  Phil. 
Tr.  Roy.  Soc,  Lond.,  1889,  1890,  clxxx,  B,  169. 

Wertheim-Salamonson,  J.  K.  A.:  Anfertigung  und  Gebrauch  dunner  versilberten  Quarz- 
faden,  Ztschr.  f.  biol.  Techn.  u.  Methodik.,  1909,  i,  35.  For  a  more  elaborate  process 
see  also  Connegieter,  H.  G. :  Leitendmachen  dunner  Quartzfaden  durch  Kathoden- 
zerstaubung  mit  nachfolgender  galvanis  cher  Versilberung,  ibid.,  1910,  ii,  21. 

Eyster,  J.  A.  E. :  Electrocardiogram  Studies,  read  before  the  the  American  Physiological 
Society,  Baltimore,  Dec.  29,  1911. 

Judin  A.:  Zur  Erklarung  der  Form  des  Elektrokardiogramms,  Zentralbl.  f.  Physiol.,  Leipz. 
and  Wien,  1908,  xxii,  365. 


THE  VENOUS   PULSE    AND   ELECTROCARDIOGRAM.        97 

Morrow,  W.  S.:  Various  Forms  of  the  Negative  or  Physiological  Venous  Pulse,  Brit.  M. 

Jour.,  Lond.,  1906,  ii,  1807.    The  Venous  Pulse,  ibid.,  1907,  i,  777. 
Knoll,  P.:  Beitrage  zur  Lehre  von  der  Blutbewegung  in  den  Venen,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1898,  lxxii,  317,  621. 
Theopold,  P.:  Ein  Beitrag  zur  Lehre  von    der  Arhythmia  perpetua,  Deutsch.  Arch.  f. 

klin.  Med.,  Leipz.,  1905,  lxxxii,  495. 
Marey,  E.  J.:   La  physiologie  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Paris,  1881. 
Fredericq,  L.,  1.  c. 

Porter,  W.  T.:  Researches  on  the  Filling  of  the  Heart,  Jour.  Physiol.,  Cam.,  1892,  xiii,  513. 
Bard,  L.:  Des  divers  details  du  pouls  veineux  les  jugulaires  chez  l'homme,  J.  de  Physiol. 

et  de  Path,  gen.,  Par.,  1906,  viii,  454. 
Hirschfelder,  A.  D.:  Some  Variations  in  the  Form  of  the  Venous  Pulse,  Bull.  Johns  Hop- 
kins Hosp.,  Bait.,  1907,  xviii,  265. 
Cushny,  A.  R.,  and  Grosh,  L.  C:  The  Venous  Pulse,  Jour.  Am.  M.  Ass.,  Chicago,  1907, 

xlix,  1254. 
Mackenzie,  J.:  The  Venous  Pulse,  Brit.  M.  J.,  Lond.,  1907,  i,  112. 
Sewall,  H.,  and  Hirschfelder,  A.  D.:  Unpublished  investigations. 
Peabody,  F.  W.:  Personal  communication. 
Sewall,  H.:    Safeguards  of   the  Heart-beat,  Am.  J.  M.  Sci.,  Phila.  and  N.  York,   1908, 

cxxxvi,  32. 
Hering,  H.  E.:    Die  Verzeichnung  des  Venepulses  am  isolierten  Kiinstlich  durchstromten 

Saugetierherzin,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1904,  cvi,  1. 
Chauveau  and  Marey:  Quoted  from  Marey,  La  Circulation  du  Sang,  etc. 
Gibson,  A.  G.:  On  a  Hitherto  Undescribed  Wave  in  the  Venous  Pulse,  Lancet,  Lond.,  1907, 

ii,  1380. 
Mackenzie,  J.:  The  Interpretation  of  the  Pulsations  in  the  Jugular  Veins,  Am.  Jour.  M. 

Sc,  Phila.  and  N.  York,  1907,  n.  s.  cxxxiv,  12. 
Rihl,  J.:  Ueber  den  Venenpuls  nach  experimenteller  Lasion  der  Trikuspidalklappe,  Ver- 

handl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1907,  xxiv,  453. 
Gibson,  G.  A.:  Certain  Clinical  Features  of  Cardiac  Disease,  Johns  Hopkins  Hosp.  Bull., 

Bait.,  1908,  xix,  361. 
Eyster,  J.  A.  E.:  Unpublished  observations. 
Hirschfelder,  A.  D.:  Inspection  of  the  Jugular  Vein;    Its  Value  and  Its  Limitations  in 

Functional  Diagnosis,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  1105. 
V.  Frey,  M.,  and  Krehl,  L.:  Untersuchungen  ueber  den  Puis,  Arch.  f.  Physiol.,  Leipz., 

1890,  31. 
Hewlett,  A.  W.:  On  the  Interpretation  of  the  Positive  Venous  Pulse,  Jour.  Med.  Re- 
search, Bost.,  1907,  xvii,  19. 
Minkowski,  O.:  Die  Registrierung  der  Herzbewegungen  am  linken  Vorhof,  Deutsch.  med. 

Wochnschr.,    1906,   xxxii,    1248.     Zur  Deutung  von   Herzarrhythmien  mittelst  des 

cesophagealen  Kardiograms,  Ztschr.  f.  klin.  Med.,  Berl.,  1907,  lxii,  371. 
Rautenberg,  E.:  Neue  Methode  der  Registrierung  der  Vorhofspulsation  vom  Oesophagus 

aus,  Deutsche  med.  Wchnschr.,  Leipz.  and  Berl.,  1907,  xxxiii,  364. 
Young,  C.  I.,  and  Hewlett,  A.  W.:  The  Normal  Pulsations  within  the  Oesophagus,  J.  M. 

Research.,  Bost.,  1907,  xvi,  427. 
Hirschfelder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Johns  Hopkins 

Hosp.  Bull.,  Baltimore,  1906,  xvii,  299. 
Einthoven,  W.:  Le  telecardiogramme,  Arch,  internat.  de  Physiol.,  Liege,  1906,  iv,  132. 

Weiteres  ueber  das  Elektrokardiogramm,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxii, 

517.    (See  also  chapter  on  Alterations  of  Rhythm.) 


ALTERATIONS   IN   CARDIAC   RHYTHM. 

The  irregularities  in  rhythm  of  the  heart  may  be  divided  first  into 
three  classes:  (1)  arrhythmias,  in  which  there  is  no  discernible  order 
in  the  occurrence  of  beats;  (2)  allorrhythmias  (altered  rhythms),  in 
which,  though  the  rhythm  is  not  regular,  yet  the  irregular  beats  occur 
according  to  a  certain  regular  system,  so  that  the  arrangement  of  these 
beats  in  one  section  of  the  tracing  can  be  prophesied  from  a  knowledge  of 
another;  and  (3)pararrhythmias  (Wenckebach),  in  which  two  separate 
rhythms  are  going  on  in  either  the  same  chamber  or  in  different  chambers 
at  the  same  time. 

ALLORRHYTHMIAS. 

A.  Of  extracardiac   origin. 

I.  Neurogenic  (sinus  arrhythmias),  due  to  more 
or  less  rhythmic  reflex  stimuli  passing  through  the  vagi  and  ac- 
celerators (toxic,  reflex  from  various  organs,  respiratory  reflexes 
from  lungs). 

a.  Associated  with  the  phases  of  respiration. 

b.  Not  associated  with  respiration — Mackenzie's  youthful  type. 

II.  Due  to  disturbances  in  the  filling  and  empty- 
ing of  the  heart  from  traction  upon  the 
heart  and  great  vessel  s — dropping  of  beats  without 
heart-block,  pulsus  paradoxus  and  Riegel's  pulse. 

B.  Of  intracardiac   origin. 

I.  Due  to  disturbance  in  the  conduction  of  normal 
impulse  s — dropping  of  beats. 

1.  Auriculo-  (atrio-)  ventricular  block. 

2.  Sino-auricular  block. 

3.  Interventricular  (?)  block  (hemisystole). 

II.  Disturbance    of    contractilit  y — pulsus  alternans,  and 

failure  to  open  the  aortic  valves. 
III.  Occurrence    of    beats    in    response    to    abnormal 
stimuli   or  increased   irritability. 

1.  Extrasystoles,  in  which  irregular  beat  is  brought  on  by  a  single  ab- 

normal stimulus. 
„     ,  ,    ,      f  Right  ventricular. 
a-Ventncular\  Left  ventricular. 

("Right  auricular  arising  near  the  superior  vena  cava 
.     .      J         (normal  site). 
b.  Auricular  <     arising  eisewhere  in  the  right  auricle. 

(Left  auricular, 
c    Auriculoventricular,  arising  in  the  cells  of  the  conduction  system. 

2.  Paroxysmal  tachycardia. 

3.  Absolutely  irregular  pulse  (auricular  fibrillation). 
98 


ALTERATIONS  IN  CARDIAC  RHYTHM. 


99 


Sinus 
arrhythmia 


AUKICULOVEN- 

TRICULAR 
HEART-BLOCK 


Alternating 

PULSE 


Auricular 
extrasystole 


Ventricular 
extraststole 


Auriculoven- 

tricular 

extraststole 


Absolute 

arrhythmia 

(auricular 

fibrillation 


Paroxysmal 
tachycardia 


Fig.  63. — Diagram  representing  various  types  of  irregular  pulse.  The  heavy  white  arrows  indi- 
cate the  site  of  origin  of  the  disturbance  of  rhythm.  The  heavy  white  lines  indicate  the  course  of  the  ab- 
normal cardiac  impulses.  RESP,  respiration;  AUR,  auricle;  A-V  or  AVB,  auriculoventricular  bundle; 
VENT,  ventricle;  CAR,  carotid  pulse;  VEN,  venous  pulse;  SIN,  sinus  region  of  the  heart;  SVC,  IVC, 
superior  and  inferior  vense  cava?,  respectively. 


100 


DISEASES  OF  THE  HEART  AND  AORTA. 

PLATE  VI. 


p     T   P    T  P     TP 

'  irtrff  iAt   -Jmra 'miTtr- 


R"       R        R        R      r  R     ' 

P     T   P    T-  |  T    P    TD    T     p    T 


A 


\A-V\ 


\ 


\   \    \ 


V 


Electrocardiogram  of  sinus  arrhythmia  (respiratory),  with  diagram  showing  the  course  of  the  impulses 
within  the  heart.1  The  white  areas  upon  the  diagram  represent  the  sinoauricular  node  of  Keith  and  Flack, 
and  the  auriculoventricular  bundle.  The  black  arrow  indicates  the  course  of  the  impulses.  A,  A-V,  V, 
impulses  in  the  auricle,  auriculoventricular  bundle  and  ventricles,  respectively. 


EX.  SYS. 


Extrasystole  arising  at  the  node  of  Keith  and  Flack  (homogenetic),  with  diagram  showing  the  course  of  the 

normal  and  extrasystolic  impulses. 


JThe  writer  is  indebted  to  Dr.  Geo.  S.  Bond  for  the  preparation  of  most  of  the  electrocardiograms 
used  throughout  the  book. 


ALTERATIONS   IN   CARDIAC   RHYTHM.  101 

I.    SINUS   ARRHYTHMIAS1    (OR    REFLEX   ARRHYTHMIAS). 

Alteration  in  cardiac  rhythm  resulting  from  intermittent  stimuli  pass- 
ing down  the  cardiac  nerves  constitutes  one  of  the  most  common  forms  of 
cardiac  allorrhythmias.  As  has  been  seen  (Chapter  III),  alterations 
of  the  pulse-rate  may  result  from  any  stimulation 
of  any  afferent  nerve,  from  skin,  muscles,  mucous  membrane, 
and  viscera,  or  from  stimuli  arising  in  the  vagal  or  accelerator  centres  in  the 
medulla. 

As  Reid  Hunt  and  Hooker  have  shown,  the  reflex  stimulation  may  cause  a  slowing  of 
the  pulse-rate  through  stimulation  of  the  vagus  centre,  or,  under  other  circumstances 
and  especially  when  of  a  different  intensity,  it  may  cause  an  acceleration  of  the  pulse- 
rate.-  Hunt  has  shown  that  this  acceleration  is  due  chiefly  to  momentary  cessation  of  the 
tonic  stimuli  in  the  vagus;  but  Hooker  proves  that  there  is  also  a  stimulation  of  the  accel- 
erators. Such  afferent  or  sensory  stimuli  may  arise  in  the  skin  and  muscles,  but  especially 
in  the  viscera  and  the  serous  and  mucous  membranes. 

Reflex  stimulation  of  this  sort  may  reach  the  medulla: 

1.  From  cortical  excitement  (emotion  or  neurasthenia). 

2.  From  intracranial  pressure  (meningitis,  brain  tumor,  etc.). 

3.  Reflexes  from  nasal  septum. 

4.  Reflexes  from  abdominal  organs  (uterus,  stomach,  intestines,  prostate,  enteroptosis). 

5.  Increased  irritability  from  toxic  agents  (tobacco,  tea,  coffee). 

6.  Adhesions  or  tumors  along  the  course  of  the  vagus. 

Mode  of  Production. — Francois-Franck  and  Koblanck  and  Roeder  have 
been  able  to  produce  such  an  arrhythmia  by  stimulating  the  mucous  mem- 
brane of  the  nasal  septum  at  a  point  just  opposite  the  middle  turbinate  bone, 
and  Stadler  and  Hirsch  have  done  so  by  stimulating  the  walls  of  the  stomach 
and  intestines.  There  is  normally  a  reflex  slowing  of  the  heart  during  swal- 
lowing, and  similar  periodic  slowing  of  the  rate  from  stimulations  of  the 
vagus  may  account  for  many  of  the  disturbances  of  rhythm  in  air-swallowers. 
Moreover,  Einthoven  has  shown,  by  recording  the  electrical  variations  in 
the  peripheral  stump  of  the  divided  vagus,  that,  with  each  inspiration,  afferent 
stimuli  are  passing  up  the  vagus,  and  these  may  evoke  reflex  responses  when 
the  entire  nervous  system  is  abnormally  sensitive. 

Occurrence. — Neurogenic  arrhythmias  are  particularly  common  in  chil- 
dren and  in  young  persons,  and  hence  are  designated  by  Mackenzie  as  the 
''youthful  type,''  but  this  is  only  because  the  cardiac,  vasomotor, 
and  respiratory  centres  are  in  more  labile  equilibrium  in  them  than  in  normal 
adults.  However,  whenever  the  nervous  system  becomes  more  irritable— 
from  the  occurrence  of  visceral  reflexes,  emotions,  or  toxic  influences  (bacterial 
toxins,  alcohol,  tobacco,  coffee,  etc.) — stimuli  (like  those  passing  up  the 
vagus)  which  are  normally  subminimal  become  effective.  Hence  allorrhyth- 
mias of  this  type  arise  in  nervous  individuals  and  in  the  so-called  functional 
cardiac  diseases  or  cardiac  neuroses  (Part  IV,  Chapter  II).  Einthoven, 
Flohil,  and  Battaerd  have  shown  that  stimuli  pass  up  the  vagi  at  each  respira- 
tory movement.  These  stimuli  are  normally  too  feeble  to  bring  about 
reflexes,  but  when  the  irritability  of  the  nervous  system  is  increased  stimuli 
which  are  ordinarily  subminimal  rise  above  the  threshold  and  give  rise  to 

1  The  term  sinus  arrhythmia  has  been  applied  to  these  forms  by  Mackenzie  because 
the  impulse  for  each  beat  arises  in  the  sinus  region  of  the  heart.  Some  extrasystoles  and 
some  cases  of  heart-block  are  also  neurogenic. 


102 


DISEASES   OF  THE   HEART  AND  AORTA. 


reflex  inhibitions  and  accelerations,  so  that  in  some  cases  there  is  a  series  of 
slow  beats  associated  with  inspiration  and  a  series  of  rapid  beats  in  expiration 
(Fig.  64),  while  in  others  the  slowing  occurs  during  expiration  and  the  rapid 
beats  are  during  inspiration.  This  latter  type  is  often  spoken  of  as  normal, 
but  in  perfectly  normal  individuals  the  rate  may  be  absolutely  regular. 

Reissner  has  shown  that  the  irregularity  is  sometimes  of  psychic  origin; 
or,  on  other  words,  that  the  stimulus  exciting  the  cardiac  nerves  may  descend 
from  the  cerebral  cortex  instead  of  ascending  by  the  usual  paths  of  afferent 
stimuli.  This  psychogenic  arrhythmia  is  not  extremely  uncommon.  Indeed, 
the  writer,  whose  pulse  has  been  regular  at  all  other  times,  experienced  such 
an  irregularity  upon  one  occasion  of  intense  anxiety  lasting  for  several  minutes. 
The  pulse  became  regular  as  soon  as  the  anxiety  passed  off;  and  has  remained 
so  for  five  years,  in  spite  of  a  severe  tonsillitis  and  tonsillectomy. 


RESPIRATION 

l_^— ^— f-4QSft        f>^— | — -^!SP^V_Ex(3^— ) — ^ls^ 

±r — %^ 

RADIAL 

*  i  a  i  t  i  l  i  - 1  i  I  1 '  1   li  t  i  1 1  LJ-JoLl 

iLM^U»> 

1                    >    Insp.      1    Exp.     1      Insp.  .     1     Exp.      1      Insp. 

Fig.  64a. — Respiratory  arrhythmia. 


Pulse 


Threshold 
stimulus 


/WMW\JWM\KJVJV 


NORMAL 


Respiratory 

Vagus 

Currents 

Fig.  64b. — Diagram  showing  the  relation  of  the  afferent  impulses  in  the  vagus  to  the  threshold  of  irrita- 
bility of  the  medulla.    +,  medullary  irritability  increased.   The  tracing  shows  the  respiratory  arrhythmia. 

As  Reyfisch  has  shown,  similar  neurogenic  allorrhythmias  occur  in 
meningitis  and  in  conditions  with  increased  intracranial 
tension  and,  as  Eyster  has  shown,  in  association  with  Cheyne-Stokes 
breathing.  Mackenzie  has  also  shown  that  there  are  many  other  cases  in 
which  neurogenic  irregularity  is  not  associated  with  the  phases  of  respiration. 
In  these  it  may  be  either  periodic  or  entirely  intermittent.  It  is  most  im- 
portant that  the  exact  mode  of  origin  of  such  stimuli  and  its  characteristics 
should  be  carefully  studied,  since  this  arrhythmia  must  be  dif- 
ferentiated from  those  of  myocardial  origin. 

Sinus  arrhythmias  also  arise  frequently  during  the  course  of  organic  or 
functional  cardiac  weakness,  and  often  result  from  administration  of  digitalis 
(Robinson  and  Draper,  Heart,  1912-1913,  iv,  97).  It  is  only  in  rare  cases 
in  which  they  may  impair  the  nutrition  of  the  heart  by  interfering  with  the 
iapidity  of  blood  flow  through  the  coronary  arteries  that  their  presence  can 
be  regarded  as  of  practical  importance. 


ALTERATIONS  IN  CARDIAC  RHYTHM.  103 

Laslett,  however,  has  reported  a  case  of  a  woman  aged  forty  in  whom  a 
sinus  arrhythmia  gave  rise  to  graver  symptoms.  The  periods  of  vagus  inhi- 
bition were  accompanied  by  prolonged  pauses  lasting  several  seconds  and 
giving  rise  to  syncope  and  a  typical  Adams-Stokes  syndrome,  although  no 
waves  suggesting  auricular  contractions  could  be  made  out  on  the  venous 
pulse.  After  atropine  the  pulse-rate  rose  to  100  and  remained  regular  for 
24  hours.  The  patient  was  also  subject  to  short  periods  of  inhibition,  during 
which  syncope  did  not  occur,  but  in  which  she  experienced  a  sensation  of 
precordial  pain  and  constriction  exactly  like  that  which  is  so  commonly  felt 
by  patients  with  the  milder  forms  of  sinus  arrhythmia  accompanying  the 
so-called  cardiac  neuroses  (as  in  the  case  of  A.  S.  quoted  on  page  698). 

In  these  cases,  though  the  relation  of  the  allorrhythmia  to  respiration 
may  be  timed  by  palpation  and  inspection,  a  careful  venous  tracing  should 
be  made  lest  an  extrasystolic  irregularity  be  diagnosed  when  it  does  not 
actually  exist. 

Characteristics  of  Sinus  Allorrhythmias. — The  striking  feature  of  these 
neurogenic  disturbances  of  rhythm  is  that  they  are  often  characterized  by 
instability  of  rhythm,  by  the  occurrence  of  rhythmic  changes 
in  rate  rather  than  by  the  interpolation  of  beats  which  differ  from  the  others 
in  character.  The  beats  usually  occur  in  short  groups,  a  few  slow  beats 
corresponding  to  a  rate  of  perhaps  50  per  minute,  alternating  with  series 
corresponding  to  a  rate  of  100  (Waller,  J.  Physiol.,  1913,  xlvi,  p.  lv).  The 
last  beat  of  the  rapid  series,  with  the  vagal  pause  following  it,  may  be 
taken  for  an  extrasystole;  but,  on  examining  the  few  beats  preceding,  it 
will  be  seen  that  this  beat  was  not  premature  and  not  due  to  an  abnormal 
stimulus.  This  is  further  demonstrated  by  the  electrocardiogram,  which 
is  in  every  respect  normal,  the  only  variations  in  form  being  shown  by  slight 
variations  in  the  height  of  the  P,  R,  and  T  waves.  Moreover,  the  beats  are 
usually  of  full  and  almost  equal  strength,  thereby  differing  from  the  feeble 
beats  of  extrasystoles.  It  is  an  irregularity  in  rhythm  rather  than  in  force, 
though  a  certain  degree  of  the  latter  may  be  present  through  the  action  of 
the  vagus  on  the  heart. 

The  rhythm  usually  becomes  regular  within  half  an  hour  after  the  hypo- 
dermic administration  of  atropine,  .0005  to  .001  Gm.  (ttu  to  -g^  gr.).  This 
rule  is  not  invariable. 

When  long  pauses  alternate  with  short  series  of  rapid  beats,  the  force 
of  the  first  large  beat  may  be  slightly  below  that  of  the  smaller  beats,  as 
shown  by  tracings  with  the  Erlanger  apparatus  at  or  near  the  maximal  pres- 
sure. With  extrasystoles  the  systolic  pressure  of  the  smaller  beats  is  usually 
less  than  that  of  the  regular  (large)  beat.  In  both  cases,  however,  this  de- 
pends upon  too  many  factors  (time  at  which  the  extrasystole  occurs,  amount 
of  systolic  output,  amount  of  peripheral  resistance,  factors  causing  the  extra- 
systole, etc.)  to  be  regarded  as  absolute  criterion  for  diagnosis. 

II.  Respiratory  (Pulsus  paradoxus  and  Riegel's  Pulse). — As  will  be  seen 
in  the  chapters  on  adherent  pericardium  (page  610)  and  enteroptosis,  traction 
upon  the  aorta  during  respiration  may  prevent  the  heart  from  emptying  itself 
and  thus  cause  the  dropping  of  a  beat  in  the  arteries.  Or,  on  the  other  hand, 
traction  upon  the  great  veins  may  produce  the  same  effect  by  preventing  the 
heart  from  filling.    When  there  are  adhesions  in  the  posterior  mediastinum 


104 


DISEASES  OF  THE  HEART  AND  AORTA. 


or  when  the  diaphragm  is  low,  this  dropping  occurs  during  inspiration  (pulsus 
paradoxus,  Kussmaul),  whereas  when  there  are  adhesions  between  the  heart 
and  the  anterior  chest  wall  it  may  occur  in  expiration  (Riegel). 

ALLORRHYTHMIAS   HAVING    THEIR   ORIGIN   WITHIN   THE   HEART. 

III.  Allorrhythmias  due  to  Failure  to  Conduct  Impulses  Generated 
Normally — Heart=block.1 — Of  this  there  are  several  types.  (1)  Auriculo- 
ventricular   Heart-block. — The  more  usual,  or  at  least  better  known, 


A  SEC. 


JUG. 


APEX 


BRACH. 


Fig.  65. — Venous  tracings  in  heart-block.    Partial  heart-block    3  : 1  rhythm)  during  pressure  on  the  vagus 

in  a  case  of  Adams-Stokes  disease. 

type  of  blocking  the  impulses  is  at  the  auriculoventricular  junction.  In 
In  this  type  no  change  occurs  in  the  origination  of  the  cardiac  impulse  or  in 
the  contraction  of  the  auricles  (atria),  but  the  conductivity  of  the  impulse 
to  the  ventricle  by  the  bundle  of  His  is  impaired.    Such  impairment  may  be 


OAi 


Tltii 


Fig.  66. — Venous  tracings  in  heart-block.     Complete  heart-block  in  a  case  of  Adams-Stokes  disease. 

(a)  functional,  from  overstimulation  of  the  vagus,  of  which  frequent 
examples  are  seen  in  every  laboratory  experiment.  Clinically  this  may  be 
seen  also  in  the  cases  of  digitalis  poisoning  and  postfebrile  bradycardia, 
especially  after  pneumonia  and  influenza,  occasionally  also  in  cases  in  which 
there  is  a  tumor  pressing  upon  the  vagus.  (6)  Organic,  from  interrup- 
tion of  the  bundle  of  His.    In  this  case  the  block  may  be  increased  by  giving 

1 A  full  discussion  may  be  found  in  Part  III,  Chapter  XI. 


ALTERATIONS  IN  CARDIAC  RHYTHM.  105 

atropine  or  anything  else  that  quickens  the  heart,  or  it  may  not  be  affected, 
(c)  There  may  be  a  combination  of  the  two  effects  (v. 
Tabora,  Gibson,  Thayer),  the  conductivity  of  the  injured  Purkinje  fibres  of 
the  bundle  being  still  further  diminished  by  the  action  of  the  vagus  upon  them, 
and  this  effect  outweighing  the  favorable  action  in  slowing  the  auricular 
rhythm. 

The  block  may  be  partial  or  complete,  depending  upon 
whether  the  ventricles  still  follow  the  lead  of  the  auricles  or  initiate  their  own 
rhythm.  Thus,  in  the  partial  block  the  ventricles  may  respond  to  only  every 
second,  third,  or  fourth,  or  even  only  every  sixteenth  contraction,  or  may 
sometimes  respond  to  every  second,  sometimes  to  every  fourth  beat,  etc. 
On  the  other  hand,  they  may  fail  to  contract  at  all  over  a  considerable  period 
(stoppage),  during  which  syncope  (Adams-Stokes  syndrome),  epileptiform 
seizures,  or  death  may  set  in  (Erlanger),  or,  after  a  stoppage  of  greater  or 
less  duration,  they  may  begin  to  beat  at  a  rhythm  of  their  own,  bearing  no 
relation  at  all  to  the  rhythm  of  the  auricles  (complete  block).  This  consti- 
tutes the  permanent  bradycardia  of  Adams-Stokes  disease. 

(2)  Sino-auricular  Block. — Sino-auricular  block  may  also  occur,  the 
cardiac  impulse  being  generated  as  usual  at  the  mouths  of  the  great  veins 
and  coronary  sinus  in  the  region  homologous  with  the  sinus  venosus  of  the 
frog,  but  may  fail  to  be  communicated  to  the  auricles. 

Keith  and  Schonberg  have  shown  that  this  could  scarcely  be  the  result  of  a  localized 
lesion,  and  would  therefore  depend  upon  the  difference  in  the  properties  and  irritability 
of  auricular  and  venous  musculature  rather  than  organic  block.     The  presence  of  such 


I        i 

APEX 

5*^^^K*flH  Hl^S 

5Bm™  BBKIBI  MBl^^B 

CA- 
ROTID 

Fig.  67. — Occasional  absence  of  apex  impulse  during  inspiration  simulating  interventricular  heart-block. 

block  is  assumed  by  August  Hoffmann  in  paroxysmal  tachycardia,  in  which  there  is  a 
sudden  doubling  or  even  quadrupling  of  the  pulse-rate  during  the  attacks,  and  by  Hewlett 
in  digitalis  poisoning.  Experimentally  they  have  been  produced  by  Erlanger  and  Black- 
man  on  the  excised  mammalian  heart,  but  both  Hirschfelder  and  Eyster  and  the  former 
observers  failed  to  do  so  in  the  heart  in  situ.  Cohn  and  Kessel  (Heart,  1912,  iii)  have 
recently  produced  such  a  block  by  excising  the  sino-auricular  node  in  the  perfused  dog's 
heart;  and  Eyster  and  Meek  (Heart,  1912-1913,  iv,  59)  have  produced  in  it  morphine  poison- 
ing. Gibson  assumes  the  existence  of  a  similar  block  in  a  case  of  Adams-Stokes  disease, 
which  he  cites,  along  with  the  block  at  the  auriculo ventricular  junction. 

(3)  Interventricular  Block  (Hemisystole). — V.  Leyden  in  1868  reported 
a  case  of  bigeminal  pulse  in  which  he  assumed  that  one  ventricle  was  con- 
tracting without  the  other. 

This  case  and  other  cases  reported  by  the  older  writers,  and  the  cases  reported  more 
recently  by  Kraus  and  Nicolai,  Hewlett  and  Schmoll,  probably  also  admit  of  a  different 
explanation.  True  hemisystole,  the  contraction  of  one  ventricle  without  the  other,  has 
never  been  produced  experimentally,  even  by  Biggs,  Barker  and  Hirschfelder,  Trendelen- 


106  DISEASES  OF  THE  HEART  AND  AORTA. 

burg  and  Cohn,  Eppinger  and  Rothberger,  who  have  cut  the  individual  branches  of  the 
His  bundle.  In  some  of  these  instances,  just  as  Knoll,  Fredericq,  Fauconnier,  and  Stassen 
had  found  for  the  intact  heart  under  vagus  stimulation,  there  was  a  very  slight  asynchro- 
nism  (x^o  to  Tf7  sec.)  between  the  contraction  of  the  two  ventricles.  Eppinger  and  Roth- 
berger have  found,  however,  that  when  one  branch  of  the  His  bundle  is  cut,  a  character- 
istic change  occurs  in  the  form  of  the  electrocardiogram,  the  ventricular  part  of  which 
then  resembles  the  form  due  to  an  extrasystole  arising  in  the  ventricle  whose  branch  is 
intact.  The  R  wave  is  sometimes  broader  than  is  found  with  ordinary  extrasystoles,  and 
the  P  wave  is  of  course  present  in  the  usual  place.  Eppinger  and  Stoerck  have  demon- 
strated the  value  of  this  finding  for  clinical  medicine  by  establishing  the  diagnosis  of  a 
patch  of  myocarditis  affecting  one  branch  of  the  bundle  but  not  the  other  in  two  cases  in 
which  their  correctness  was  proved  by  autopsy.  Since  their  studies  similar  cases  have 
been  encountered  and  correctly  diagnosed  during  life.  An  example  of  this  is  shown  in 
Plate  XI  from  a  case  under  the  care  of  Drs.  S.  Marx  White  and  R.  E.  Morris  in  the  Uni- 
versity Hospital,  Minneapolis.  Such  tracings  must,  however,  be  carefully  differentiated 
from  simple  ventricular  hypertrophy.  It  must  be  admitted,  however,  that  the  electro- 
cardiogram in  these  cases  does  not  differ  very  much  from  that  found  in  simple  hypertrophy, 
and  confusion  with  the  latter  is  possible.  The  number  of  cases  reported  thus  far  is  too 
limited  to  judge  of  the  ultimate  estimate  of  this  criterion  for  diagnosis. 

IV.  Diminution  in  Contractile  Power — Pulsus  alternans. — When  the 
contractile  power  of  the  heart  diminishes,  or,  more  frequently,  when  the 
rate  is  increased  to  the  point  that  the  heart  has  some  difficulty  in  carrying 
out  effectual  contractions,  it  is  found  that  the  alternate  contractions  are  of 
different  size,  some  larger,  some  smaller,  giving  rise  to  the  condition  known 


>Mfy\J\j\JW 

AN- 

f3- 

■ach: 

Fig.  68. — Alternating  pulse  in  a  case  of  paroxysmal  tachycardia. 

as  pulsus  alternans  or  alternating  pulse.1  Pulsus  alternans  can  be  diagnos- 
ticated clinically  by  feeling  or  listening  over  the  artery  below  a  sphyg- 
momanometer cuff.  If  the  rate  is  regular  and  the  number  of  pulse  beats 
passing  below  the  cuff  falls  to  half  when  the  pressure  is  raised  to  a  point 
less  than  the  systolic,  a  pulsus  alternans  is  present. 

Experimentally  this  can  be  readily  shown  by  throwing  induction  shocks  into  the 
heart  at  a  rate  which  it  can  barely  follow.  A  pulsus  alternans  invariably  results  (Hirsch- 
felder,  Hering).  After  a  few  seconds  or  minutes  the  heart  has  gained  its  full  contractility 
and  the  alternating  character  disappears,  only  to  reappear  when  it  begins  to  weaken. 
The  same  phenomenon  is  also  seen  in  attacks  of  paroxysmal  tachycardia  (Fig.  68).  Pul- 
sus alternans  is  also  present  in  some  cases  of  angina  pectoris  (Mackenzie).  It  then  indicates 
that  the  heart  is  in  a  weakened  condition. 

V.  Dropping  of  Beat  Owing  to  Too  Low  Contractility. — If  the  auricle  be 
stimulated  directly  at  a  rate  still  more  rapid,  it  can  no  longer  follow  every 
single  stimulus,  but,  occasionally  one  beat  is  dropped  out,  just  as  is  the  case 
in  a  partial  heart-block,  although  the  stimulus  is  being  applied  directly  to 
the  auricle,  which  intermits  a  little. more  rapidly,  and  it  follows  only  alter- 
nate stimuli.  If  the  irritability  of  the  auricle  be  now  suddenly  increased, 
as  by  pouring  warm  salt  solution  over  it,  it  will  suddenly  respond  with  a 
contraction  to  each  instead  of  to  alternate  stimuli,  or  it  may  respond  occa- 

1  Extrasystoles,  giving  typical  electrocardiograms,  may  occur  midway  between  regu- 
lar beats  and  give  rise  to  an  alternating  pulse. 


ALTERATIONS  IN  CARDIAC  RHYTHM. 


107 


sionally  to  all  and  occasionally  to  only  alternate  stimuli,  giving  an  allorrhyth- 
mia  1:1  +  2:1.  Thus  we  may  have  allorrhythmias  simulating  partial  heart- 
blocks  on  the  one  hand,  and  extrasystoles  on  the  other,  due  merely  to  general 
decrease  in  the  irritability  of  the  entire  musculature  without  any  special 
disturbance  in  conductivity;  and  just  such  inotrophic  and  bathmotrophic 
variations  may  be  responsible  for  many  of  the  so-called  veno-auricular 
heart-blocks,  such  as  have  been  described  by  Hewlett  and  Wenckebach. 


IRREGULARITIES  DUE  TO  THE  GENESIS  OF  ABNORMAL  IMPULSES. 

EXTRASYSTOLES. 

In  the  majority  of  all  cases  of  cardiac  arrhythmia  and  almost  all  of  those 
associated  with  severe  functional  or  organic  heart  disease,  the  disturbance  of 
rhythm  is  due  to  the  presence  of  beats  which  arise  at  an  abnormal  site  within 
the  heart. 

The  simplest  form  of  abnormal  impulse  is  seen  in  the  single  abnormal 
beat  (extrasystoles,  Engelmann;  premature  systole,  Marey,  Mackenzie) 
which,  as  Marey  has  shown,  sets  in 
almost  immediately  when  a  single  elec- 
trical or  mechanical  stimulus  is  applied 
to  the  heart  at  any  instant  of  diastole. 
During  the  period  of  systole  and  dur- 
ing the  instant  before  it,  an  external 
stimulus  does  not  alter  the  cardiac 
rhythm,  and  the  heart  is  said  to  be  in 
its  refractory  period. 

Extrasystoles  may  arise  in  any 
part  of  the  heart  either  as  the  result  of 
definite  external  stimuli  or  as  the  result 
of  some  change,  organic  or  functional, 
in  the  part  of  the  heart  wall  where 
it  arises.  Such  a  condition  is  often 
brought  about  by  overstretching  of 
the  heart  wall  as  a  result  of  inability 
of  the  chamber  to  empty  itself,  a  con- 
dition which  is  readily  brought  about 
by  clamping  the  aorta  or  by  increasing 
the  peripheral  resistance,  and  which  is 
very  commonly  met  with  in  the  ven- 
tricles when  the  heart  is  failing  or  the 
blood-pressure  too  high,  in  the  left  au- 
ricle in  the  severer  grades  of  mitral  stenosis  or  regurgitation  (mitralized  pulse). 

Extrasystoles  may  also  arise  in  perfectly  strong  hearts  with  normal 
blood-pressure  when  the  irritability  of  the  latter  is  increased  by  some  toxic 
action,  such  as  nicotin,  digitalis,  or  the  more  or  less  obscure  nitrogenous  sub- 
stances which  are  absorbed  from  the  intestines  during  intestinal  putrefac- 
tion. It  is  possible  that  they  may  also  be  produced  reflexly  from  irritation 
of  the  gastro-intesfcinal  tract;  but,  though  extrasystoles  are  relatively  common 
in  otherwise  healthy  persons  suffering  from  flatulence  and  tympanites,  no 


Fig.  69. — Response  of  frog's  ventricle  to 
abnormal  stimuli.  (After  Marey.)  Electric 
shock  thrown  into  it  at  the  instant  marked 
by  the  nick  in  the  base  line  and  by  the 
dotted  line. 


108  DISEASES  OF  THE  HEART  AND  AORTA. 

one  has  as  yet  reported  their  production  experimentally  from  stimulation  of 
the  gastro-intestinal  tract,  and  the  mechanism  by  which  they  arise  in  these 
cases  is  still  obscure. 

Lewis  has  produced  ventricular  extrasystoles  by  ligating  one  of  the 
descending  branches  of  the  coronary  arteries,  and  a  similar  association  with 
coronary  sclerosis  is  sometimes  noted  clinically,  but  whether  the  extrasystole 
then  arises  as  the  result  of  weakening  of  the  muscle  and  overstretching  of  the 
wall  or  from  an  increased  irritability  of  the  fibres  undergoing  localized  asphyxia 
cannot  be  stated  definitely.  That  the  latter  is  not  the  case  would  appear 
probable  from  the  fact  that  extrasystoles  are  not  common  in  the  correspond- 
ing stages  of  general  asphyxia;  and,  moreover,  other  localized  injuries,  such 
as  injury  of  the  heart  muscle  by  injection  of  alcohol,  iodine,  silver  nitrate, 
etc.,  are  not  followed  by  extrasystoles  (Barker  and  Hirschfelder). 

Extrasystoles  of  Neurogenic  Origin. — Quite  recently  Rothberger  and 
Winterberg  have  been  able  to  induce  extrasystoles  by  stimulation  of  the  left 
accelerator  nerves,  but  only  in  animals  whose  cardiac  irritability  had  already 
been  greatly  enhanced  by  intravenous  injections  of  barium  or  calcium  chloride. 
The  latter  required  doses  ten  times  greater  than  the  former.  Such  extra- 
systoles probably  are  closely  analogous  to  those  met  with  clinically  in  persons 
suffering  from  indigestion. 

Physiologically  the  condition  of  the  heart  in  which  extrasystoles  occur 
is  one  of  increased  irritability,  of  which  there  are  several  stages.  Hirschfelder 
has  shown  that  if  the  dog's  heart  muscle  be  stimulated  with  a  very  weak 
alternating  current,  no  change  in  rhythm  occurs;  if  the  current  be  made 
stronger,  occasional  extrasystoles  set  in;  if  it  be  still  stronger,  there  is  a 
sudden  acceleration  of  the  rate,  which  rises  at  one  bound  to  almost  double 
the  previous  rate,  and  at  some  time  after  cessation  of  the  stimulus  subsides 
as  suddenly  to  the  original  rate;  while  with  maximal  stimuli  the  contractions 
suddenly  change  from  the  ordinary  coordinate  systoles  to  a  series  of  inco- 
ordinate worm-like  contractions  (fibrillary  contraction  or  fibrillation),  in 
which  each  fibre  or  group  of  fibres  contracts  by  itself  and  the  surface  of  the 
chamber  appears  like  a  mass  of  writhing  earthworms. 

As  regards  irritability,  therefore,  the  extrasystoles  may  be  regarded  as 
the  first  stage  in  the  scale. 

This  scale  of  intensity  is  seen  more  or  less  clearly  in  the  action  of  certain 
heart  poisons  such  as  digitalis  and  aconite;  and,  moreover,  finds  its  analogon 
in  the  realm  of  pure  physical  chemistry. 

Bredig  and  Wilke  have  found  that  a  similar  irregularity  occurs  in  rhythmic 
chemical  reactions,  such  as  the  catalysis  of  hydrogen  peroxide  by  mercury, 
when  the  intensity  of  the  current  generating  them  is  increased.  The  record 
from  a  slightly  increased  current  at  first  resembles  that  due  to  single  extra- 
systoles; a  greater  increase  shows  marked  acceleration  and  irregularity. 

Extrasystoles  may  arise  spontaneously  in  any  part  of  the  heart  wall, 
in  the  right  or  left  auricle,  the  right  or  left  ventricle,  or  in  the  auriculo ventric- 
ular bundle.  Indeed,  as  Lewis  and  Wybauw  have  proved,  they  may  arise 
in  various  parts  of  the  same  chamber,  and  the  site  of  origin  may  in  many 
cases  be  identified  by  means  of  the  electrocardiogram. 

As  a  rule,  the  extrasystole  occurs  very  early  in  diastole,  and  the  heart  is 
still  in  the  refractory  period  when  the  next  impulse  should  arise,  so  that  the 


ALTERATIONS  IN  CARDIAC  RHYTHM.  109 

latter  is  replaced  by  a  long  pause  (compensatory  pause).  Occasionally, 
however,  especially  when  the  cardiac  irritability  is  increased,  the  next  impulse 
may  set  in  at  the  regular  time,  and  the  compensatory  pause  may  be  omitted. 
Under  these  circumstances  the  extr asystole  is  said  to  be  "interpolated." 

Ventricular  Extrasystoles. — Ventricular  extrasystoles  are  always  accom- 
panied by  full  bigemini  and  usually  by  a  single  large  flapping  venous  pulsa- 
tion of  very  characteristic  appearance  which  sweeps  upward  over  the  sterno- 
cleidomastoid, while  the  normal  beats  and  the  auricular  extrasystoles  are 
usually  accompanied  by  smaller  double  undulations  which  do  not  reach 
higher  than  the  lower  border  of  this  muscle  and  are  often  barely  visible. 

The  jugular  tracing  of  a  ventricular  extrasystole  shows  a  relatively  large 
wave,  sometimes  single  and  sloping,  often  in  plateau  form,  and  occasionally 
with  a  crest  which  is  surmounted  by  a  second  smaller  undulation,  produced 
by  the  contraction  of  the  auricle  which  takes  place  at  its  regular  time,  as 
though  the  ventricle  were  beating  regularly.  It  is  impossible  to  differentiate 
by  means  of  the  venous  tracing  between  extrasystoles  arising  in  the  right 


RAD.  p  £ 

Or.C  7-11-7^  93p  AM 

Fig.  70. — Tracing  from  the  right  jugular  vein  and  radial  artery  of  a  patient  showing  ventricular 
extrasystoles  (E,  E).  The  extrasystoles  are  shown  as  very  large  waves  not  preceded  by  an  A  wave.  (Kind- 
ness of  Dr.  R.  E.  Morris.) 

ventricle  and  those  having  their  origin  in  the  left.  In  many  cases  this  may 
be  guessed  at  with  more  or  less  accuracy  by  a  knowledge  of  the  general 
conditions  of  stasis  and  lesions,  extrasystoles  accompanying  aortic  disease, 
the  high  blood-pressure  of  nephritis,  etc.,  being  usually  left  sided,  those 
accompanying  mitral  stenosis  and  congenital  heart  disease  arising  usually 
in  the  right. 

The  definite  differentiation  between  right  ventricular  and  left  ventricular 
extrasystoles  can  always  be  made  by  means  of  the  electrocardiograph,  which 
gives  typical  tracings  (Kraus  and  Nikolai,  Kahn),  especially  when  taken  in 
the  second  lead  (D2,  right  hand  to  left  foot).  The  curves  thus  obtained  are 
simple  diphasic  variations.  In  right  ventricular  extrasystoles  there  is  a  very 
large  upstroke,  higher  than  that  corresponding  to  the  regular  beats  and  of 
longer  duration,  followed  by  a  slow  fall  to  below  the  base  line;  while  in  the 
case  of  the  left-sided  extrasystoles  the  curve  is  the  mirror  image  of  the  right, 
and  starts  off  with  a  very  deep  depression  below  the  line  which  is  followed  by 
a  slower  rise  above  it  (Plate  VII).  Occasionally  extrasystoles  arising  some- 
times in  one  ventricle  and  sometimes  in  the  other  may  be  met  with  in  the 
same  patient  and  even  in  different  parts  of  the  same  tracing  (Plate  VIII). 

If  the  extra  stimulus  be  applied  to  the  ventricle,  the  latter  responds 
with  a  premature  contraction,  then  usually  but  not  always  misses  the  next 
impulse  from  the  auricle  and  pauses  for  a  while,  until  the  second  impulse 


110 


DISEASES  OF  THE  HEART  AND  AORTA. 
PLATE  VII. 


Kindness  of  Interstate  Medical  Journal. 

Tracing  showing  auricular  extrasystoles  arising  from  an  abnormal  site  (heterogenetic),  with  diagram  showing 
the  course  of  the  extrasystolic  impulse.    The  P  waves  of  the  extrasystoles  are  inverted. 


R 


LXS^S 


■  --,?■  -timwrmmm 


V,y,'Yffiw.""ii  it immmmmmam 


A 


A-V 


V 


Tracing  taken  in  Dl,  showing  an  extrasystole  arising  in  the  right  ventricle,  with  diagram.    The  extra- 
systole  is  followed  by  a  contraction  of  the  auricles  (P  wave)  occurring  at  the  usual  time. 


ALTERATIONS  IN  CARDIAC  RHYTHM. 

PLATE  VIII. 


Ill 


A 


A-V         \ 


5 


V 


Kindness  of  Interstate  Medical  Journal. 

Tracing  taken  in  D2t  showing  an  extrasystole  arising  in  the  left  ventricle,  with  diagram. 


f*V*"*^ 


!*«*%< 


R.EXST5 


LDCSYS 


Tracing  taken  in  D2,  showing  one  extrasystole  arising  in  the  right  ventricle  and  one  arising  in  the 

left  ventricle. 


112  DISEASES  OF  THE  HEART  AND  AORTA. 

from  the  auricle  reaches  it.  We  have,  therefore,  a  normal  contraction,  a 
premature  contraction,  and  the  subsequent  pause  (which  together  may  be 
termed  a  bigeminus),  lasting  as  long  as  two  regular  contractions.  The  bi- 
geminus  may  be  spoken  of  as  a  ''full  bigeminus"  when  it  lasts 
through  two  full  cardiac  cycles,  and  a  "shortened 
bigeminus"  when  the  duration  of  regular  systole  + 
ex  t  r  as  y  s  t  o  1  e  +  s  u  bs  e  q  u  en  t  pause  is  less  than  two 
cardiac    cycles. 

Auricular  Extrasystoles. — When,  however,  the  extra  stimulus  is  applied 
to  the  great  veins  or  the  auricle,  the  bigeminus  lasts  less  than  two  cardiac 
cycles  if  the  stimulus  follows  closely  upon  the  regular  contraction,  and  exactly 
equal  to  two  cycles  if  it  is  applied  late  (Hirschf elder  and  Eyster).  If  the 
stimulus  is  applied  early,  the  auriculo ventricular  (atrioventricular)  conduc- 
tion time  (a-c)  interval  is  slowed.    Later  in  the  cycle  it  is  unchanged. 


JUG. 


BRACH. 


Fig.  71. — Tracings  from  the  jugular  vein  and  brachial  artery  of  a  patient  with  trigeminal  pulse  due 
to  the  regular  occurrence  of  two  auricular  extrasystoles  (E,  E)  after  each  regular  systole.  The  a  wave 
and  general  form  of  the  venous  pulse  are  the  same  for  the  regular  and  the  auric u  ar  extrasystoles. 

The  two  forms  of  extrasystoles  occur  clinically  and  may  be  differentiated 
by  the  analysis  of  the  venous  pulse;  the  extrasystoles  of  auricular  (atrial) 
origin  often  give  rise  to  shortened  bigemini,  while  ventricu- 
lar extrasystoles  always  cause  full  bigemini.  In  the 
tracings  of  auricular  extrasystoles  one  can  see  the  auricular  wave  before  the 
ventricular  even  in  the  extrasystole;  the  ventricular  showing  a  single  large 
wave  due  to  ventricular  systole,  sometimes  with  the  notch  due  to  the  con- 
traction of  the  auricle  from  reversed  conduction  of  the  impulse.  Occasionally 
ventricular  extrasystoles  can  be  distinguished  on 
inspection  by  the  large  flapping  ''single''  pulsa- 
tion in  the  jugular  vein  which  accompanies  them,  in  contrast 
to  the  double  venous  pulse  of  the  normal  beats  and  the  auricular  extrasystoles 
(Hirschf  elder). 

The  electrocardiograms  of  auricular  systoles  do  not  show  the  large  and 
striking  variations  that  accompany  ventricular  extrasystoles.  Indeed,  when 
the  extra  stimulus  arises  in  the  vicinity  of  the  superior  vena  cava,  the  waves 
accompanying  the  extra  stimulus  differ  from  the  normal  only  in  being  a  little 
lower  and  in  the  fact  that  they  occur  much  earlier  than  the  normal.  When, 
however,  the  extrasystole  arises  at  an  abnormal  site  (ectopic  impulses),  such 
as  the  region  of  the  inferior  vena  cava  or  the  left  auricle,  the  P  wave  is  in- 
verted and  somewhat  modified  in  form. 

Auricular  extrasystoles  occur  most  commonly  in  the  irregularities  accom- 
panying mitral  disease  and  in  patients  suffering  from  paroxysmal  tachycardia 


ALTERATIONS  IN  CARDIAC  RHYTHM.  113 

and  paroxysmal  irregularity  during  the  intervals  between  attacks.  In  the 
latter  case  especially  they  are  liable  to  arise  at  an  abnormal  site.  It  seems 
probable  that  in  the  latter  groups  the  extrasystoles  represent  a  lower  degree 
of  the  hyperexcitability  which  finds  its  expression  in  the  paroxysms. 

A  further  advance  in  the  clinical  study  of  extrasystoles  is  due  to  the  clinical  use  of 
the  electrocardiogram  by  Einthoven  and  his  pupils,  and  more  recently  by  Kraus  and  Nik- 
olai, Hering,  and  Lewis. 

Einthoven  called  attention  to  the  presence  of  certain  very  peculiarly  formed  electro- 
cardiograms obtained  from  irregularly  acting  hearts.  Kraus  and  Nikolai  were  able  to 
reproduce  these  abnormal  waves  by  producing  extrasystoles  in  dogs;  and  found  that  extra- 
systoles arising  in  the  right  and  left  ventricles  respectively  produced  curves  which  were 
the  inverse  of  one  another  (Plate  VI). 

Kahn  in  Hering's  laboratory  has  been  able  to  confirm  these  findings  in  great  part. 
However,  he  calls  attention  to  the  fact  that  they  do  not  hold  absolutely,  and  shows  that 
stimuli  applied  to  neighboring  points  in  right  and  left  ventricles,  near  the  apex,  may  elicit 
electrocardiograms  which  differ  only  slightly  from  one  another. 

Stimuli  which  Cause  Extrasystoles. — The  question  as  to  the  nature  of 
the  stimulus  which  gives  rise  to  extrasystoles  in  man  is  of  the  greatest  practical 
importance,  for  many  writers  (especially  Fr.  Muller)  are  of  the  belief  that 
they  never  occur  unless  the  heart  muscle  is  diseased.  On  the  other  hand, 
Mackenzie,  whose  observations  have  been  extended  over  a  period  of  fifteen 
years,  regards  them  as  of  no  special  significance  either  in  prognosis  or  in 
influencing  the  patient's  manner  of  life.  He  mentions  having  advised  one  of 
his  patients  to  continue  playing  football  in  spite  of  his  extrasystoles,  and 
adds  that  the  extrasystoles  disappeared! 

Experimentally  it  has  been  shown  by  Knoll,  Marey,  Hering,  and  others  that  ventric- 
ular extrasystoles  may  be  produced  whenever  either  the  left  ventricle  or  the  right  is  pre- 
vented from  emptying  itself  {i.e.,  by  clamping  the  aorta  or  the  pulmonary  artery).  In 
man  they  are  also  most  common  in  conditions  in  which  there  is  a  high  blood-pressure  and 
the  heart  is  just  beginning  to  fail  (chronic  nephritis,  myocarditis,  aortic  insufficiency), 
and  probably  fails  to  discharge  a  sufficient  amount  of  its  contents.  This  probably  acts  as 
a  stimulus  for  a  second  extrasystole,  as  is  frequently  seen  (pulsus  trigeminus).  Ventricular 
extrasystoles  are  most  common  in  hearts  whose  rate  is  slow  and  hence  which  discharge 
a  large  amount  of  blood.  They  are  particularly  common  at  the  end  of  the  first  third  of 
diastole  when  the  filling  of  the  ventricle  is  nearing  completion.  The  ventricular  fibres  are 
stretched  more  or  less  by  the  influx,  and  in  conditions  of  increased  irritability  the  stretch- 
ing of  the  fibres  may  act  as  a  stimulus  and  give  rise  to  the  extrasystoles. 

Similar  conditions  are  observed  with  reference  to  the  auricle.  Dr.  Cameron,  in  the 
writer's  laboratory,  observed  an  instance  of  permanent  bigeminal  pulse  in  a  dog  due  to 
the  presence  of  a  bubble  of  air  in  the  right  auricle.  The  air  had  entered 
from  a  hypodermic  syringe  during  an  intravenous  injection.  When  the  bubble  was 
massaged  out  of  the  auricle  the  bigeminal  pulse  disappeared.  It  seems  not  improba- 
ble that  mural  thrombi  may  play  a  similar  role,  though  it  is  certain  that  this  is  not 
always  the  case. 

Auricular  extrasystoles  may  also  be  produced  experimentally  by  causing  a  steno- 
sis at  the  auriculoventricular  orifices  (Hirschf elder).  Clinically  they  occur  quite  com- 
monly in  mitral  disease  and  most  frequently  begin  at  the  time  of  the  v  wave,  the  very  in- 
stant in  the  cycle  at  which  the  auricle  is  most  distended  (Fig.  71).  Nevertheless,  it  must 
be  confessed  that  much  remains  to  be  learned  regarding  the  nature  of  the  stimulus  or 
stimuli,  and  the  actual  functional  significance  of  extrasystoles. 

Palpitation  with  Extrasystoles. — Extrasystoles  are  very  frequently 
associated  clinically  with  cardiac  hyperesthesia  in  the  form  of  palpitation, 
so  that  many  clinicians  erroneously  regard  all  irregularities  with  palpitation 


114  DISEASES  OF  THE  HEART  AND  AORTA. 

as  extrasystolic.  However,  it  is  possible  that  this  hypersensibility  about 
the  heart  may  have  some  causal  relation,  since  Hornung  has  shown  that 
extrasystoles  in  the  dog  are  most  readily  produced  by  stimulating  in  the 
vicinity  of  the  cardiac  nerves — auriculo(atrio) ventricular  and  interventricular 
grooves — and  that  they  cannot  be  produced  after  cocainizing  the  epicardium. 
As  stated  above,  Rothberger  and  Winterberg  have  produced  them  by 
stimulation  of  the  cervical  sympathetic  branches,  and  stimuli  along  the 
sympathetics  may  also  be  responsible  for  their  occurrence  in  cases  of 
gastro-intestinal  disease.  It  is  certain  that  they  are  often  brought  on 
by  constipation  and  flatulence  in  certain  persons,  but  whether  there  is  a 
myocardial  lesion  already  present  in  these  cases  is  a  still  open  question. 

Ineffectual  Contractions. — When  the  extrasystole  occurs  early  in  diastole, 
the  heart  may  not  have  recovered  from  the  effect  of  the  last  systole  sufficiently 
to  generate  a'1  forcible  contraction.  The  aortic  valves  are  not  opened.  The 
aortic  second  of  the  extrasystole  disappears  and  the  sounds  change  from 

1—2—3—4 1—2,  etc.,  to  1—2—3 1—2,  etc.     By  beating 

time  to  the  regular  beats  it  is  sometimes  possible  to  note  that  the  total  rhythm 
is  unchanged  by  occasional  ventricular  extrasystoles.  Such  extrasystoles  cor- 
respond to  impulses  on  the  apex  and  jugular  tracings  but  not  on  the  carotid. 

The  variations  in  the  force  of  the  extrasystoles  or  in  the  beats  of  the 
absolutely  irregular  pulse  are  great.  Occasionally,  especially  when  the  extra- 
systoles occur  early  in  the  cardiac  cycle  and  there  is  a  high  peripheral  resist- 
ance, the  intracardiac  pressure  may  not  reach  the  aortic  pressure  and  the 
aortic  valves  are  not  opened.  The  systole  has  been  ineffectual  (Frustrane 
Contractionen,  Hochaus  and  Quincke).  The  compensatory  pause  after  these 
may  be  so  long  and  the  circulation  may  be  so  poor  that  actual  syncope  simu- 
lating the  Adams-Stokes  syndrome  (W.  B.  James)  may  take  place  in  the 
interval  between  the  regular  beats.  On  the  other  hand,  a  great  deal  of  cardiac 
energy  has  been  expended  without  opening  the  cardiac  valves  and  without 
propelling  any  blood.    This  increases  the  cardiac  fatigue. 

Bigeminal  and  Trigeminal  Pulses  due  to  Extrasystoles. — Very  common 
forms  of  extrasystolic  irregularity  are  those  in  which  the  extrasystoles  recur 
after  each  regular  beat;  thus  we  may  find  every  beat  followed  by  a  single 
extrasystole  and  compensatory  pause,  so  that  the  pulse  beats  occur  in  pairs 
separated  by  pauses  (pulsus  bigeminus),  or  there  may  be  two  extrasystoles 
following  regularly  after  each  regular  systole  (pulsus  trigeminus),  as  in  Fig. 
71.  These  may  be  of  either  the  auricular  or  the  ventricular  type,  dependent 
upon  the  site  of  the  origin  of  the  irregularity  or  of  the  so-called  auriculo(atrio) 
ventricular  type  referred  to  below.  As  stated  above,  it  is  sometimes  difficult 
to  differentiate  the  auricular  extrasystolic  groups  from  the  youthful  type  of 
arrhythmia,  but  this  may  usually  be.  accomplished  by  the  use  of  a  sufficiently 
large  dose  of  atropine. 

As  Hering  has  shown,  ventricular  extrasystoles  frequently  disappear 
under  atropine  or  any  other  influence  by  which  the  pulse-rate  is  accelerated, 
so  that  the  normal  stimuli  fall  in  at  about  the  periods  at  which  the  abnormal 
stimuli  would  have  fallen.  The  form  of  the  venous  pulse  in  ventricular 
extrasystoles  is,  however,  characteristic. 

Auriculo(Atrio)  ventricular  Extrasystoles.— It  is  also  claimed  by  Hering 
and  Rihl,  Mackenzie  and  Wenckebach,  Lohmann,  Schmoll,  Mackenzie  and 


ALTERATIONS  IN  CARDIAC  RHYTHM. 


115 


Morrow,  and  others  that  extrasystoles  may  arise  in  the  Purkinje  cells  of  the 
conduction  system,  and  that  such  extrasystoles  are  char- 
acterized by  a  shortening  in  the  conduction  time 
(a-c  interval  on  the  venous  pulse),  for  the  impulse  is  conducted  simultaneously 
in  both  directions. 


VOLUME  OF 
VENTRICLES 


BLOOD- PRESSURE 


SECONDS 


Fig.  72. — Volume  curve  of  the  ventricles,  showing  the  dilatation  which  followed  the  entrance  of 
an  air-bubble  into  the  right  auricle.  (Kindness  of  Dr.  Cameron.)  The  extrasystoles  drive  very  little 
blood  into  the  aorta.    DIL,  dilatation. 

Cushny  has  found  the  same  thing  in  dogs  poisoned  with  aconite,  and  Hirschfelder  has 
repeatedly  produced  them  in  hearts  whose  excitability  was  increased  by  faradization. 
Rothberger  and  Winterberg  have  found  that  such  extrasystoles  give  rise  to  a  characteristic 
electrocardiogram  with  a  very  small  P  wave  which  occurs  just  before  the  R.    Correspond- 


Fig.  73. — Extrasystoles  with  shortened  conduction  time,  supposed  to  arise  in  the  auriculoventricular  bundle. 

ing  to  the  two  ventricles,  extrasystoles  arising  in  the  two  branches  of  the  bundle  give 
absence  of  the  P  wave,  a  rather  small  R,  and  an  inverted  T. 

Gaskell  has  shown  in  frogs  that  if  the  tissue  at  the  auriculoventricular  junction  was 
touched  with  a  probe  a  series  of  extrasystoles  set  in  both  auricles  and  ventricle.  And  Bond 
has  been  able  to  watch  this  process  in  the  frog,  in  which  he  could  see  the  auriculoventricular 


Fig.  74. — Variation  in  conduction  time  (a-c)  in  a  case  of  mitral  stenosis. 


muscle  fibres  contract  first,  and  this  was  followed  by  the  contractions  of  auricles  and  of 
the  ventricle,  which  contracted  at  apparently  the  same  instant.  In  mammals  it  cannot  be 
decided  whether  the  fibres  of  the  conduction  system  conduct  or  merely  contract,  but  extra- 
systoles in  which  auricles  and  ventricles  contract  simultaneously  (nodal  extrasystoles) 
are  occasionally  met  with.    Lohmann  also  observed  them  persisting  after  the  tissue  in  the 


11G 


DISEASES  OF  THE  HEART  AND  AORTA. 


vicinity  of  the  His  bundle  had  been  stimulated.  In  a  later  investigation  upon  the  excised 
heart  Lohmann  poisoned  the  region  of  the  venae  cavae  by  means  of  cotton  soaked  in  for- 
malin. He  then  sometimes  saw  extrasy stoles  set  in  spontaneously.  The  auricles  and  ven- 
tricles sometimes  contracted  simultaneously,  sometimes  there  were  ventricular  extrasystoles. 


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Fig.  75. — Tracing  from  right  jugular  vein  and  left  radial  artery  showing  absolute  arrhythmia  due 
to  auricular  fibrillation.  The  jugular  pulse  shows  no  evidence  of  a  waves  and  shows  the  ventricular  type 
of  pulsation.  One  ineffectual  systole  (I)  is  too  weak  to  open  the  aortic  valves  and  hence  appears  on  the 
jugular  but  gives  no  sign  upon  the  radial  pulse.     (Kindness  of  Dr.  R.  E.  Morris.) 

Upon  the  clinical  side  there  is  some  positive  evidence.  Peculiar  extra- 
systoles  often  occur  between  attacks  of  paroxysmal  tachycardia,  but  occa- 
sionally also  in  cases  with  simple  valvular  lesions.  Keith  has  found  patches 
of  fibrous  myocarditis  in  the  vicinity  of  the  His  bundle  in  cases  which  had 

car.1 


VES. 
AES. 

A-VES. 


CMC         V|C^"\        QIC      V 


A-V  BLOCK 


SINO-AURICULAR  BLOCK 
VAGAL  SLOWING 


ic    vAl?  V  3dir  vA~l5    ^5J_S    v 


Q  c  v  ac  vA      ac  vacvA       ac  vac 
c-  v        aic    a,c  v         a.c    a,<- 


Fig.  76.- 


-Diagram   showing  the  alterations  of  rhythm  which  may  cause  a  pulsus  bigeminus. 
indicate  the  incidence  of  stimuli  ori. 


The  arrows 


shown  these  extrasystoles,  and  thinks  that  they  irritated  the  cells  in  the 
vicinity,  but  such  scars  are  very  common,  and  elsewhere  in  the  heart  are 
not  known  to  act  as  irritative  lesions.  Moreover,  the  writer  has  never  been 
able  to  produce  them  by  pressure  upon  the  bundle  with  an  Erlanger  clamp, 
injection  of  mercury  into  the  left  branch  of  the  bundle,  etc.  So  that  in  spite 
of  the  interest  in  the  subject  it  must  be  admitted  that  the  occurrence  of 
extrasystoles  with  shortened  conduction  time  cannot  be  as  yet  regarded  as 
absolute  proof  of  a  lesion  near  the  His  bundle,  but  only  to  heightened  excita- 
bility of  the  latter. 

Prognosis  and  Treatment  of  Extrasystoles. — From  the  stand-point  of 
prognosis  and  treatment  patients  with  extrasystoles  may  be  divided  into  two 
groups : 


ALTERATIONS  IN  CARDIAC  RHYTHM.  117 

1.  Extrasy stoles  in  otherwise  normal  hearts. 

2.  Extrasystoles  in  weak  or  overworked  hearts. 

Occasional  extrasystoles  occur  in  many  persons  who  are  otherwise  healthy. 
If  they  are  not  rendered  more  frequent  by  exercise  they  may  usually  be  dis- 
regarded, but  if  exercise  increases  their  frequency  they  are  often  signs  of 
deeper  myocardial  involvement.  Quite  frequently  they  may  entirely  dis- 
appear when  the  pulse-rate  is  quickened  by  atropine,  nitroglycerin,  or  even 
by  exercise.  Mackenzie,  indeed,  cites  the  case  of  a  young  professional  football 
player  who,  though  otherwise  healthy,  was  troubled  by  occasional  extrasys- 
toles and  had  been  condemned  by  various  physicians  to  a  life  of  invalidism  on 
this  account,  whose  heart  became  regular  again  as  soon  as  he  began  to  enter 
into  the  heat  of  a  game,  which  he  played  in  his  best  form  without  the  slightest 
inconvenience. 

The  extrasystoles  in  themselves  under  these  conditions  do  not  demand 
treatment,  unless  they  are  accompanied  by  palpitation  which  distresses  the 
patient,  and  in  that  case  avoidance  of  excitement  and  fatigue  and  of  an  over- 
loaded stomach,  temporary  abstinence  from  tea,  coffee,  alcohol,  and  tobacco 
(and,  if  necessary,  the  administration  of  bromides  may  be  resorted  to)  is  the 
rule  in  young  persons  with  otherwise  normal  hearts. 

In  those  cases  which  are  secondary  to  flatulence,  constipation,  and 
gastro-intestinal  fermentation,  the  pulse  may  become  regular  as  soon  as  these 
conditions  are  remedied.  If  these  do  not  suffice,  small  doses  of  digitalis  may 
be  given,  but  larger  doses  are  more  likely  to  increase  the  irritability  of  the 
heart,  and  hence  the  occurrence  of  extrasystoles,  than  to  depress  it. 

On  the  other  hand,  in  persons  with  valvular  disease  or  with  high  blood- 
pressure  the  presence  of  extrasystoles  may  be  regarded  as  an  indication  that 
the  ventricles  are  not  driving  out  blood  well  at  each  systole,  and  therefore 
they  may  be  a  forerunner  of  impending  danger.  This  is  especially  true  when 
the  number  is  increased  by  exertion  and  accompanied  by  dyspnoea.  More- 
over, it  must  be  borne  in  mind  that  Lewis  has  produced  ventricular  extra- 
systoles by  ligating  the  descending  branch  of  one  of  the  coronary  arteries ;  and 
the  occurrence  of  extrasystoles  as  the  result  of  coronary  disease,  especially  in 
elderly  individuals,  must  always  be  borne  in  mind;  but  neither  the  presence 
of  coronary  sclerosis  nor  of  any  organic  lesion  whatever  can  be  diagnosed 
from  the  presence  of  ventricular  extrasystoles. 

In  weakened  or  overworked  hearts,  regardless  of  the  definite  anatomical 
diagnosis,  the  presence  of  extrasystoles  constitutes  a  definite  indication  for 
digitalis  and  the  usual  treatment  of  cardiac  overstrain. 

Various  Types  of  Allorrhythmia  which  May  Result  in  a  Bigeminal  Pulse. 
— It  must  be  borne  in  mind  that  the  bigeminal  pulse  is  not  pathognomonic 
of  any  single  disturbance  of  function,  but  may  occur  in  any  of  the  following- 
conditions  (Fig.  76):  (1)  recurring  ventricular  extrasystoles;  (2)  recurring 
auricular  extrasystoles;  (3)  recurring  auriculo ventricular  extrasystoles;  (4) 
recurring  slight  auriculoventricular  heart-block,  the  ventricle  failing  to 
follow  every  third  beat;  (5)  recurring  sino-auricular  block  (?),  the  auricles 
failing  to  respond  to  every  third  impulse;  (6)  recurring  vagal  prolon- 
gation of  every  alternate  diastole.  Similar  conditions  hold  for  the 
trigeminal  pulse,  except  that  two  extrasystoles  or  regular  beats  are  inter- 
polated before  the  pause. 


118  DISEASES  OF  THE  HEART  AND  AORTA. 

AURICULAR     FIBRILLATION     (ABSOLUTE     ARRHYTHMIA;     DISORDERLY     RHYTHM; 
PULSUS   IRREGULARIS   PERPETUUS;   PAROXYSMAL   IRREGULARITY). 

One  of  the  commonest  and  most  characteristic  forms  of  arrhythmia  is 
that  which  is  seen  in  many  old  cases  of  mitral  stenosis  and  myocarditis  in 
which  the  pulse  has  become  permanently  irregular.  The  beats  come  in  groups 
in  which  no  order  is  discernible;  an  irregularity  in  force  and  rhythm  devoid 
of  definite  relation  to  the  phases  of  respiration  or  of  indications  of  heart- 
block,  and  free  from  the  pairs  of  trios  and  associated  beats  which  are  charac- 
teristic of  extrasystolic  arrhythmias.  No  two  parts  of  the  curve  resemble  one 
another,  and,  in  contrast  to  the  extrasystolic  arrhythmias,  weak  beats  may 
follow  the  longer  pauses  just  as  well  as  strong  beats.  On  this  account  it  was 
termed  "absolute  arrhythmia"  or  "disorderly  rhythm"  by  Mackenzie, 
and,  on  account  of  its  frequency  among  the  cases  of  persistent  arrhythmia, 
the  designations  "pulsus  irregularis  perpetuus"  (Hering),  "arrhythmia 
perpetual"  (Gerhardt),  and  "perpetual  arrhythmia"  (Hewlett)  were  applied 
to  it  also. 

The  patients  are  usually,  but  by  no  means  always,  weak,  cyanotic,  and 
subject  to  shortness  of  breath  upon  the  slightest  exertion.  Their  jugular  veins 
are  full  and,  owing  to  the  increased  venous  pressure,  stand  out  prominently 
across  the  sternocleidomastoid,  showing  the  pouches  above  the  venous  valves. 
Often  there  is  little  or  no  pulsation,  but  in  many  cases  a  "single"  venous  pulse 
may  be  made  out  with  one  impulse  accompanying  the  pulse  in  the  carotid. 

When  a  tracing  of  the  venous  pulse  is  taken,  this  wave  is  seen  to  be  of 
the  ventricular  type,  a  single  plateau  or  an  M-shaped  crest  throughout  ven- 
tricular systole,  with  no  indications  whatever  of  an  auricular  contraction 
(a  wave  absent).  Occasionally,  as  in  Fig.  47,  there  is  no  positive  pulsation, 
but  the  midsystolic  (x)  depression  becomes  so  deep  as  to  represent  the  most 
prominent  wave  upon  the  tracing.  Tracings  taken  from  the  oesophagus  in 
this  form  of  arrhythmia  show  only  the  contractions  of  the  ventricle  (Hewlett, 
Clerc  and  Esmein). 

The  exact  nature  of  this  form  of  arrhythmia  was  long  a  matter  of  doubt. 
Mackenzie,  at  first,  relying  upon  the  absence  of  the  a  wave  and  the  general 
form  of  the  pulse,  believed  that  the  auricles  were  absolutely  paralyzed,  and 
that  the  impulse  no  longer  arose  at  the  usual  site  but  in  the  tissue  of  the  His 
bundle  at  the  node  of  Tawara;  and  accordingly  he  designated  this  form  of 
arrhythmia  as  "nodal  rhythm."  Later  he  thought  that  the  auricles  and 
ventricles  were  contracting,  and  hence  the  wave  of  auricular  contraction 
superposed  upon  the  c  wave  could  not  be  made  out.  In  support  of  this  view, 
he  presented  the  findings  in  a  number  of  autopsies,  by  Keith,  of  patients  who 
had  died  with  this  form  of  arrhythmia  in  which  there  were  sclerotic  myocardial 
lesions  (supposed  to  be  irritative)  in  the  vicinity  of  the  His  bundle. 

Cushny  and  Edmunds  and  Hewlett,  as  the  result  of  experiments  upon 
dogs,  suggested  that  this  form  of  irregularity  might  result  from  fibrillation 
of  the  auricles.  J.  Mac  William  (J.  Physiol,  1887,  iii,  296)  had  noted  that  such 
fibrillary  movements  readily  occurred  in  hearts  of  high  degree  of  irritability 
and  that  they  were  inhibited  by  vagus  stimulation.  F.  Philips,  a  pupil  of 
Fredericq  (Arch.  Internat.  de  Physiol.,  1904-05,  ii,  271),  produced  such  arrhyth- 
mias in  dogs  and  showed  that  they  were  associated  with  fall  of  blood-pres- 
sure.   Fredericq  showed  that  after  destroying  the  A-V  bundle  auricular  fibril- 


ALTERATIONS  IN  CARDIAC  RHYTHM. 


119 


lation  no  longer  produced  arrhythmia  of  the  ventricle;  but  the  association  of 
this  condition  with  the  common  clinical  arrhythmia  was  not  definitely  proved 
until  1909,  when  Rothberger  and  Winterberg  and  Lewis  showed  that  the 
electrocardiogram  in  such  cases  assumed  a  very  characteristic  form,  upon 
which  the  two  ventricular  waves  (R  and  T)  are  well  marked,  but  the  single 
presystolic  (P)  wave  is  absent,  and  replaced  by  a  series  of  undulations  irregu- 
lar in  size,  in  form,  and  in  rate,  and  taking  place  continuously  throughout 


Fig.  77. — Perpetual  arrhythmia  of  the  ventricles.     (After  Jolly  and  Ritchie.)    The  small  wavelets  (a)  are 

due  to  auricular  flutter. 

systole  and  diastole  of  the  ventricle.  The  average  rate  of  these  fibrillar  con- 
tractions varies  from  about  450  to  about  1000  per  minute;  the  slower  ones 
being  larger  and  approaching  more  nearly  to  forcible  contractions,  the  rapid 
ones  smaller  and  feebler  and  approximating  a  condition  of  absolute  paralysis. 

Moreover,  exactly  the  same  form  of  electrocardiogram  and  exactly  the 
same  irregularity  could  be  produced  in  dogs  when  the  auricles  were  caused 
to  fibrillate  by  faradization  or  other  means,  and  this  form  of  electrocardio- 
gram corresponded  to  no  other  known  condition. 

These  fibrillations,  as  is  seen  from  the  electrical  variations,  are  accom- 
panied by  impulses  which  may  pass  down  the  His  bundle  and  stimulate  the 
ventricles,  but  which  do  so  at  a  rate  too  fast  for  the  latter  to  follow,  and  hence 
they  respond  to  only  occasional  stimuli.  In  the  dog  this  may  give  rise  to 
either  a  regular  rate  at  about  doubled  velocity  or  to  an  absolute  arrhythmia, 
but  in  man  the  electrocardiograph  shows  that  auricular  fibrillation  always 
brings  about  an  irregular  rhythm. 

Fibrillary  contractions  of  the  auricle  are,  as  Cushny  and  Edmunds  and 
Rihl  have  shown,  too  feeble  to  produce  any  definite  waves  upon  the  venous 
pulse,  and  hence  the  latter  assumes  the  ventricular  type,  often  showing 
small  undulations  during  diastole. 

The  ventricular  type  of  venous  pulse,  on  the  other  hand,  does  not  always 
correspond  to  an  auricular  fibrillation,  but,  as  Lewis  has  shown,  whenever 
a  ventricular  pulse  accompanies  a  perfectly  regular  rhythm  in  man,  the 
electrocardiograph  shows  that  the  auricle  is  still  contracting  (P  wave  present). 


120 


DISEASES  OF  THE  HEART  AND  AORTA. 


The  finer  and  coarser  forms  may  have  some  clinical  significance,  for  the 
coarser  type  occurs,  as  a  rule,  in  cases  in  which  compensation  is  established 
or  nearly  so,  while  the  type  of  finer  contractions  is  more  common  in  cases 
with  badly  broken  compensation.  Occasionally,  indeed,  a  reversion  from  the 
finer  to  the  coarser  type  of  contraction  occurs  in  the  same  patient,  accompany- 
ing improvement  in  the  clinical  condition,  but  it  is  doubtful  whether  this 
manifestation  may  be  regarded  as  of  importance  in  prognosis. 


RV  EXSYS 


L.V.   EXSYS 


Fig.  78. — Diagram  showing  abnormal  electrocardiograms  and  the  structures  in  which  they  arise. 

R.ACCEL,  electrocardiogram  resulting  from  stimulation  of  the  right  accelerator  nerve;  P,  S,  T 
waves  increased,  R  wave  diminished. 

L.ACCEL,  effect  of  stimulating  the  left  accelerator;  P  and  R  waves  diminished,  S  wave  increased, 
T  wave  inverted. 

A.  FIBRILL,  auricular  fibrillation,  P  wave  absent,  replaced  by  numerous  small  undulations. 

SUP  V.C.EXSYS,  right  auricular  extrasystole  arising  in  the  vicinity  of  the  lower  end  of  the 
superior  vena  cava  (especially  in  the  vicinity  of  the  Keith-Flack  node) ;  all  the  waves  normal. 

INF  V.C.EXSYS,  right  auricular  extrasystole  arising  in  the  vicinity  of  the  inferior  vena  cava; 
P  wave  inverted. 

L.A.EXSYS,  extrasystole  arising  in  the  left  auricle;  P  wave  inverted. 

R.V.HYPERT,  hypertrophy  of  the  right  ventricle,  all  the  waves  normal,  but  R  wave  increased. 

L-  V-  HYPERT,  all  waves,  but  especially  the  R  wave  inverted;  or  S  wave  increased. 

RV  EXSYS,  extrasystole  arising  in  the  right  ventricle,  showing  an  absence  of  the  P  wave,  and  an 
abnormal  ventricular  wave,  consisting  of  a  large  initial  wave  followed  by  a  depression  and  a  second 
smaller  wave. 

LV  EXSYS,  extrasystole  arising  in  the  left  ventricle,  showing  a  large  initial  depression  followed  by 
a  large  slow  wave. 

A-V  EXSYS,  extrasystole  arising  in  the  node  of  Tawara  or  the  His  auriculoventricular  bundle, 
accompanied  by  synchronous  contraction  of  auricles  and  ventricles,  showing  absence  of  the  P  wave  and 
slightly  abnormal  ventricular  waves. 

R  A-V  B,  electrocardiogram  due  to  a  myocardial  lesion  affecting  the  right  branch  of  the  auriculo- 
ventricular bundle;  P  wave  normal,  other  waves  resembling  those  due  to  a  left  ventricular  extrasystole. 

L  A-V  B,  electrocardiogram  due  to  a  myocardial  lesion  affecting  the  left  branch  of  the  auriculoven- 
tricular bundle. 

The  presence  of  auricular  fibrillation  does  not  exclude  the  other  forms 
of  disturbance,  but  it  may  be  accompanied  by  sinus  arrhythmias,  extrasys- 
toles,  and  even  heart-block  in  the  same  patient. 

Although  auricular  fibrillation  gives  rise  to  the  most  common  form  of 
perpetual  irregularity,  it  is  by  no  means  always  perpetual. 


ALTERATIONS  IN  CARDIAC  RHYTHM. 
PLATE  IX. 


121 


%/^^H^i^u 


ik/v 


wm*  t 


A 


%A-V\         \ 


V 


Absolute  arrhythmia  due  to  auricular  fibrillation  of  the  coarse  type,  with  diagram  showing  the  origin  and 

transmission  of  the  impulses. 


] 

c;"-  as,  . 


||i|W]iiip|ii|il|l|i|lll|l"|it'll||l|l|l|ITl1llll|l||ll1|||ll 


A 


i^A-A 


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V 


Absolute  arrhythmia  due  to  auricular  fibrillation  of  the  fine  type,  with  diagram  showing  the  origin  and 

transmission  of  the  impulses. 


122  DISEASES  OF  THE  HEART  AND  AORTA. 

Cases  are  frequently  encountered,  especially  in  incipient  heart-failure 
of  mitral  stenosis  or  myocardial  insufficiency,  in  which  the  irregularity  sets 
in  only  occasionally,  often  arising  suddenly  and  subsiding  suddenly,  as  is  the 
case  with  true  paroxysmal  tachycardia,  with  which  it  is  closely  associated. 
The  rate  remains  rapid  and  irregular  for  a  period  which  may  vary  from  a 
few  minutes  to  hours,  days,  or  weeks,  during  which  the  patient  usually  feels 
weak,  often  a  little  light-headed  or  giddy,  and  with  a  feeling  of  fluttering  in 
the  chest  and  sometimes  definite  precardial  oppression,  and  shortness  of 
breath  on  slight  exertion.  The  attacks  may  at  any  time  subside  suddenly 
and  spontaneously  to  the  regular  rate  which  is  normal  for  the  patient,  whose 
health  and  vigor  are  then  suddenly  restored,  just  as  is  the  case  in  idiopathic 
paroxysmal  tachycardia.  Occasionally,  as  in  a  case  reported  by  Lewis,  true 
paroxysmal  tachycardia  passes  into  this  form  of  arrhythmia,  a  transition 
which  is  not  strange,  since,  as  Hirschfelder  has  shown,  the  functional  disturb- 
ances are  clearly  allied,  and  indeed  seem  to  represent  a  difference  of  degree  of 
hyperirritability  rather  than  an  essential  difference  in  mode  of  origin.  More- 
over, as  Lewis  and  Fox  have  shown,  paroxysms  of  absolute  irregularity  usually 
become  more  and  more  frequent,  more  and  more  prolonged,  and  finally  merge 
into  a  condition  of  permanent  irregularity,  whereas  paroxysmal  tachycardia 
may  persist  for  decades  without  increase  in  severity  or  impairment  of  the 
general  health — and  without  definite  association  with  any  organic  lesion. 

Anatomically  the  usual  lesions  of  myocarditis  are  found  in  these  cases, 
but  in  addition  Schonberg,  Keith  and  Ivy  Mackenzie,  and  Hedinger  have 
never  failed  to  find  lesions  in  the  superior  vena  cava  at  the  veno-auricular 
junction  (node  of  Keith  and  Flack).  In  view  of  the  fact  that  from  a  physio- 
logical stand-point  the  condition  corresponds  merely  to  a  condition  of  hyper- 
irritability of  the  auricular  tissue,  it  is  still  questionable  whether  all  cases 
correspond  to  definite  lesions  of  the  myocardium. 

Mechanical  Effect  of  Arrhythmia  on  the  Circulation. — The  mechanical 
effect  of  any  arrhythmia  is  to  slow  the  circulation,  as  may  be  easily  seen  from 

the  volume  curve  of  the 
heart  during  a  period  of 
irregularity.  This  slowing 
in  itself  tends  to  bring  on 
cyanosis,  increase  the  CO2 
in  the  blood,  and,  as  Cam- 
eron has  shown,  to  dimin- 

Fig.  79. — Effect  of  arrhythmia  on  the  circulation,  blood-  .  ' 

pressure,  and  volume  of  the  ventricles.    Tracing  from  a  dog's  ISh    the    tone    01    the     heart 

heart  stimulated   irregularly  with   induction   shocks.      7,  I,  I,  TrmcrOo     in     +hia    -nro-tr  C\r\ 

ineffectual    systoles;    DIL,    dilatation.      Upstrokes   on   volume  "'UfeLie     m     l^»     Wd,y.        Un 

curve  represent  outflow  from  the  ventricles.  the    Other    hand,    the     long 

pauses  cause  an  increase  of 
pressure  in  the  veins,  and  the  influx  of  venous  blood  under  a  relatively 
increased  pressure  acting  upon  cardiac  muscle,  whose  tone  is  diminished, 
tends  to  overdistend  the  heart  (as  seen  in  Fig.  79).  The  over-distention,  by 
increasing  the  diameter  of  the  ventricular  chamber,  increases  the  hydrostatic 
pressure  upon  its  walls  and  causes  it  to  work  at  a  disadvantage.  Thus  is 
established  the  vicious  circle  of  the  irregular  heart: 

Overfilling  of  heart 

t  I 

Slowing  of  circulation  ■< Irregularity 


ALTERATIONS  IN  CARDIAC  RHYTHM.  123 

The  effect  is  most  marked  in  the  auricles,  where  tone  changes  show  themselves 
in  more  marked  degree  than  in  the  ventricles,  and  over-distention  sets  in  and 
facilitates  fibrillation.  When  the  auricles  are  fibrillating,  the  genesis  of  efficient 
stimuli  becomes  more  difficult,  it  is  harder  to  accelerate  the  pulse  during 
exercise,  etc.,  and  consequently  it  becomes  easier  for  CO2  to  accumulate  in 
the  blood  in  the  irregular  than  in  the  regular  heart,  and  the  heart  in  this 
condition  is  per  se  permanently  weakened.  < 

Effect  of  Digitalis  in  Arrhythmia  due  to  Auricular  Fibrillation. — The 
most  striking  results  that  are  ever  obtained  from  the  use  of  digitalis  in  heart 
diseases  are  obtained  in  the  arrhythmias  due  to  auricular  fibrillation.  The 
pulse-rate,  it  is  true,  does  not  become  regular,  but  its  rapid  rate  can  be  dimin- 
ished almost  at  will  by  the  use  of  the  drug;  and  the  slowing  of  the  pulse-rate 
almost  invariably  ushers  in  an  improvement  in  the  clinical  condition.  This 
is  due  to  the  fact  that  many  of  the  symptoms  are  due  merely  to  the  rapidity 
of  the  heart  rate  and  the  number  of  premature  and  ineffectual  contractions 
rather  than  to  the  fact  that  the  rate  is  an  irregular  one,  or  even  to  the  absence 
of  effectual  contractions  of  the  auricle.    W.  B.  James  regards  the  number  of 

rate  over  the  heart 

ineffectual  contractions  (pulse  deficit)  as  shown  by  the  ratio : 

rate  at  wrist 

as  indicative  of  clinical  condition,  a  relatively  high  ratio  indicating  cardiac 

weakness,  a  fall  forward  indicating  improvement. 

The  action  of  digitalis  in  auricular  fibrillation  is  due  almost  entirely  to 
the  blocking  of  the  impulses  that  pass  from  the  auricles  to  the  ventricles. 
The  impulses  due  to  fibrillation  are  in  the  main  more  easily  blocked  than 
those  due  to  coordinate  contractions,  and  a  mild  degree  of  heart-block  is  thus 
easily  introduced  by  which  any  desired  number  of  impulses  may  be  cut  off 
from  crossing  the  His  bundle,  and  thus  almost  any  desired  pulse-rate  can  be 
attained.  This  action  of  digitalis  is  due  almost  entirely  to  stimulation  of 
the  vagi,  for  Mackenzie  has  shown  that  the  rapid  heart  rate  is  resumed 
upon  the  administration  of  atropin.  It  is  only  in  the  later  stages  of  digitalis 
action,  as  Hirschfelder  has  shown  in  animals,  that  a  purely  muscular  effect 
of  digitalis  which  is  independent  of  the  vagi  and  uninfluenced  by  atropin  is 
brought  about. 

Although  it  is  always  possible  with  any  individual  to  give  digitalis  to 
the  point  of  complete  heart-block,  the  best  effects  are  obtained,  as  Mackenzie 
has  shown,  after  a  very  considerable  reduction  in  rate  has  been  obtained. 
The  optimum  rate  varies  with  different  individuals  dependent  largely  upon 
the  circulation  in  the  coronary  arteries  and  in  the  medulla,  but  it  is  usually 
advisable  to  administer  enough  of  the  drug  to  bring  the  pulse -rate  down  to 
70  or  80  per  minute  in  about  a  week.  This  is  usually  accompanied  by  striking 
improvement  of  clinical  symptoms.  Each  case  has  its  own  optimum  rate 
at  which  greatest  vigor  and  fewest  symptoms  are  met.  Mackenzie  finds 
that  this  may  be  as  low  as  48  per  minute  without  inducing  any  symptoms 
save  those  of  improvement,  but  though  this  level  may  occasionally  be  reached, 
the  writer  has  found  that  it  is  necessary  to  proceed  slowly  in  reducing  the 
rate  much  below  70;  and  the  latter  stages  of  the  reduction  should  be  accom-_ 
plished  very  slowly.  On  the  other  hand,  if  digitalis  is  pushed  too  far,  weakness 
of  the  ventricles  sets  in,  and  the  patient's  health  may  suffer. 


124  DISEASES  OF  THE  HEART  AND  AORTA. 

Paroxysmal  Tachycardia  and  Auricular  Flutter. — Cotton  in  1867  de- 
scribed a  peculiar  condition  in  which  attacks  of  extreme  tachycardia  were 
present,  leaving  the  heart  quite  normal  in  the  interim.  Similar  cases  were 
reported  by  Bensen,  Nothnagel,  Proebsting,  Priesendorfer,  Pribram,  and 
Bristowe,  who  considered  them  to  be  due  to  a  sort  of  vagus  neurosis.  Bou- 
veret,  however,  regarded  the  condition  as  a  distinct  clinical  entity,  of  which 
he  was  able  in  1889  to  collect  over  twenty  cases  from  the  literature,  and  which 
he  designated  as  "essential  (or  idiopathic)  paroxysmal  tachycardia  (tachy- 
cardie  paroxystique  essentielle) . "  According  to  Bouveret,  this  condition  is 
characterized  by  attacks  in  which  the  pulse  suddenly  attains  a  rapidity  (200 
to  300  per  minute)  which  is  never  seen  in  any  other  condition,  even  in  the 
gravest  heart  failures.  These  attacks  last  from  several  minutes  to  several 
days  or  even  weeks,  and  subside  as  suddenly  as  they  come.  They  sometimes 
recur  for  years  and  often  for  decades  without  seriously  interfering  with  life 
and  general  health  of  the  patient;  or,  on  the  other  hand,  an  attack  sometimes 
ends  in  death. 

Bouveret's  clinical  description  was  so  complete  that,  though  many  cases 
were  subsequently  reported,  little  that  was  essential  was  added  until  Aug. 
Hoffmann  in  1900  called  attention  to  the  fact  that  the  paroxysms  of  tachy- 
cardia began  and  ceased  with  extreme  suddenness,  and  showed  by  excellent 
tracings  that  the  complete  change  of  rate  often  occurred  within  the  period 
of  a  single  cardiac  cycle.  Moreover,  he  showed  that  this  change  of  rate  was 
an  exact  doubling,  trebling,  or  quadrupling  of  the  previous  rate,  and  ended 
by  halving,  quartering  or  dropping  to  one-third.  For  example,  the  normal 
pulse-rate  being  70,  the  rate  during  an  attack  might  be  140,  210,  280  per 
minute,  and  vice  versa.  Hoffmann  regarded  this  sudden  complete  change  of 
rate  as  characteristic  of  the  essential  or  idiopathic  paroxysmal  tachycardia, 
in  contrast  to  the  simple  tachycardia  of  exercise,  excitement,  or  convalescence, 
in  which  the  change  of  rate  is  due  to  loss  of  vagus  tone  and  comes  on  by  a 
gradual  increase  of  rate  during  a  period  of  from  one  to  several  minutes.  Such 
a  tachycardia  rarely  exceeds  120  to  140  per  minute.  Even  though  it  may 
give  rise  to  sharp  attacks  coming  on  more  or  less  suddenly  and  accompanied 
by  palpitation,  it  is  not  to  be  regarded  as  idiopathic  (essential)  paroxysmal 
tachycardia,  but  will  be  considered  under  the  simple  nervous  affections  of 
the  heart  (Part  IV,  Chapter  II). 

Occurrence  and  Associated  Lesions. — Paroxysmal  tachycardia  is  equally 
common  in  both  sexes  (Bouveret,  Hoffmann).  It  occurs  at  all  ages,  frequently 
beginning  in  early  childhood  and  persisting  for  decades.  On  the  other  hand, 
it  frequently  occurs  in  old  persons,  as  in  G.  R.,  who  was  72  years  of  age. 
It  is  not  infrequent  in  otherwise  healthy  pregnant  women,  in  whom  it  is  a 
very  annoying  feature.  It  is  particularly  common  in  mitral  stenosis,  as  are 
also  the  related  conditions,  auricular  flutter  and  auricular  fibrillation. 

Effects  on  Circulation. — The  effect  which  these  paroxysms  of  tachycardia 
exert  upon  the  circulation  is  primarily  due  to  the  deficient  filling  of  ventricles 
during  the  short  diastoles.  As  Yandell  Henderson  has  shown,  the  ventricles 
fill  to  their  normal  extent  only  when  the  pulse-rate  is  moderately  slow.  When 
the  pulse  becomes  rapid,  the  ventricles  do  not  have  time  to  fill,  and,  since  the 
period  of  systole  is  never  much  less  than  0.2  second,  it  is  evident  that  when 
the  heart-rate  is  much  above  200  the  period  during  which  filling  can  take 


ALTERATIONS  IN  CARDIAC  RHYTHM. 


125 


place  is  very  short  and  little  blood  can  enter  the  ventricles.  The  volume  of 
the  heart  remains  small.  As  a  result  of  this  condition,  blood  stagnates  in 
auricles  and  veins,  venous  pressure  rises  (to  30  cm.  H20  in  one  case  examined 
by  Eyster  and  Hooker),  and  with  it  there  come  engorgement  of  the  liver  and 
oedema  of  the  extremities.  Stasis  also  occurs  in  the  pulmonary  veins,  ushering 
in  oedema  and  dyspnoea,  and  sometimes  these  symptoms  of  broken  pulmonary 
compensation  dominate  the  scene  (see  page  207). 

On  the  other  hand,  the  arterial  pressure  falls,  because,  as  the  filling  of 
the  ventricle  is  small,  the  amount  which  is  driven  out  into  the  arteries  is 
diminished  correspondingly.  This  fall  in  blood-pressure  is  usually  accom- 
panied by  pallor  and  often  by  symptoms  of  cerebral  anaemia,  exactly  as  occurs 
in  hemorrhage,  surgical  shock,  or  other  conditions  in  which  the  amount  of 
blood  in  the  arteries  is  diminished.  Other  organs  also  suffer  from  anaemia, 
and  finally  also  the  heart  itself,  which  may  give  signs  of  weakening,  first 
evinced  by  lowered  tonus  and  dilation.  It  is  evident  that  hearts  whose  coro- 
nary arteries  are  sclerotic  would  suffer  more  readily  than  those  with  normal 
blood  supply. 

Mechanism  of  Paroxysmal  Tachycardia. — These  tachycardias  differ 
fundamentally  from  the  changes  in  heart  rate  such  as  those  produced  by 


f^M^IWVM^^uMr/W 


Fig.  80a. — Venous  pulse  in  a  case  of  paroxysmal  tachycardia  (G.  D.  R.).  (Kindness  of  the  Johns 
Hopkins  Hospital  Bulletin.)  A.  During  the  attack  (pulse-rate  144  per  minute).  Ventricular  type  of 
venous  pulse,  no  a  wave  discernible,  c,  carotid  wave.  Time  of  the  carotid  wave.  B.  Tracing  taken  five 
minutes  later,  just  after  cessation  of  the  attack.  Pulse-rate  80.  Venous  pulse  of  the  normal  auricular 
type,  conduction  time  {a-c  interval)  normal.  C.  Tracing  from  the  same  case  taken  during  a  period  of 
irregularity  a  few  days  later,  showing  extrasystoles  with  shortened  conduction  time.  The  intervals  are 
measured  in  millimetres  upon  a  uniformly  running  drum. 

motion  or  exercise,  for  the  latter  are  produced  by  changes  in  the  nerve  im- 
pulses governing  the  heart  rate  while  the  extreme  tachycardias  are  associated 
with  increased  irritability  of  the  heart  muscle. 

Tachycardias  of  purely  neurogenic  origin  set  in  gradually  and  subside 
gradually,  while  those  of  myogenic  origin  set  in  at  a  single  leap  up  to  maximum 
rate  within  one  or  two  cardiac  cycles.  MacWilliam,  Hirschfelder  and  Lewis 
have  shown  that  these  tachycardias  are  more  closely  associated  with  extra- 


126 


DISEASES  OF  THE  HEART  AND  AORTA. 


systoles  and  auricular  fibrillation  than  they  are  with  the  neurogenic  tachy- 
cardias of  emotion  and  exercise. 

If  the  irritability  of  the  heart  muscle  is  increased  by  gradually  increasing 
faradic  stimulation,  the  first  effect  produced  is  an  extrasystolic  arrhythmia, 
the  next  a  tachycardia  of  regular  rate,  and  the  maximal  stimuli  induce  fibril- 
lation. All  of  these  effects,  like  the  corresponding  clinical  conditions,  set  in 
suddenly  and  subside  suddenly,  within  the  period  of  one  or  two  cardiac 
cycles;  and  the  gap  to  or  from  the  tachycardia  or  fibrillation  is  often  bridged 
by  one  or  two  extrasystoles. 

Assuming  that  tachycardias  of  this  variety  are  associated  with  increased 
irritability  of  certain  regions  of  heart  muscle,  it  would  be  only  natural  to 
expect  that  any  region  whose  irritability  was  thus  increased  would  become 
the  pace-maker  of  the  heart;  and  that  therefore  dependent  upon  the  site  of 
the  pace-maker,  we  would  encounter  tachycardias  arising  at  the  sino-auricular 
node  where  the  normal  beats  arise  (homogenetic)  or  at  other  regions  of  the 
heart  (heterogenetic) . 

This  is  exactly  borne  out  by  clinical  experience,  so  that,  sometimes  by 
means  of  the  venous  pulse  tracing  and  almost  always  by  means  of  the  electro- 
cardiogram, we  can  differentiate  several  other  types  of  tachycardia  even 


ii. 


in. 


IV. 


Fig.  806. — Diagram  showing  the  various  types  of  tachycardia.  I.  Simple  non-paroxysmal  tachy- 
cardia, showing  the  gradual  increase  and  gradual  decrease  in  rate.  JUG,  venous  pulse;  A,  auricular  im- 
pulses; V,  ventricular  impulses;  A-V,  auriculoventricular  conduction.  II.  Paroxysmal  tachycardia,  with 
persistent  auricular  contraction  and  ending  in  auriculoventricular  heart-block  (2  :  1  rhythm).  III.  Parox- 
ysmal tachycardia  due  to  impulses  arising  in  the  auriculoventricular  bundle  (auriculoventricular  tachy- 
cardia).    IV.  Paroxysmal  tachycardia  due  to  impulses  arising  in  the  ventricle  (ventricular  tachycardia). 

though  these  may  all  have  the  same  pulse-rates.  Thus,  we  may  have  a 
heterogenetic  auricular  tachycardia  arising  at  some  site 
in  the  walls  of  the  auricles  but  not  at  the  sino-auricular  node.  This  is  char- 
acterized by  the  presence  of  an  auricular  (a)  wave  upon  the  venous  pulse 
and  by  an  inversion  of  the  P  wave  upon  the  electrocardiogram.  We  may 
also  encounter  a  tachycardia  which  is  brought  on  when  the  cells  of  the  auric- 
uloventricular node  of  the  His  bundle  undergo  an  increased  rhyth- 
micity  and  become  the  pace-makers;  and  in  this  case  the  a  wave  upon  the 
venous  pulse  closely  approaches  or  fuses  with  the  c  wave  so  that  there  is  a  very 
much  shortened  a-c  interval,  or  when  there  is  absolute  fusion  a  short  but  high 
and  steep  wave  corresponding  to  the  c  wave.  The  electrocardiogram  also  un- 
dergoes characteristic  changes;  the  P-R  interval  may  become  tremendously 
reduced  (to  as  short  as  .03  to  .05  seconds)  or  the  P  wave  may  become  fused 


PLATE  X. 


D  I 


DII 


D  III 


Electrocardiograms  from  a  patient  with  a  lesion  of  the  right  branch  of  the  His  bundle,  verified  at 
autopsy.  (Kindness  of  Dr.  R.  E.  Morris.)  DII  shows  a  splitting  of  the  R  wave  and  of  the  depression 
following  it   (S  depression)  . 


ALTERATIONS  IN  CARDIAC  RHYTHM.  127 

with  the  R  wave;  or  the  P  wave  may  follow  the  R  wave  and  appear  as  a  small 
notch  between  the  R  and  T,  following  the  former  at  less  than  .1  second 
interval. 

Such  a  shifting  of  the  site  of  the  pace-maker  from  the  sino-auricular 
region  to  the  auriculoventricular  bundle  may  be  induced  experimentally  by 
cooling  the  former  with  ice  while  leaving  the  latter  region  undisturbed;  or 
it  may  be  met  with  during  perfusion  of  the  isolated  mammalian  heart  when 
the  conditions  of  temperature,  etc.,  are  not  at  their  optimum. 

Still  further  the  ventricle  may  become  the  pace-maker  and  aventric- 
ular  tachycardia  may  set  in  in  which  the  ventricle  may  become  the 
pace-maker  and  the  auricles  may  follow  them  (idioventricular  rhythm)  or 
in  which  conduction  may  be  impaired  and  the  ventricles  alone  may  participate 
in  the  rhythm,  while  a  ventriculo-auricular  heart-block  sets  in.  These  condi- 
tions are  characterized  by  a  ventricular  form  of  venous  pulse  and  by  an 
electrocardiogram  showing  for  all  beats  curves  which  correspond  to  those  of 
ventricular  extrasy stoles.  Thus,  as  might  be  expected,  two  forms  of  ventricular 
tachycardia  are  encountered,  one  corresponding  to  a  right  ventricular  com- 
plex or  curve,  the  other  to  a  left  ventricular.  Just  as  in  the  case  of  left 
and  right  ventricular  extrasystoles,  the  two  curves  are  the  mirror  images  of 
one  another. 

Such  tachycardias  may  give  rise  not  only  to  regular  but  also  to  irregular 
pulse-rates  even  though  the  rate  of  the  pace-maker,  whether  auricular  or 
auriculoventricular,  remains,  itself,  regular.  This  is  due  to  the  fact  that  the 
auriculoventricular  bundle  may  be  somewhat  overwhelmed  and  fatigued  by 
the  frequent  impulses  imposed  upon  it  and  fail  to  transmit  more  than  a  certain 
number;  so  that  a  partial  heart-block  may  set  in,  without  any  lesion  of  the 
auriculoventricular  bundle.  This  partial  block  may  be  uniform  and  give 
rise  to  a  regular  rate  of  the  ventricle  one-half,  one-third,  or  one-fourth  that 
of  the  auricle;  or  the  failures  of  conduction  may  occur  at  irregular  intervals 
and  an  absolute  arrhythmia  may  be  set  up,  due  to  the  irregular  intermingling 
of  groups  with  1  :  1,  2  :  1,  3  :  1,  4  :  1  block. 

Auricular  Flutter. — Paroxysmal  acceleration  of  the  auricles,  due  to 
increased  rhythmicity  or  irritability  at  either  the  normal  pace-maker  or  at 
some  abnormal  site,  may  give  rise  to  an  interesting  form  of  arrhythmia 
which  may  closely  simulate  the  absolute  arrhythmia  due  to  auricular  fibrilla- 
tion. This  arrhythmia  which  was  first  described  by  Jolly  and  Ritchie  repre- 
sents what  may  be  described  as  a  paroxysmal  regular  tachycardia  of  the 
auricles  themselves  accompanied  by  either  paroxysmal  tachycardia,  by  an 
irregularity  of  the  ventricles  or  by  heart-block.  This  is  due  to  irregularity 
either  in  the  conduction  of  the  impulse  or  in  the  ventricular  response  itself; 
so  that  the  heart  rate  and  arterial  pulse  are  represented  by  irregularly  inter- 
spersed series  of  1:1,  2:1,  3:1,  4:1,  auriculoventricular  block  with  an 
auricular  rate  so  rapid  that  the  relation  may  be  only  difficultly  discernible. 
As  is  the  case  of  true  paroxysmal  tachycardia,  these  contractions  of  the  auricle 
are  coordinate  systoles  of  the  entire  auricle  and  give  rise  to  distinct  and  uni- 
form waves  upon  the  venous  pulse  and  electrocardiogram  (Plate  XII,  B), 
each  ventricular  cycle  representing  a  definite  multiple  of  these  auricular  cycles. 

This  condition  represents  a  true  heart-block  superposed  upon  a  paroxys- 
mal tachycardia  or  condition  of  increased  cardiac  irritability.    It  differs  from 


128  DISEASES  OF  THE  HEART  AND  AORTA. 

paroxysmal  tachycardia  only  by  the  coincident  occurrence  of  block;  from  the 
ordinary  heart-block  only  by  the  coincident  occurrence  of  extreme  tachy- 
cardia in  the  auricles,  and  from  auricular  fibrillation,  which  it  outwardly 
resembles,  only  by  the  fact  that  the  latter  is  due  to  incoordinate  contractions. 
This  seems  to  represent  a  difference  only  in  degree  of  irritability  according 
to  the  scale  shown  on  page  108;  and  clinical  evidence  shows  frequent  transi- 
tions from  either  form  to  the  two  others.  In  spite  of  the  element  of  heart- 
block,  however,  there  is  but  rarely  any  organic  injury  of  the  bundle  present 
in  this  condition;  and  the  disturbance  of  conduction  is  due  merely  to  the 
functional  inability  of  the  His  bundle  to  conduct  all  the  rapid  impulses  that 
reach  it  from  above.  This  is  either  fatigue  of  the  bundle  or  is  due  to  the 
fact  that  the  impulses  are  too  weak  to  affect  it.  That  such  an  arrhythmia 
may  result  from  a  succession  of  regular  impulses  too  rapid  for  the  heart  to 
follow  has  been  shown  by  Hirschfelder,  who  stimulated  the  right  auricle  of 
a  series  of  dogs  with  weak  rapid  rhythmic  electric  stimuli  and  found  that  an 
arrhythmia  frequently  resulted  due  to  the  interpolation  of  successions  of 
1  :  1,  2  :  1  rhythms  in  a  manner  that  could  not  be  predicted.  Strengthening 
the  stimuli  or  slowing  the  rate  both  caused  a  return  to  1  :  1  response;  weaken- 
ing the  stimuli  or  quickening  their  rate  increased  the  irregularity  of  the 
response. 

Physiological  Summary. — The  pathological  physiology  of  paroxysmal 
tachycardia  may  therefore  be  summed  up  as  follows: 

Underlying  causes:   Increased  irritability  of  cardiac  muscle. 

Predisposing  factors  for  an  attack:  Slight  reflex  stimulations  of  cardiac 
nerves. 

Condition  during  attack:  "Doubling"  or  multiplication  of  pulse-rate, 
with  or  without  auricular  fibrillation. 

Mechanical  effects  on  the  circulation,  to  which  these  symptoms  are 
referable : 

1.  Systemic  stasis,  high  venous  pressure. 

2.  Pulmonary  stasis,  high  pressure  in  pulmonary  veins. 

3.  Ansemia  of  brain,  kidneys,  and  heart,  from  low  arterial  pressure. 
Symptoms. — Although  attacks  of  tachycardia  sometimes  run  their  course 

without  the  patient's  knowledge,  it  is  more  common  for  them  to  be  accom- 
panied by  symptoms.    These  symptoms  may  be  grouped  as  follows: 

1.  Symptoms  of  cardiac  excitability. 

2.  Those  due  to  engorgement  of  systemic  veins  (failure  of  right  ventricle). 

3.  Those  due  to  engorgement  of  pulmonary  veins  (failure  of  left  ventricle) . 

4.  Those  due  to  cerebral  ansemia. 

1.  Palpitation,  a  feeling  of  discomfort  or  oppression  in  the  pre- 
cordium  and  weakness  are  the  most  common  symptoms.  This  is  often 
worse  just  at  the  end  of  the  attack,  and  may,  as  in  Hay's  case,  resemble  the 
symptoms  of  angina  pectoris.  In  this  case  there  was  also  hyperesthesia  of 
the  precordium  and  neck.  The  latter  may  be  due  to  engorgement  of  the 
cervical  veins,  just  as  in  angina  pectoris  it  may  be  referred  from  the  heart 
(Mackenzie) . 

2.  Besides  the  above-mentioned  feeling  of  fulness  in  the  neck,  the  patient 
often  has  a  similar  feeling  in  the  abdomen  from  distention  of  the  liver,  and 
swelling  of  the  feet  commonly  appears  before  the  end  of  the  attack. 


PLATE  XI. 


Electrocardiograms  showing  auricular  and  ventricular  tachycardia.  (Kindness  of  Dr.  J.  M.  Black- 
ford, of  the  Mayo  Clinic.)  A,  electrocardiogram  from  a  woman  suffering  from  attacks  of  palpitation  and 
suddenly  developing  tachycardia,  with  a  ventricular  rate  rising  from  150  to  300  per  minute,  showing  tachy- 
cardia of  the  auricular  type  (auricular  nutter).  B,  electrocardiogram  from  the  same  patient,  showing 
auricular  flutter  between  attacks.  The  patient  has  been  receiving  digitalis.  Subsequently  auricular 
fibrillation  set  in.  C,  electrocardiogram  taken  during  an  attack  of  ventricular  tachycardia  in  a  man  aged 
sixty-two.    Pulse  rate,  150  per  minute. 


PLATE  XII 


Electrocardiogram  from  patient,  showing  (A)  partial  heart-block  (2:1  rhythm)  after  digitalis  with 
(B)  sudden  onset  of  auricular  flutter  and  auricular  fibrillation  and  (C)  return  to  normal  (1  :  1  rhythm) ,  all 
within  a  period  of  a  few  minutes.    (Kindness  of  Dr.  R.  E.  Morris.) 


ALTERATIONS  IN  CARDIAC  RHYTHM.  129 

3.  Dyspnoea  is  frequent.  It  is  striking  that  this  may  occur  without 
any  change  in  the  rate  of  respiration,  even  in  cases  with  severe  myocardial 
changes  (Romberg).  No  doubt  this  is  associated  with  engorgement  and  high 
pressure  in  the  pulmonary  veins.  It  is  often  accompanied  by  cough  and  the 
expectoration  of  mucus,  sometimes  containing  large  endothelial  cells  with 
blood  pigment  (Herzfehlerzellen).  Occasionally  there  is  actual  haemoptysis 
(in  three  of  Bouveret's  eleven  cases)  during  the  attack.  Actual  pulmonary 
oedema  may  indeed  set  in,  as  in  Pribram's  case — a  young  woman,  otherwise 
healthy,  whose  attacks  were  so  severe  that  "the  pulse  became  barely  palpable. 
The  patient  fell  into  a  state  of  collapse,  and  finally  oedema  appeared  in  the 
lower  part  of  the  lungs.  At  the  moment  when  death  seemed  imminent, 
when  collapse  was  at  its  height,  she  gave  a  cry  of  anguish ;  it  seemed  to  her  as 
though  something  were  taken  out  of  her  neck,  and  the  scene  suddenly  changed. 
The  pulse  fell  to  76,  became  large  and  full,  and  the  collapse  disappeared." 

On  the  other  hand,  this  sudden  change  does  not  always  occur,  and  death 
sometimes  supervenes  during  the  attack. 

The  venous  stasis  also  leads  to  albuminuria,  though  in  the  milder  attacks 
the  urine  may  be  increased  and  of  low  specific  gravity. 

4.  The  fall  in  arterial  pressure  usually  brings  about  symptoms  of  cere- 
bral anaemia;  weakness,  vertigo,  and  even  extreme  nervousness  is  the  rule 
during  the  attacks,  accompanied  by  restlessness,  loss  of  appetite,  and  inability 
to  sleep.  Even  syncope  may  occur.  In  a  gentleman  whom  the  writer  ex- 
amined some  years  ago  these  syncopal  attacks  had  led  several  prominent 
physicians  to  diagnose  Adams-Stokes  syndrome;  when,  as  was  shown  by  the 
examination  and  subsequent  observation,  the  cerebral  anaemia  resulted  not 
from  bradycardia  but  from  tachycardia.  Fortunately,  these  attacks  have  a 
tendency  to  become  milder.  Dr.  Lyon  writes,  three  years  after  the  first 
examination,  that  this  patient  "is  now  able  to  play  cards,  go  fishing,  and  do 
almost  anything  in  a  quiet  way  during  attacks." 

PHYSICAL   SIGNS. 

Physical  signs  are  absent  between  attacks  of  paroxysmal  tachycardia. 
During  the  attacks  the  face  is  usually  pale,  the  expression  anxious,  the  pupils 


126 

ah  rv 


V 

SKj 

Fig.  80c. — Slightly  more  intense  stimulation.     Tachycardia,  with  quickened  conduction,  outlasting  the 
period  of  stimulation.     Time  in  seconds. 

are  equal,  the  veins  of  the  neck  are  seen  to  be  engorged  and  often  to  show  a 
positive  "single"  pulsation  accompanying  each  systole  (sometimes  due  to 
transitory  tricuspid  insufficiency) ,  perhaps  due  to  the  feebleness  of  the  auric- 
ular contractions.  The  tumultuous  heart  action  is  often  seen  in  a  precordial 
heaving  and  well-marked  apex  beat.  The  area  of  cardiac  dulness  is  rarely 
increased  except  toward  the  end  of  the  attack.  It  is  usually  unchanged  or 
decreased  in  size,  corresponding  to  the  diminished  filling  of  the  ventricles. 
This  diminution  in  the  size  of  the  heart  during  an  attack  has  been  seen  with 
9 


130  DISEASES  OF  THE  HEART  AND  AORTA. 

the  fluoroscope  by  Hoffmann,  Dietlen,  and  others,  and  it  can  be  demonstrated 
in  the  experimental  paroxysms.  Towards  the  end  of  severe  attacks  dilatation 
sets  in  from  cardiac  weakness. 

The  heart  sounds  may  be  unchanged,  but  usually  become  short  and  some- 
what muffled.  There  is  often  embryocardia.  It  is  very  common  to  hear  a 
soft  systolic  over  the  right  ventricle  and  apex,  perhaps  due  to  a  mitral  or 
tricuspid  insufficiency  of  the  papillary  type. 

Sometimes  the  cardiac  rhythm  is  irregular,  owing  to  inability  of  the 
ventricles  to  follow  all  the  impulses  from  the  sinus  and  auricles  or  to  the 
presence  of  extrasystoles.  The  liver  often  is  felt  to  be  enlarged,  and  often 
shows  a  systolic  pulsation  during  attacks  (tricuspid  insufficiency),  but  ascites 
rarely  occurs.    (Edema  of  the  ankles  and  feet  is  very  frequent. 

Case  of  Paroxysmal  Tachycardia. 

G.  D.  R.,  a  hotel-keeper  aged  72,  was  admitted  to  the  Johns  Hopkins  Hospital  on 
February  22,  1906,  complaining  of  palpitation  of  the  heart.  The  family  history  and  per- 
sonal history  were  negative.  The  patient  had  always  been  a  robust  man,  had  had  no  infec- 
tious diseases  and  no  other  cardiac  manifestations. 

The  first  attack  of  palpitation  and  tachycardia  came  on  suddenly  after  retiring  one 
evening  twenty  years  before  admission.  It  caused  him  great  fear,  but  no  pain.  The  attack 
lasted  six  hours  and  left  him  weak  but  otherwise  well.  Attacks  similar  in  character  recurred 
once  a  month  until  the  winter  of  1905-1906,  when  they  became  more  severe  and  began  to 
occur  once  or  twice  a  week.  During  the  attacks  he  passed  large  amounts  of  urine.  He 
never  noticed  palpitation  between  attacks  of  tachycardia. 

The  patient  was  a  large,  well-nourished  man  of  good  color.  His  pupils  were  equal  and 
reacted  well  to  light  and  during  accommodation. 


CAROTID  PRESSURE 


VOLUME  OF  VENTRICLES 


VENOUS  PRESSURE  s: 


Fig.  80d. — Diagram  showing  the  effect  of  a  paroxysm  of  tachycardia  upon  the  circulation.     The  under- 
lined portion  indicates  the  paroxysm. 

The  thorax  was  rather  barrel-shaped;  the  percussion  note  was  hyperresonant,  and  the 
breath-sounds  were  clear,  though  distant.  The  cardiac  impulse  was  neither  seen  nor  felt, 
but  the  apex,  as  made  out  by  percussion  and  auscultation,  was  situated  in  the  fifth  left 
interspace  11  cm.  from  the  midline.  The  cardiac  dulness  extended  up  to  the  upper  border 
of  the  third  rib,  but  could  not  be  made  out  to  the  right  of  the  sternum.  The  sounds  were 
distant,  but  clear.  The  pulse-rate  between  attacks  was  64  per  minute.  It  was  usually 
regular  in  force  and  rhythm,  of  good  volume  and  rather  high  tension;  the  blood- pressure 
ranged  from  165  to  190,  the  minimum  from  100  to  115. 

The  abdomen  was  large  and  flabby,  with  considerable  panniculus.  Liver  and  spleen 
were  not  palpable.  The  examination  was  otherwise  negative.  The  venous  pulse  between 
attacks  was  usually  normal. 

On  February  23  and  March  1  and  15  the  patient  had  attacks  of  tachycardia,  in  which 
his  pulse-rate  rose  suddenly  from  80  to  88  per  minute  to  a  height  of  144  to  160  per  minute. 
The  attack  of  March  15  began  just  after  returning  from  the  closet,  where  he  had  passed  a 
soft,  fluid  stool.  Tracings  made  from  the  patient  during  this  attack  showed  what  is  probably 
a  ventricular  type  of  venous  pulse  during  the  attack.  When  the  latter  ceased,  however, 
the  pulse  resumed  the  normal  auricular  type.  There  was  no  sign  of  auriculoventricular 
block.  Excitement  incident  to  being  shown  at  the  clinic  precipitated  a  second  attack  on 
March  15,  which  was  not  relieved  by  the  application  of  an  ice-bag,  yawning,  deep  breathing, 
pressure  on  the  vagus,  in  front  of  the  sternocleidomastoid,  nor  by  administration  of  spiritus 
setheris  nitrosi,  amyl  nitrite,  or  digitalin.  The  attack  ceased  spontaneously  within  an 
instant,  at  3.10  p.  m. 

On  March  21  his  pulse  was  irregular,  due  to  the  presence  of  numerous  extrasystoles 
with  shortened  conduction  time  (auriculoventricular?).    These  subsided,  however,  leaving 


ALTERATIONS  IN  CARDIAC  RHYTHM.  131 

his  pulse  regular.    On  March  24  his  pulse  remained  at  76  in  spite  of  the  administration  of 

2  mg.  atropine.     Even  rapid  walking  while  he  was  under  the  influence  of  the  atropine 
did  not  bring  on  an  attack,  nor  did  the  administration  of  amyl  nitrite  on  March  24. 

Clinical  Picture  of  Auricular  Flutter. — Cases  of  auricular  flutter  may 
present  the  clinical  picture  in  symptoms  and  signs  of  either  paroxysmal 
tachycardia,  auricular  fibrillation  or  heart-block,  dependent  upon  the  manner 
in  which  the  ventricle  happens  to  respond  to  the  tachycardia  of  the  auricles. 
As  a  matter  of  fact,  all  three  types  occur,  often  two  of  them  occurring  in  the 
same  patient  at  different  stages  of  the  disease. 

The  following  case  is  taken  from  the  excellent  book  of  W.  T.  Ritchie 
("Auricular  Flutter,"  Green  and  Co.,  Edinburgh,  1914). 

The  patient,  aged  59,  had  no  antecedent  history  of  acute  rheumatism  or  valvular 
disease,  but  for  several  years  he  had  been  subject  to .  paroxysmal  attacks  of  tachycardia 
in  which  the  ventricles  beat  irregularly  at  a  rate  of  about  158  per  minute;  and  there  had 
been  a  syncopal  seizure  on  one  occasion.  From  each  of  these  attacks  the  patient  had 
made  a  rapid  and  speedy  recovery  after  the  heart  had  regained  its  normal  rhythm.  The 
last  attack  of  flutter  began  five  months  before  the  patient's  death.  Dyspnoea,  palpitation, 
Cheyne-Stokes  breathing  and  insomnia  were  the  dominant  symptoms.  The  auricles  were 
beating  rhythmically  at  a  rate  of  333-340  per  minute.  The  auricular  waves  in  the  jugular 
veins  were  of  large  size.  Meanwhile  the  ventricular  rate  was  about  110  per  minute,  and 
the  rhythm  was  notably  irregular,  for  although  the  auriculoventricular  ratio  was  often 

3  : 1,  it  frequently  varied  between  2  :  1,  3  : 1,  and  4  :  1.    The  ventricles  could  not  be  retarded 
by  compression  of  the  vagus  on  either  side. 

The  symptoms  of  cardiac  failure  becoming  more  urgent,  the  daily  dose  of  digitalis 
tincture  was  increased  to  1  drachm.  Four  days  later  the  large  auricular  waves  disappeared 
from  the  jugular  veins,  the  venous  pulse  acquired  the  ventricular  form,  and  the  arterial 
pulse  became  wholly  irregular.  The  auricular  flutter  had  apparently  passed  into  fibrillation. 
Subsequently  the  ventricles  became  dilated,  the  mitral  valve  incompetent,  and  the  urine 
scanty  and  albuminous.  The  auricles  apparently  remained  in  fibrillation  for  three  and  a 
half  months.  Thereafter,  during  the  fortnight  preceding  the  fatal  issue  and  while  the  admin- 
istration of  digitalis  was  still  being  continued,  periods  of  auricular  fibrillation,  with  ventricu- 
lar arrhythmia,  alternated  with  others  in  which  the  ventricles  were  beating  rhythmically  at 
a  rate  of  64-80  per  minute. 

DIAGNOSIS. 

In  the  cases  in  which  the  pulse-rate  is  above  160  per  minute  the  diagnosis 
rarely  presents  any  difficulty,  for  the  tachycardias  of  simple  nervous  origin, 
on  the  one  hand,  and  those  of  organic  cardiac  disease  rarely  reach  that  height. 
But  in  the  border-line  case  in  which  the  tachycardia  is  about  140,  the  diag- 
nosis may  be  difficult.  The  crucial  point  in  the  differentiation  lies  in  the 
suddenness  of  the  change  of  rate,  and  for  this  it  is  important  to  have  observed 
the  beginning  and  the  end  of  an  attack,  the  sudden  rise  to  maximum  rate 
within  a  few  seconds  indicating  idiopathic  paroxysmal  tachycardia,  while  a 
gradual  step-like  or  progressive  rise  indicates  a  simple  tachycardia.  Thus, 
while  the  patient  G.  R.  exemplifies  the  idiopathic  condition,  the  following 
case  is  typical  of  the  simple  tachycardia. 

The  diagnosis  of  auricular  flutter  may  be  made  with  certainty  from  the 
electrocardiogram,  which  shows  great  tachycardia  of  the  auricle  with  intervals 
between  the  P  waves  which  are  regular  in  form  and  uniform  in  spacing,  though 
the  intervals  between  the  R  waves  may  be  irregular  or  of  much  longer  dura- 
tion. The  P-R  interval  is  usually  uniform  in  duration.  The  venous  pulse 
shows  numerous  A  waves  between  the  ventricular  C  waves  just  as  in  ordinary 
heart-block,  only  with  much  shorter  intervals.  As  these  wavelets  are  often 
visible,  it  is  sometimes  possible  to  make  the  diagnosis  of  auricular  flutter 


132  DISEASES  OF  THE  HEART  AND  AORTA 

from  a  simple  inspection  of  the  venous  pulse,  by  noting  the  great  discrepancy 
between  the  auricular  rate  and  that  of  the  ventricles.  These  wavelets  may 
be  shown  much  more  distinctly  by  the  card  or  shadow  methods  described  on 
page  72,  or  the  corresponding  sounds  may  sometimes  be  heard  upon  placing 
the  stethoscope  bell  over  the  jugular  bulb  as  recommended  by  Josue. 
All  the  manoeuvres  in  raising  and  lowering  the  patient  in  order  to  bring  out 
the  wavelets  of  the  venous  pulsation  are  of  course  even  more  necessary 
for  the  diagnosis  of  auricular  nutter  than  for  the  coarser  pulsations  of  other 
conditions. 

TREATMENT. 

As  regards  the  treatment  of  paroxysmal  tachycardia  various  methods 
have  been  employed.  The  first  essential  is  to  put  the  patient  into  the  best 
possible  physical  condition,  to  treat  any  anaemia,  digestive  disturbance, 
constipation,  disturbance  of  vision,  heaving,  enteroptosis,  or  other  conditions 
which  may  bring  about  reflex  irritations;  to  stop  the  use  of  tea,  coffee,  tobacco, 
and  alcohol,  and  so  to  arrange  the  life  of  the  patient  as  to  do  away  with  mental 
excitement,  worry,  over-exertion,  and  fatigue.  If  necessary,  a  "rest  cure" 
may  be  resorted  to.  These  measures  may  do  much  to  diminish  the  frequency 
of  the  attacks,  but  often  the  latter  do  not  disappear  altogether.  Small  doses 
of  digitalis  or  aconite  may  be  tried  in  the  interim  between  attacks,  in  the 
hopes  of  keeping  them  down  by  increasing  the  action  of  the  vagus;  or  potassium 
bromide  or  valerian  may  be  given,  in  the  hope  of  quieting  the  nervous  system; 
but  the  desired  result  is  only  occasionally  obtained. 

The  application  of  an  ice-bag  to  the  precordium  sometimes  relieves  the 
symptoms,  but  only  rarely  is  a  sufficient  cardiac  sedative  to  stop  an  attack. 

Exercise  for  Stopping  the  Attacks. — Fairbrother  states  that  he  has  been 
able  to  stop  his  own  attacks  by  sudden  or  violent  exercise,  such  as  running 
or  jumping.  In  like  manner  a  young  physician  with  mitral  stenosis  who 
was  under  the  writer's  observation  suffered  from  paroxysms  which  for  years 
resisted  treatment  with  rest,  digitalis,  strophanthin,  potassium  bromide, 
aconite,  pressure  on  the  vagus,  and  deep  breathing;  but  they  have  disap- 
peared since  he  has  been  doing  hard  work  in  the  hospital.  Needless  to 
say,  such  exertions  in  a  layman  should  always  be  under  the  care  of  a 
physician. 

The  paroxysms  themselves  may  sometimes  be  stopped  by  various 
mechanical  methods  which  stimulate  the  vagi;  deep  inspirations  (Nothnagel), 
especially  yawning,  "squeezing  arms  and  elbows  tightly  against  the  chest 
while  holding  breath  and  compressing  abdomen"  (Valsalva's  experiment  with 
elbows  compressed  against  chest)  (Hay),  swallowing,  especially  of  ice-water, 
or  belching,  may  be  successful. 

Max  Herz  has  found  it  possible  to  suppress  many  troublesome  attacks 
in  his  patients  by  bringing  about  belching  in  the  following  manner:  The 
patient  is  made  to  sit  down,  fill  his  mouth  with  water,  bend  his  head  back- 
ward as  far  as  possible,  and  swallow.  This  not  only  brings  about  a  desire  to 
belch,  but  also  facilitates  the  eructation  of  a  large  amount  of  gas,  and  fre- 
quently brings  the  attack  to  a  close.  Needless  to  say,  care  should  be  taken 
that  the  belching  does  not  pass  over  into  continuous  air  swallowing  and  that 
the  patient  does  not  acquire  this  pernicious  habit  (see  page  706). 


ALTERATIONS  IN  CARDIAC  RHYTHM.  133 

When  belching  fails  to  stop  the  attack,  vomiting  may  be  resorted  to, 
and  frequently  proves  an  effectual  though  unpleasant  method.  Tickling  the 
pharynx  with  the  finger  is  usually  sufficient  to  bring  it  about,  especially  after 
swallowing  some  water.    Emetics  need  not  be  used. 

One  of  the  oldest  and  best  procedures  (Bensen,  1880)  is  pressure  upon 
the  vagus  just  to  the  left  of  the  thyroid  cartilage.  The  nerve  which  is  just 
behind  the  carotid  artery  is  pressed  very  firmly  against  the  vertebrae  and 
held  tightly  for  two  or  three  minutes.  In  a  considerable  number  of  cases 
this  stops  the  attack,  but  in  many  it  fails,  or  succeeds  for  a  moment  and 
then  the  tachycardia  is  resumed  (Priesendorf er) ,  just  as  is  the  case  in  the 
experimental  auricular  fibrillation.  The  patient  should  never  do  this  for 
himself,  as  it  sometimes  leads  to  heart-block  with  fainting  and  convulsions 
(see  page  579). 

To  quiet  the  attack  after  its  onset  drugs  are  of  little  avail.  Morphine, 
bromides,  etc.,  and  other  sedatives  may  diminish  the  intensity  of  the  symp- 
toms, but  do  not  slow  the  heart-rate.  The  administration  of  a  few  whiffs 
of  chloroform,  of  amyl  nitrite,  nitroglycerin,  Hoffmann's  anodyne,  strychnine, 
digitalis  and  its  derivatives  (digitalin,  digalen)  is  without  effect.  Aconite 
also,  though  the  best  stimulant  for  the  vagus,  was  without  clinical  effect  in 
the  one  case  in  which  the  writer  used  it,  and  has  proved  equally  unsatis- 
factory in  the  hands  of  others. 

Digitalis  and  its  derivatives  are  usually  without  effect.  Though  large 
doses  of  strophanthin  sometimes  stop  auricular  fibrillation  in  animals,  intra- 
venous injection  of  strophanthin  has  not  given  satisfactory  results  in  three 
cases  of  paroxysmal  tachycardia  to  whom  it  was  administered  in  the  Johns 
Hopkins  Hospital.  In  cases  of  auricular  flutter  digitalis  is  of  little  avail  for 
the  flutter  itself,  but  digitalis  in  large  doses  tends  to  increase  the  irritability 
of  the  heart  muscle  and  by  this  means  it  sometimes  helps  to  convert  auricular 
flutter  into  auricular  fibrillation.  After  this  transformation  has  set  in  the 
digitalis  may  then  be  pushed  further  to  bring  about  slowing  of  the  ventricular 
rate  by  inducing  block  at  the  His  bundle.  This  is  a  rather  desperate  pro- 
cedure, for  it  leads  to  the  production  of  a  condition  which  in  itself  represents 
a  higher  degree  of  functional  disturbance  than  the  original  condition  for  which 
treatment  was  begun,  but  in  cases  in  which  the  tachycardia  is  leading  to  heart 
failure  it  may  become  the  last  resort. 

It  has  been  seen  that  cases  of  paroxysmal  tachycardia  do  not  respond 
well  to  the  administration  of  digitalis  because  the  stimulation  of  the  vagi 
produced  by  the  latter  is  not  strong  enough  to  quiet  the  excited  auricles  nor 
to  block  the  impulses  which  they  send  across  the  His  bundle.  On  the  other 
hand,  digitalis  acts  well  in  auricular  fibrillation  when  the  feeble  impulses  are 
easily  blocked.  Hirschf  elder  has  shown  that  the  effectiveness  of  digitalis  in  this 
condition  depends  upon  the  intensity  of  the  impulses  coming  down  from  the 
auricles. 

However,  when  the  results  of  all  methods  of  treatment  have  been  taken  into 
account,  one  is  inclined  to  share  the  feelings  expressed  by  Mackenzie  when  he 
wrote:  "In  my  early  days  I,  too,  thought  I  knew  how  to  stop  attacks,  but  more 
extended  experience  has  shown  me  that  when  they  stopped  it  was  from  some 
cause  unknown  to  me  and  which  was  independent  of  any  means  I  employed." 


134  DISEASES  OF  THE  HEART  AND  AORTA. 

DIFFERENTIAL   DIAGNOSIS   OF   ARRHYTHMIAS   BY   ORDINARY  PHYSICAL 

EXAMINATION. 

Inspection  of  the  Venous  Pulse. — A  quite  accurate  functional  analysis 
of  arrhythmias  is  possible  by  simple  inspection  of  the  venous  pulse.  For  a 
satisfactory  examination  of  the  venous  pulse  it  is  necessary  first  of  all  to  place 
the  patient  in  such  a  position  that  a  good  visible  pulsation  is  present,  the 
normal  venous  pulse  is  not  a  true  expansile  pulsation  like  the  carotid  pulse, 
but  is  determined  by  a  series  of  collapses  and  fillings  of  the  vein.  The  vein 
collapses  when  the  pressure  within  it  is  less  than  atmospheric,  i.e.,  the  pres- 
sure upon  its  walls,  namely,  atmospheric  pressure;  it  fills  when  the  pressure 
within  it  is  greater  than  atmospheric;  when  it  is  constantly  below  atmos- 
pheric pressure  the  vein  remains  empty;  when  it  is  constantly  above  it  the 
vein  remains  full.  The  vein  alternately  collapses  and  expands  and  gives  a 
good  pulsation  when  the  mean  pressure  is  about  zero,  and  in  order  to  maintain 
the  mean  pressure  at  zero  it  may  be  necessary  in  some  cases  to  make  the 
patients  sit  up,  in  other  cases  to  cause  them  to  lie  flat  and  even  to  elevate 
the  feet. 

"  Having  obtained  a  pulsation  which  is  easily  seen  in  the  right  jugular 
fossa  the  next  step  is  the  inspection  of  the  pulsation.  In  order  to  do  this 
with  ease  and  accuracy  we  may  avail  ourselves  of  some  of  the  well-known 
principles  of  physiological  psychology.  It  is  well-known  that  if  we  appre- 
ciate light  objects  most  readily  when  they  are  contrasted  with  a  dark  back- 
ground or  a  shadow,  that  we  appreciate  the  movement  of  an  object  best  when 
it  is  contrasted  with  a  fixed  point,  and  that  we  recognize  the  amount  of  any 
change  in  visual,  auditory  or  tactual  sensation  but  when  the  amount  of  the 
change  represents  a  considerable  fraction  of  the  original  impression. 

"  We  recognize  a  change  in  weight  from  5  to  10  Gm.  better  than  a  change 
from  20  to  25  Gm.  We  recognize  a  change  in  length  of  a  band  from  five  to 
ten  millimetres  better  than  that  of  another  changing  from  twenty  to  twenty- 
five.  It  is  impossible  to  make  use  of  all  these  principles  of  psychology  in  the 
study  of  the  venous  pulse  by  merely  holding  up  a  bit  of  card  next  to  the  jugular 
vein,  as  shown  in  Plate  XIII,  so  that  both  the  card  and  the  skin  contrast  sharply 
against  the  dark  shadow  between  them,  and  it  is  possible  to  hold  the  card  in 
such  'a  way  that  this  band  of  shadow  becomes  narrowed  to  two  or  three  milli- 
metres as  the  vein  fills  and  widens  to  four  to  six  millimetres  as  it  collapses; 
so  that  the  visual  impression  of  the  width  of  the  shadow  is  alternately  doubled 
and  halved.  Or  the  card  may  be  held  in  such  a  way  that  the  shadow  is  just 
obliterated  when  the  vein  is  full  and  appears  as  a  wide  slit  when  the  vein 
collapses;  and  then  the  impression  is  one  of  a  series  of  flashes  interrupted  by 
shadows  like  the  dots  and  dashes  of  a  Morse  code.  In  accordance  with  the 
laws  of  psychology  these  impressions  are  much  easier  to  time  than  is  the 
simple  movement  of  one  area  of  skin  against  another  area  of  white  skin  as  a 
background,  and  a  greater  accuracy  of  diagnosis  is  therefore  possible  by  this 
method. 

"  Characteristics  of  Venous  Pulsations. — Viewed  in  this  way  the  normal 
or  'double'  venous  pulse  appears  as  a  double  flash  accompanying  each  beat 
of  the  heart  or  pulsation  in  the  carotid  artery,  interrupted  by  shadows  of 
perfectly  regular  duration. 

"  A  sinus  arrhythmia  may  in  most  cases  be  diagnosed  by  the  fact  that  it 


ALTERATIONS  IN  CARDIAC  RHYTHM.  135 

is  usually  composed  of  a  series  of  2-4  short  beats,  each  with  a  'double' 
venous  pulse,  alternating  with  a  series  of  2-4  long  ones,  also  with  'double' 
pulsations. 

*'  The  venous  pulse  is  either  absent  or  normal  in  appearance;  and  the  veins 
of  the  neck  are  usually  rather  empty,  often  barely  discernible,  and  there  is 
little  or  no  irregularity  in  force,  discernible  to  the  palpating  finger  or  made 
out  by  the  dropping  of  a  few  of  the  beats  as  the  pressure  is  raised  in  a  blood- 
pressure  cuff  upon  the  arm.  Moreover,  in  most  cases  they  are  accentuated 
in  deep  inspiration  or  in  deep  expiration,  but  disappear  when  the  breath  is 
held.  The  serial  character  of  the  beats  is  made  out  better  in  listening  over 
the  heart  than  in  palpation  at  the  wrist." 

In  the  irregularities  due  to  pericardial  adhesions  (pulsus  paradoxus  and 
Riegel's  pulse)  there  may  be  irregularity  in  force  and  not  in  rhythm,  the 
veins  of  the  neck  dilate  in  one  or  the  other  phase  of  respiration,  and  this 
corresponds  to  the  period  when  the  pulse  is  smaller  or  entirely  absent. 

"A  pulsus  alternans  may  be  diagnosed  when,  without  irregularity 
in  rhythm,  there  is  irregularity  in  force  and  the  alternate  beats  are  found  to 
be  weaker,  and  the  beats  felt  at  the  wrist  fall  to  exactly  half  the  original  rate 
and  remain  regular  when  the  artery  is  gradually  compressed  above  the  wrist 
with  the  finger  or  by  means  of  a  blood-pressure  cuff  on  the  upper  arm.  The 
rate  of  the  beats  still  felt  remains  regular.  Here,  again,  care  must  be  taken 
to  exclude  a  dicrotic  pulse.  The  latter  will  usually  disappear  while  the  arm 
is  allowed  to  hang  down  perpendicularly  at  the  side.  In  the  dicrotic  pulse 
the  sounds  heard  over  the  heart  are  half  as  frequent  as  the  impulses  felt  at 
the  wrist." 

When  extrasystoles  are  present  we  find  a  pair  or  trio  of  beats  at 
the  wrist  followed  by  a  long  compensatory  pause,  whereas  over  the  jugular 
we  can  distinguish  clearly  between  auricular  and  ventricular  extrasystoles."  * 

The  heart  sounds  come  in  groups — lub,  dub,  tut,  up  (1,  2,  3,  4:  pause) 
(1,  2,  3,  4,  5,  6:  pause) — of  sounds  of  approximately  equal  loudness,  never 
that  of  the  distant  ticking  character  of  the  auricular  or  third  heart  sounds. 

They  are  as  loud  and  distinct  for  the  extrasystoles  as  for  the  normal 
beat,  but  the  former  are  occasionally  accompanied  by  systolic  murmurs  even 
though  there  are  none  accompanying  the  regular  beats. 

When  the  extrasystoles  are  too  weak  to  open  the  aortic  valves,  a  dis- 
crepancy will  be  noted  between  the  number  of  beats  over  the  heart  and  the 
number  of  beats  felt  at  the  wrist  or  over  the  carotids,  and  the  missed  beat 
will  be  accompanied  by  only  one  heart  sound  instead  of  two,  for  the  second 
sound,  ordinarily  due  to  closure  of  the  aortic  valve,  drops  out.  The  groups 
of  sounds  will  therefore  be  (1,  2,  3:  pause;  1,  2,  3,  4,  5:  pause,  etc.). 

"  The  auricular  extrasystoles  appear  as  pairs  of  waves  occurring  early  but 
otherwise  exactly  like  the  pulsation  for  the  normal  beats,  while  the  ventricular 
extrasystoles  are  readily  distinguished  as  large  long  waves  which  frequently 
run  from  the  jugular  fossa  along  the  course  of  the  external  jugular  vein  across 
the  sternocleidomastoid  muscle,  giving  the  largest  and  most  characteristic 
pulsation  that  one  encounters.  If  the  extrasystoles  diminish 
or  disappear  under  exercise  they  are  of  little  prog- 

1  Quoted  from  A.  D.  Hirschfelder  Virginia  Medical  Semi-Monthly,  1914,  xvtii,  576. 


136  DISEASES  OF  THE  HEART  AND  AORTA. 

nostic  significance;  but  if  they  are  increased  in  number  by  exercise 
they  may  be  regarded  as  indications  of  an  overloaded  heart  and  may  be  con- 
sidered as  an  early  sign  of  cardiac  weakness.  Occasionally,  as  in  one  of  the 
patients  to  be  mentioned  later,  one  may  encounter  a  third  heart  sound  that 
is  loud  and  sharp — the  sounds  accompanying  normal  beats,  though  when  they 
are  too  weak  to  open  the  aortic  valves  only  one  sound  may  be  heard  with  the 
extra  beat  instead  of  two.  Occasionally  as  in  one  of  the  cases  to  be  mentioned 
again  in  connection  with  heart-block,  one  may  encounter  a  third  heart  sound 
so  loud  and  sharp  that  it  might  be  mistaken  for  one  of  these  ineffectual  extra- 
systoles  which  does  not  open  the  aortic  valves.  The  latter  can  be  readily 
excluded,  however,  by  the  fact  that  the  third  heart  sound  is  not  usually  heard 
over  the  entire  precordium,  while  the  sound  of  an  extrasystole  is  as  well  heard 
everywhere  over  the  heart  as  the  sounds  of  the  normal  beats.  It  may,  more- 
over, be  differentiated  by  the  fact  that  the  third  sound  is  accompanied  by 
only  a  single  small  wave  upon  the  jugular  pulse,  while  the  auricular  extra- 
systoles  are  accompanied  by  a  double  wave  and  the  ventricular  extrasystoles 
are  accompanied  by  the  single  large  characteristic  wave.  In  the  case  men- 
tioned, the  electrocardiogram  showed  that  there  was  a  third  heart  sound. 

"In  auricular  fibrillation  one  often  finds  full  veins  and  a  high  venous 
pressure  so  that  the  patient  may  have  to  sit  up  in  order  to  obtain  a  good 
venous  pulsation,  this  pulsation  is  single  in  character,  that  is,  beat  for  each 
beat  in  the  carotid,  but  there  is  no  regular  pairing  or  trebling  of  the  beats 
and  the  rhythm  is  absolutely  free  from  definite  sequence.  The  waves  are 
usually  smaller  than  those  of  ventricular  extrasystoles,  so  that  it  is  often 
possible  to  diagnose  the  latter  even  in  the  presence  of  auricular  fibrillation 
from  the  interpolation  of  occasional  waves  which,  though  much  larger  than 
the  rest,  are  not  preceded  by  a  long  pause.  The  venous  pulsation  of  auricular 
fibrillation  may  be  differentiated  from  that  of  tricuspid  insufficiency  by  the 
fact  that  the  latter  is  often  accompanied  by  a  regular  pulse,  but  some  cases 
of  extrasystoles  accompanied  by  a  tricuspid  insufficiency  are  particularly  hard 
to  differentiate  from  auricular  fibrillation.  This  can  be  done,  however,  by 
paying  attention  to  the  interspersing  of  pairs  or  trios  of  beats  in  the  midst  of 
regular  series,  and  the  feasibility  of  this  diagnosis  is  best  shown  by  the  fact 
that  it  was  made  correctly  in  a  number  of  cases  by  our  third  year  students. 
Auricular  flutter  with  an  irregular  pulse  can  sometimes  be  differ- 
entiated from  auricular  fibrillation  by  the  presence  of  a  very  fine  tremulous- 
ness  or  series  of  very  rapid  small  undulations  over  the  vein  during  diastole. 

"  Auriculo ventricular  extrasystoles  cannot  be  differentiated  from  ventric- 
ular extrasystoles  by  simple  inspection,  as  both  give  rise  to  large  waves,  but 
the  ventricular  forms  are  so  much  more  frequent  in  the  more  common  condi- 
tions of  circulatory  or  gastro-intestinal  disturbances,  while  the  auriculo- 
ventricular  are  most  liable  to  be  met  with  between  the  attacks  of  paroxysmal 
tachycardia. 

"  Differences  between  right  and  left  ventricular  extrasystoles  cannot  be 
made  out;  but  the  site  may  be  suspected  in  many  cases  from  a  knowledge 
of  the  conditions  within  the  circulation,  for  the  extrasystole  usually  arises 
in  the  ventricle  which  is  most  heavily  over-worked.  Thus,  in  aortic  disease 
and  high  blood-pressure  they  are  most  likely  to  arise  in  the  left  ventricle;  in 
mitral  disease  and  broken  pulmonary  compensation  they  are  most  likely  to 


ALTERATIONS  IN  CARDIAC  RHYTHM.  137 

arise  in  the  right.  It  must  always  be  borne  in  mind,  however,  that  this  rule 
is  far  from  absolute,  for  local  impairment  in  coronary  circulation  may  entirely 
reverse  the  conditions. 

"  The  most  interesting  condition  for  physical  diagnosis  has  been  the  condi- 
tion of  heart-block. 

"  The  existence  of  heart-block  can  always  be  suspected  when  the  pulse- 
rate  is  below  42.  The  diagnosis  can  frequently  be  made  from  the  presence  of 
more  than  two  pulsations  over  the  jugular  vein  for  each  beat  in  the  carotid, 
and  by  hearing  from  one  to  three  low  ticking  auricular  sounds  over  the  heart 
in  diastole.  Very  often  this  finding  may  be  corroborated  by  the  presence  of 
a  corresponding  number  of  very  slight  shocks  or  beats  just  discernible  upon 
the  radial  pulse  between  the  big  beats  when  the  artery  is  very  lightly  palpated. 

"  Stokes,  in  his  famous  report  in  1846,  stated  that  hewasable  to  distinguish 
in  the  pauses  between  the  large  beats  in  the  jugular  and  the  loud  sounds  over 
the  heart  small  waves  and  distant  sounds  which  we  now  know  were  due  to  the 
contractions  of  the  auricle.  By  this  observation  Stokes  possessed  all  the  data 
necessary  to-day  for  the  complete  functional  diagnosis  of  heart-block  with  the 
differentiation  between  partial  and  complete  block.  If  he  had  noticed  that 
in  spite  of  the  regularity  of  the  large  or  ventricular  beats  the  number  of  small 
waves  over  the  jugular  and  the  number  of  soft  sounds  over  the  heart  varied 
in  successive  diastoles,  he  could,  without  hesitation,  have  made  the  diagnosis 
of  complete  heart-block.  If,  however,  the  number  of  wavelets  and  of  auricular 
sounds  remained  constant  during  ten  or  more  successive  diastoles,  he  could 
have  diagnosed  partial  heart-block. 

"  In  listening  for  the  sounds  produced  by  the  contracting  auricle  it  is 
important  to  rest  the  bell  of  the  stethoscope  as  lightly  as  possible  upon  the 
chest  wall.  They  are  best  heard  at  the  apex  or  over  the  tricuspid  area.  If 
one  bear  in  mind  the  fact  that  one  or,  with  very  fast  beating  auricles,  two 
beats  of  the  auricle  can  be  concealed  by  the  extraction  of  the  ventricle  it  may 
be  possible  to  state  exactly  the  degree  of  block,  whether  two  to  one,  three  to 
one,  or  four  to  one. 

"  We  have  encountered  a  number  of  cases,  however,  which  show  plainly 
the  pitfalls  to  be  avoided  in  the  diagnosis  of  heart-block.  The  most  common 
of  these  is  found  in  many  of  the  medical  students  taking  the  laboratory  work 
in  physiology — young  athletes  of  twenty  to  twenty-five,  whose  pulse  rates 
upon  lying  down  after  dinner  while  their  comrades  apply  the  polygraph  fall 
about  forty-five  per  minute.  Coincident  with  this  there  is  seen  an  extra 
wave  (the  h  wave  of  Hirschfelder,  b  wave  of  A.  G.  Gibson),  upon  the  venous 
pulse,  and  a  distant  ticking  sound  exactly  like  the  auricular  sound  in  heart- 
block  is  heard  over  the  heart.  This  is  merely  the  normal  third  heart  sound, 
whose  frequent  occurrence  has  been  so  well  described  by  Thayer.  Heart- 
block  can  be  excluded  by  simply  causing  the  subject  to  make  a  few  swift 
arm  movements,  which  will  accelerate  his  pulse  and  cause  the  third  heart 
sound  and  the  h  wave  to  disappear  at  once,  but  will  leave  a  partial  heart- 
block  unaffected  or  increased  in  degree.  During  the  current  year  we  encount- 
ered one  patient  with  a  heart  rate  of  44  per  minute ;  in  spite  of  the  most  careful 
observation  at  the  time  of  admission  we  were  unable  to  make  out  more  than 
one  sound  and  that  a  well-defined  third  sound  during  diastole.  The  next  day, 
however,  after  rest  in  bed,  the  ventricular  rate  had  fallen  a  little  and  in  about 


138  DISEASES  OF  THE  HEART  AND  AORTA. 

every  seventh  diastole  two  distant  ticking  sounds  could  be  made  out  and  the 
diagnosis  of  complete  heart-block  became  possible.  On  the  other  hand,  in  a 
patient  with  mitral  stenosis,  there  was  never  more  than  one  wavelet  between 
beats,  and  her  ventricular  rate  was  often  paired.  Corresponding  to  this  the 
venous  pulse  was  sometimes  double  and  sometimes  single.  The  most  likely 
diagnosis  in  this  case  seemed  to  be  extrasystoles  sometimes  auricular  and 
sometimes  ventricular,  a  disturbance  which  electrocardiographic  studies  have 
shown  to  be  of  very  common  occurrence. 

"  In  this  case,  however,  the  electrocardiograph  showed  us  that  we  were 
dealing  with  a  complete  heart-block  in  which  the  rate  of  the  ventricle  was 
almost  the  same  as  that  of  the  auricle,  so  that  at  the  time  of  the  single  pulsa- 
tion the  auricle  was  contracting  during  ventricular  systole.  This  condition 
could  scarcely  be  made  out  by  simple  methods  and  might  have  caused  some 
difficulty  upon  a  venous  tracing.  Had  we  suspected  the  heart-block,  however, 
we  might  have  obtained  more  satisfactory  data  by  accelerating  pulse  rate 
with  exercise.  The  sounds  of  extrasystoles  which  frequently  occur  in  the 
course  of  heart-block  should  not  be  confused  with  those  due  to  the  auricular 
systoles,  because,  as  is  well  known,  the  former  are  as  loud  as  the  sounds  of  the 
normal  beats  and  are  therefore  five  or  six  times  as  loud  as  the  sounds  of  the 
auricular  contractions.  This  is  well  shown  in  a  tracing  (Plate  XIII,  Fig.  10) 
taken  with  a  Lilienstein  cardiophone.  The  ventricular  sounds  are  shown  as 
1  and  2;  the  auricular  are  lettered  a.  Even  when  the  extrasystole  is  so  feeble 
that  it  does  not  open  the  aortic  valves  and  therefore  causes  no  pulse  wave 
and  gives  rise  to  only  a  single  heart  sound,  its  loudness  should  differentiate 
it  readily  from  the  auricular  sounds,  and  the  presence  of  the  large  character- 
istic wave  upon  the  jugular  pulse  should  certainly  do  so. 

"  These  represent  a  few  of  the  conditions  in  which  fairly  accurate  observa- 
tions and  trustworthy  inferences  can  be  made  by  the  ordinary  methods  with- 
out recourse  to  elaborate  apparatus,  though  it  is  desirable  to  control  them 
with  the  latter  wherever  possible.  However,  the  functional  analysis  of  cardiac 
arrhythmias  is  one  which  can  in  most  cases  be  made  by  the  general  practitioner 
almost  as  accurately  as  can  the  diagnosis  of  valvular  lesions,  and  it  should 
be  taught  to  the  student  along  with  the  latter  in  the  routine  courses  of  physical 

diagnosis." 

BIBLIOGRAPHY. 

For  general  discussion  of  alterations  of  cardiac  rhythm  the  reader  may  consult: 
Wenckebach,  K.   F.:  Die  Arhythmie  als  Ausdruck  bestimmter  Functionsstorungen  des 

Herzens,  Leipz.,  1903.    Les  irregularites  du  coeur,  Arch,  des  malad.  du  cceur,  Par., 

1908,  i,  65. 
Mackenzie,  J.:  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903.    New 

Methods  of  Studying  Affections  of  the  Heart,  Brit.  M.  J.,  Lond.,  1905,  i,  519,  587, 

702,  759,  812.    Diseases  of  the  Heart,  Lond.,  1908. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  Am.  Jour.  M.  Sc, 

Phila.,  1906,  cxxxii,  378.    Recent  Studies  upon  the  Circulation  and  their  Importance 

to  the  Practice  of  Medicine,  Jour.  Am.  M.  Assoc,  Chicago,  1908,  li,  473. 
Hewlett,  A.  W. :  Some  Common  Cardiac  Arrhythmias,  Internat.  Clin.,  Phila.,  1907,  17th 

ser.,  iv,  47. 
Gerhardt,  D. :  Die  Unregelmassigkeiten  des  Herzschlages,  Ergebn.  d.  innere  Med.,  Berl., 

1908,  ii,  418. 
Dock,  Geo. :  Recent  Advances  in  the  Study  of  Heart  Disease,  Wisconsin  M.  J.,  Aug.,  1907. 
Bard.  L.:  Des  divers  types  d'arhythmie  cardiaque  observes  en  clinique,  Sem.  m6d.,  Par., 

1909. 


PLATE  XIII. 


Fig.   1. — Card  held  against  the  skin  over  the  jug-  Fig.  2. — Same  with  vein  collapsed,  shadow  wide, 

ular  vein — vein  full,  shadow  between  the   skin  and        as  at  the  instant  of  the  x  and  y  depressions, 
card  is  narrow  at  the  instant  of  the   a  and  v  waves 
on   the  venous   pulse.       (Plate  from   the     Virginia 
Medical  Semi-Monthly,   1914,  xviii,  573.) 


^\>Vv^/VVvA/v 


■    ■        1    ■ ■_■ ■_! ■_■- 


Fig.  3. — Normal  double  venous  pulse.    The  black  bands  indicate  the  corresponding  waves  on  the  pulsation. 


a         a 


I    ■ 111! ■_■ l_X 

AE 
Fig.  4. — Venous  pulse  and  waves  of  an  auricular  extrasystole  (AE),  showing  "double"  venous  pulse. 


!_■    I  i 


1 


J_i Li 


VE 


Fig.  5. — Venous  pulse  with  ventricular  extrasystole  (VE),  showing  the  large  "single"  venous  pulse,  accom- 
panying the  extrasystole. 


PLATE  XIII    (Continued). 


■    ■■Ill 

Fig.  6. — Positive  "single"  venous  pulse  with  absolute  arrhythmia,  accompanying  ventricular  fibrillation. 


■         ■ 


Fig.  7. — Similar  "single"  venous  pulse  with  small  wavelets  due  to  auricular  flutter. 


Fig.  8.- 


-Venous  pulsation  in  partial  heart-block,  a  constant  number  of  small  auricular  waves,   two  in 
each  diastole,  occurring  between  the  larger  ventricular  waves. 


Fig.  9. — Venous  pulsation  in  complete  heart-block,  showing  a  varying  number  of  auricular  waves  in  suc- 
cessive diastoles. 


. -  .■•  i  ,    •■   ■  .■■....■■  ' 


•  :,,'■.,;  .'■  '...•:         '         , 


Fig.  10. — Tracing  of  heart  sounds  from  a  patient  with  complete  heart-block  and  ventricular  extra- 
systoles,  showing  the  very  low  auricular  sounds  (a)  in  contrast  to  the  louder  ventricular  sounds  (1,2)  which 
accompany  both  the  regular  beats  and  the  extrasystole  (VE). 


ALTERATIONS  IN  CARDIAC  RHYTHM.  139 

Hoffmann,  A.:  Ueber  die  klinische  Bedeutung  der  Herzarhythmie,  Deutsch.  med.  Wchn- 

schr.,  Leipz.,   1906,  xxxii,   1682.     Neuere  Fortschritte  in  der  Diagnostik  der  Herz- 

krankheiten,  Deutsch.  med.  Wchnschr.,  Leipz.,  1908,  xxxiv,  13. 
Hunt,  R. ;  Direct  and  Reflex  Acceleration  of  the  Mammalian  Heart,  Am.  J.  Physiol.,  Bost., 

1899,  h,  395. 
Hooker,  D.  R. :  May  Reflex  Cardiac  Acceleration  Occur  Independently  of  the  Cardio- 

inhibitory  Centre?     Ibid.,  1907,  xix,  417. 
Mackenzie,  J. :  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903. 
Frangois-Franck,  Ch.  A. :  Contribution  a  l'etude  experimental  des  nevroses  reflexes  d'ori- 

gine  nasale,  Arch,  de  physiol.  de  Phomme,  Par.,  1889,  5  ser.,  i,  538.     Contribution 

a  l'etude  de  l'innervation  vasodilatatrice  de  la  muqueuse,  ibid.,  1889,  i. 
Koblanck  and   Roeder,    H. :  Experimentelle   Untersuchungen  zur  reflektorischen   Herz- 
arhythmie, Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxv,  377. 
Stadler,  E.,  and  Hirsch,  C. :  Meteorismus  und  Kreislauf,  Mitth.  a.  d.  Grenzgeb.  d.  Med.  u. 

Chir.,  Jena,  1906,  xv,  449. 
Reyfisch:    Klinische  und  experimentelle  Erfahrungen  ueber  Reizungen  des  Herzvagus, 

Berl.  klin.  Wchnschr.,  1905,  1468. 
Reissner,  O. :  Ueber  unregelmassige  Herztatigkeit  auf  psychischer  Grundlage,  Ztschr.  f. 

khn.  Med.,  Berl.,  1904,  liii,  234. 
Einthoven,  W.,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A.:  On  Vagus  Currents  Examined  with 

the  String  Galvanometer,  Quart.  Jour.  Exper.  Physiol.,  Lond.,  1908,  i,  243. 
Eyster,  J.  A.  E. :  Clinical  and  Experimental  Observations  upon  Cheyne-Stokes  Respiration, 

Jour.  Exper.  M.,  New  York  and  Lancaster,  1906,  viii,  565. 
Kussmaul,  A.:  Ueber  schwieliege  Mediastino-pericarditis  und  paradoxen  Puis,  Berl.  khn. 

Wchnschr.,  1873,  x,  433,  445,  461. 
Riegel,  F. :  Ueber  extrapericardiale  Verwachsungen,  ibid.,  1877,  xiv,  657. 
Keith,  A.,  and  Flack,  and  Schonberg:  See  Chapter  I. 

Hewlett,  A.  W.:  Digitalis  Heart  Block,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  47. 
Erlanger,  J.,  and  Blackman,  J.  R. :  A  Study  of  the  Relative  Rhythmicity  and  Conductivity 

in  Various  Regions  of  the  Auricles  of  the  Mammalian  Heart,  Am.  J.  Physiol.,  Bost., 

1907,  xix,  125. 
Hoffmann,  Aug. :  See  chapter  on  Paroxysmal  Tachycardia. 
Hirschf elder,  A.  D.,  and  Eyster,  J.  A.  E.:  Extrasystoles  in  the  Mammalian  Heart,  Am.  J. 

Physiol.,  Bost.,  1907,  xviii,  222. 
Kraus,   Fr.,   and  Nikolai:  Ueber  das  Elektrokardiogramm  unter  normalen  und  patho- 

logischen  Verhaltnissen,  Berl.  klin.  Wochnschr.,  1907,  765,  811. 
Kahn,  R.  H. :  Ueber  das  Elektrokardiogramm  kimstlich  ausgeloster  Herzschlage  Zentralbl. 

f.  Physiol.,  Leipz.  and  Vienna,  1909,  xxiii,  444. 
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ii,  139. 
Biggs,  L.  N.  H.:  Investigation  of  the  Bundle  of  His  in  Rabbits'  Excised  Hearts  Perfused 

with  Locke's  Fluid,  Brit.  M.  J.,  Lond.,  1908,  i,  1419. 
Barker,  L.  F.,  and  Hirschfelder,  A.  D. :  The  Effects  of  Cutting  the  Branch  of  the  His  Bundle 

Going  to  the  Left  Ventricle,  Arch.  Int.  Med.,  Chicago,  1909,  iv,  193. 
Cohn,  A.  E.,  and  Trendelenburg,  W. :  Untersuchungen  zur  Physiologie  des  Uebergangs- 

bundels  am  Saugetierherzen   nebst  mikroskopische  Nachprufung,   Arch.  f.   d.   ges. 

Physiol.,  Bonn,  1910,  cxxxi,  1. 
Eppinger,  J.,  and  Rothberger,  J. :  Ueber  die  Folgen  der  Durchschneidung  der  Tawarascher 

Schenkel  des  Reizleitungssystems,  Ztschr.  f.  klin.  Med.,  Berl.,  1910,  lxx,  1. 
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Liege,  1907,  v,  122. 
Knoll,  Phihp:  Ueber  Incongruenz  in  der  Thatigkeit  der  beiden  Herzhalften,  Sitzungsb. 

d.  k.  Akad.  d.  Wissensch.  Math-naturw.  CI.,  Vienna,  1890,  xcix,  31-53,  6. 
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internat.  de  physiol.,  1906,  iv,  60. 
Stassen,  M.:  De  l'ordre  de  succession  des  differentes  phases  de  la  pulsation  cardiaque  chez 

le  chien,  Arch,  internat.  de  physiol.,  1907,  v,  600. 
Von  Leyden,  E.:  Ueber  ungleichzeitige  Kontraction  beider  Ventrikel,  Arch.  f.  path.  Anat., 

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Kraus,  F.,  and  Nicolai,  G.  F. :  Ueber  die  funktionelle  Sohdaritat  der  beiden  Herzhalften, 

Deutsche  med.  Wchnschr.,  1908,  xxxiv,  1. 


140  DISEASES  OF  THE  HEART  AND  AORTA. 

Aschoff,  L.,  and  Tawara,  S. :  See  chapter  on  Acute  Myocarditis. 

Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Johns  Hopkins  Hosp. 
Bull.,  Bait.,  1906,  xvii,  337. 

Hering,  H.  E.:  Ueber  Herzalternans,  Miinchen.  med.  Wochnschr.,  1908,  lv,  1417. 

Mackenzie,  J.:  See  chapter  on  Angina  Pectoris. 

Wenckebach,  K.  F.:  Beitrage  zur  Kenntniss  der  menschhchen  Herztatigkeit,  Arch.  f. 
Physiol.,  1906,  1907,  i. 

Lewis,  T. :  The  Experimental  Production  of  Paroxysmal  Tachycardia  and  the  Effects  of 
Ligation  of  the  Coronary  Arteries,  Heart,  Lond.,  1909-1910,  i,  98. 

Hirschfelder,  A.  D.:  The  Functional  Disturbances  in  Paroxysmal  Tachycardia,  Arch. 
Int.  Med.,  Chicago,  1910,  vi,  380.  Recent  Studies  upon  the  Electrocardiogram  and 
upon  the  Changes  in  the  Volume  of  the  Heart,  Interstate  M.  J.,  St.  Louis,  1911, 
xviii,  557. 

Bredig,  G.,  and  Wilke,  D.:  Erregung  und  Beeinflussung  katalytischer  Pulsationen  durch 
elektrische  Strome,  Bioc.  Ztschr.,  Berl.,  1908,  xi,  67. 

Lewis,  T.:  Galvanometric  Curves  Yielded  by  Cardiac  Beats  Generated  in  Various  Areas 
of  the  Auricular  Musculature,  the  Pace-maker  of  the  Heart,  Heart,  Lond.,  1910, 
ii,  23. 

Lewis,  T.,  Oppenheimer,  B.  S.,  and  Oppenheimer,  A. :  The  Site  of  Origin  of  the  Pace-maker 
of  the  Mammalian  Heart-beat;  The  Pace-maker  of  the  Dog,  ibid.,  1910,  ii,  147. 

Wybauw:  Sur  le  pointe  d'origine  de  la  systole  cardiaque  dans  l'oreillette  droite,  Arch, 
internat.  de  physiol.,  Liege,  1910,  x,  78. 

Rothberger,  C.  J.,  and  Winterberg,  H. :  Ueber  die  experimentelle  Erzeugung  extrasystolis. 
cher  Tachycardie  durch  Acceleransreinzung,  Zentralbl.  f.  Physiol.,  Leipz.  and  Wien 
1911,  xxv,  189,  and  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1911,  cxlii,  461. 

Engelmann:  Ueber  die  Leitung  der  Bewegungsreize  im  Herzen,  Arch.  f.  d.  ges.  Physiol., 
Bonn,  1894,  lvi,  149.    Ueber  die  Ursprung  der  Herzbewegungen,  ibid.,  lxv. 

Cushny,  A.  R.,  and  Matthews,  S.  A.:  On  the  Effects  of  Electrical  Stimulation  of  the  Mam- 
malian Heart,  Jour.  Physiol.,  Camb.,  1897,  xxi,  214. 

Hirschfelder,  A.  D.:  Inspection  of  the  Jugular  Vein;  its  Value  and  its  Limitations  in  Func- 
tional Diagnosis,  Jour.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  1105. 

Lewis,  T. :  Single  and  Successive  Extrasystoles,  Lancet,  Lond.,  1909,  i. 

Miiller,  Fr. :  Nervous  Affections  of  the  Heart,  Arch.  Int.  Med.,  Chicago,  1908,  i,  1. 

Mackenzie,  J.:  Diseases  of  the  Heart,  Lond.,  1908. 

Knoll,  Ph.:  Ueber  die  Veranderungen  des  Herzschlages  bei  reflectorischer  Erregung  des 
vasomotorischen  Nervensystems,  sowie  bei  Steigerung  des  intracardialen  Drucks 
liberhaupt,  Sitzungsber.  d.  k.  Akad.  d.  Wissensch.,  Wien,  Abth.  Ill,  1872,  lxv-lxvi,  195. 

Marey:  La  circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Par.,  1881. 

Hering,  H.  E. :  Zur  experimentellen  Analyse  des  unregelmassigen  Herzschalges,  Arch.  f. 
d.  ges.  Physiol.,  Bonn,  1900,  lxxxii.  Ueber  continuierliche  Herzbigeminie,  Deutsch. 
Arch.  f.  klin.  Med.,  Leipz.,  1904,  lxxix,  175.  Ergebnisse  experimenteller  und  klinischer 
Untersuchungen  ueber  den  Vorhofvenenpuls  bei  Extrasystolen,  Ztschr.  f.  exper.  Path, 
u.  Therap.,  Berl.,  1905,  i,  26;  also  his  pupils. 

Rihl,  J.:  Experimentelle  Analyse  des  Venenpulses  bei  den  durch  Extrasystolen  verur- 
sachten  Unregelmassigkeiten  des  Saugethierherzens,  ibid.,  1905,  i,  43. 

Pan,  O. :  Ueber  das  Verhalten  des  Venenpulses  bei  den  durch  Extrasystolen  verursachten 
Unregelmassigkeiten  des  menschhchen  Herzens,  ibid.,  1905,  i,  56. 

Hirschfelder,  A.  D. :  The  Volume  Curve  of  the  Ventricles  in  Experimental  Mitral  Stenosis 
and  Its  Relation  to  Physical  Signs,  Johns  Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  319. 

Mackenzie,  J.:  The  Extrasystole,  Quart.  J.  M.,  Oxford,  1908,  i,  481. 

Gerhardt,  D.:  Beitrag  zur  Lehre  von  den  Extrasystolen,  Deutsch.  Arch.  f.  klin.  Med., 
Leipz.,  1905,  lxxxii,  509. 

Hoffmann,  Aug.:  Arhythmie  des  Herzens,  Deutsch.  med.  Wchnschr.,  Leipz.,  1906,  xxxii, 
1682.  Ueber  die  Entstehung  der  Extrasystolenirregularitat,  Miinchen.  med.  Wchn- 
schr., 1907,  liii,  1987. 

Dehio,  K. :  Einfluss  des  Atropins  auf  arhythmische  Herztatigkeit,  Deutsch.  Arch,  f .  klin. 
Med.,  Leipz.,  1894,  hi,  97. 

Hering,  H.  E. :  Experimentelle  Untersuchungen  ueber  Herzunregelmassigkeiten  an  Affen, 
Ztschr.  f.  exper.  Path.  u.  Therap.,  Berl.,  1906,  ii,  525. 

Hering,  H.  E.,  and  Rihl,  J.:  Ueber  atrioventrikulare  Extrasystolen,  ibid.,  1906,  ii,  510. 


ALTERATIONS  IN  CARDIAC  RHYTHM.  141 

Gaskell,  W.  H.:  The  Properties  of  Cardiac  Muscle,  Schafer's  Text-book  of  Physiology, 

Lond.,  1900,  ii. 
Lohmann,  A.:  Zur  Automatic  der  Bnickenfasern  des  Herzens,  Arch.  f.  Physiol.,  Leipz., 
1904,  431;  and  Supplbd.,  265.     Ueber  der  Funktion  der  Bruckenfasern  an  Stelle  der 
grossen  Venen  die  Fiihrung  der  Herztatigkeit  beim  Saugetiere  zu  ubernehmen,  Arch. 
f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxiii,  628. 
Mackenzie,  J. :  Inception  of  the  Rhythm  of  the  Heart  by  the  Ventricles,  Brit.  M.  J.,  Lond., 
1904,  i,  529.     Abnormal  Inception  of  the  Cardiac  Rhythm,  Quart.  J.  M.,  Oxford, 
1907,  i,  39. 
Mackenzie,  J.,  and  Wenckebach,  K.  F. :  Ueber  an  der  Atrioventrikulargrenze  ausgeloste 

Systolen  beim  Menschen,  Arch.  f.  Physiol.,  Leipz.,  1905. 
Rothberger,  J.,  and  Winterberg,  H. :  Ueber  die  Beziehungen  der  Herznerven  zur  atrioven- 

tricularen  Automatie  (nodal  rhythm),  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1910,  cxxxv,  559. 
Schmoll,  E. :  Paroxysmal  Tachycardia,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1907,  cxxxiv,  662. 
Mackenzie,  R.,  and  Morrow,  W.  S.:  Cardiac  Arrhythmia  due  to  Extrasystoles  Originating 

in  the  Bundle  of  His,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1908,  cxxxv,  534. 
Cushny,  A.  R. :  See  chapter  on  the  Action  of  Drugs. 
Hering,  H.  E. :  Ueber  die  haufige  Kombination  von  Kammervenenpuls  mit  Pulsus  irregularis 

perpetuus,  Deutsch.  med.  Wchnschr.,  Leipz.,  1906,  213. 
Gerhard't,   D. :  Arhythmia  perpetua  des  Puis,   Deutsch.  med.  Wchnschr.,   Leipz.,   1907, 

xxxiii,  448. 
Hewlett,  A.  W. :  On  the  Interpretation  of  the  Positive  Venous  Pulse.  J.  M.  Research,  1907- 

1908,  xvii,  119.     Clinical  Observations  on  Absolutely  Irregular   Hearts,  J.  Am.  M. 

Assoc,  Chicago,  1903,  li,  655. 
Theopold,  J.:  Ein  Beitrag  zur  Lehre  von  der  Arhythmia  perpetua,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1907,  xc,  77. 
Hering,  H.  E.:  Das  Elektrocardiogramm  des  Pulsus  irregularis  perpetuus,    ibid.,   1908, 

xciv,  205. 
Mackenzie,  J. :  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Edinb.  and  Lond., 

1902;  Diseases  of  the  Heart,  2d  Ed.,  N.  Y.,  1910. 
Clerc,  A.,  and  Esmein,  Ch.:  Etude  critique  de  la  pulsation  cesophagienne  chex  l'homme, 

Arch,  de  mal.  d.  cceur,  etc.,  Par.,  1910,  iii,  1. 
Lewis,  T. :  Auricular  Fibrillation:  A  Common -Clinical  Condition,  Brit.  M.  J.,  Lond.,  1909, 

ii,  1528;  Auricular  Fibrillation,  Heart,  Lond.,  1910,  i,  306. 
Rothberger,  J.,  and  Winterberg,  H.:  Vorhofflimmern  und  Arythmia  perpetua,  Wien.  klin. 

Wchnschr.,  1909,  xxii,  1091. 
Winterberg,  H. :  Studien  iiber  Herzflimmern,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxviii, 

471. 
Radasewsky:  See  chapter  on  Chronic  Myocarditis.     Ueber  die  Muskelkrankungen  der 

Vorhofe  des  Herzens,  Ztschr.  f.  klin.  Med.,  Berl.,  xxvii. 
Schonberg,  S. :  Ueber  Veranderungen  im  Sinusgebiete  des  Herzens  bei  chronischer  Arhyth- 

mie,  Frankf.  Ztschr.  f.  Path.,  1908,  ii,  153. 
M tiller,    G. :  Ungewohnliche   Dilatation  des    Herzens  und  Ausfall  der  Vorhofsfunktion, 

Ztschr.  f.  klin.  Med.,  Berl.,  lvi,  520. 
Quincke,  and  Hochhaus,  J.:  Ueber  frustrane  Herzcontractionen,  Deutsch.  Arch.  f.   klin. 

Med.,  Leipz.,  1894,  liii,  414. 
James,  W. :  Clinical  Study  of  Some  Arrhythmias  of  the  Heart,  Am.  Jour.  M.  Sc,   Phila. 

and  N.  York,  1908,  cxxxvi,  469. 
Hirschfelder,  A.  D. :  Contributions  to  the  Study  of  Auricular  Fibrillation,  Paroxysmal 

Tachycardia,    and   the   So-called  Auriculo-  (Atrio-)  ventricular   Extrasystoles,    Johns 

Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  322. 
Hoffmann,  A. :  Neue  Beobachtungen  ueber  Herzjagen,  Deutsch.  Arch.  f.  klin.  Med.,  1903, 

lxxviii,  39. 
Cushny,  A.  R.,  and  Edmunds,  C.  W. :  Paroxysmal  Irregularity  of  the  Heart  and  Auricular 

Fibrillation,  Am.  Jour.  M.  Sc,  Phila.,  1907,  cxxxhi,  66;  and  Studies  in  Pathology, 

Quatercentenary  Public,  Aberdeen  Univ. 
Engelmann,  1.  c 
Trendelenburg,  W. :  Untersuchungen  ueber  das  Verhalten  des  Herzmuskels  bei  rhythm- 

ischer  elektrischer  Reizung,  Arch.  f.  Physiol.,  Leipz.,  1903,  271. 
Ritchie,  W.  T.:  Auricular  Flutter,  Edinb.  and  Lond.,  1914. 


142  DISEASES  OF  THE  HEART  AND  AORTA. 

Hirschfelder,  1.  c,  Fibrillar  Contraction  of  the  Heart,  J.  Physiol.,  1887,  viii,  296. 
Lewis,  T. :  The  Mechanism  of  the  Heart-Beat,  Lond. 

Paroxysmal  Tachycardia. 
Bouveret,  L.:  De  la  tachycardie  paroxystique  essentielle,  Rev.  de  Med.,  Far.,  1889,  ix, 

753,  836. 
Hoffmann,  Aug.:  Die  parozysmale  Tachycardie   (Anfalle  von  Herzjagen),  Wiesb.,   1900. 

Pathologie  und  Therapie  der  Herzneurosen,  u.s.w.,  Wiesb.,  1901.    Neue  Beobachtungen 

ueber  Herzjagen,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1903,  lxxviii,  39.     Ueber  Ver- 

doppelung  der  Herzfrequenz,  Ztschr.  f.  klin.  Med.,  Berl.,  1904,  liii,  206. 
Rihl,  J.:  Analyse  von  fiinf  Fallen  von  Ueberleitungstorungen,  Ztschr.  f.  exp.  Path.  u. 

Therap.,  Berl.,  1905,  ii,  83. 
Schmoll,  E.:  Paroxysmal  Tachycardia,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1907,  cxxxiv,  662. 
Mackenzie,  J.:  On  the  Inception  of  the  Rhythm  of  the  Heart  by  the  Ventricles,  Brit.  M.  J., 

Lond.,  1904,  i,  529.    New  Methods  in  the  Study  of  Affections  of  the  Heart,  ibid.,  1905, 

i,  813.    Abnormal  Inception  of  the  Cardiac  Rhythm,  Quart.  M.  J.,  Oxford,  1S07,  i,  39. 

The  Extrasystole :  A  Contribution  to  the  Functional  Pathology  of  the  Primitive  Cardiac 

Tissue,  ibid.,  1908,  i,  182  and  481.    Diseases  of  the  Heart,  Lond.,  1908. 
Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Bull.  Johns  Hopkins 

Hosp.,  Bait.,  1906,  xvii,  337. 
Hay,  J.:  Paroxysmal  Tachycardia,  Edinb.  M.  J.,  1907,  N.  S.  xxi,  40. 
Peabody,  F.  W.:  A  Note  on  the  Venous  Pulse  in  Paroxysmal  Tachycardia,  Arch.  Int.  Med., 

Chicago,  1909,  iv,  432. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttg.,  1906. 

The  complete  bibliography  of  cases  will  be  found  in  the  monograph  of  Hoffmann  and 

the  articles  of  Reinhold,  Schlesinger,  and  Schmoll. 
Gerhardt,  D.:  Beitrage  zur  Lehre  von  den  Extrasystolen,  Deutsch.  Arch.  f.  klin.  Med., 

Leipz.,  1905,  lxxxvii,  509. 
Lommel,  F.:  ibid.,  1905,  lxxxii,  495. 
Bayliss,  W.  M.,  and  Starling,  E.  H.:  On  Some  Points  in  the  Innervation  of  the  Mammalian 

Heart,  J.  Physiol.,  Camb.,  1892,  xiii,  407. 
Gaskell,  W.  H. :  Schaefer's  Text-book  of  Physiology,  Edinb.  and  Lond.,  1900,  ii. 
Lohmann,  A.:  Zur  Automatie  der  Bruckenfasern  des  Herzens,  Arch.  f.  Physiol.,  Leipz., 

1904,  431,  and  Suppl.,  265. 
Hering,  H.  E.,  and  Rihl,  J.:  Ueber  atrioventrikulare  Extrasystolen,  Ztschr.  f.  exp.  Path. 

u.  Therap.,  Berl.,  1906,  ii,  510.    Experimentelle  Untersuchungen  ueber  Herzunregel- 

massigkeiten  an  Affen,  ibid.,  1906,  ii,  525. 
Hirschfelder,   A.  D.:  The   Functional   Disturbances  in   Paroxysmal   Tachycardia,    Arch. 

Int.    Med.,  Chicago,  1910,    vi,    380;    Recent    Studies    upon    the    Electrocardiogram 

and  upon  the  Changes  in  the  Volume  of  the   Heart,    Interstate   M.   J.,    St.    Louis, 

1911,  xviii,  557. 
Lewis,  T.,  and  Silberberg,  M.  D. :  Paroxysmal  Tachycardia  Accompanied  by  the  Ventricular 

Form  of  Venous  Pulse,  Quart.  J.  M.,  Oxford,  1911,  v,  5. 
Lewis,  T.,  and  Schleiter,  H.  G.:  The  Relation  of  Regular  Tachycardias  of  Auricular  Origin 

to  Auricular  Fibrillation,  Heart,  Lond.,  1912,  iii,  173. 
Agassiz,  C.  D.  S.:  Paroxysmal  Tachycardia  Accompanied  by  the    Ventricular  Form  of 

Venous  Pulse,  ibid.,  1912,  iii,  193. 
Hoffmann,  A. :  Fibrillation  of  the  Ventricles  at  the  End  of  an  Attack  of  Paroxysmal  Tachy- 
cardia in  Man,  ibid.,  iii,  213. 
Hirschfelder,  A.  D.:  Contributions  to  the  Study  of  Auricular  Fibrillation,  Paroxysmal 

Tachycardia,   and  the  so-called  Auriculo-   (atrio-)   ventricular  Extrasystoles,   Bull. 

Johns  Hopkins  Hosp.,  Bait.,  1908,  xix,  323. 
Cushny,  A.  R.,  and  Edmunds,  C.  W.:  Paroxysmal  Irregularity  of  the  Heart  and  Auricular 

Fibrillation,  Am.  J.  M.  Sc,  Phila.  and  N.  Y.,  1907,  cxxxiii,  66.    Studies  in  Pathology, 

Quart.  Publ.,  Aberdeen  Univ.,  1907. 
Hunt,  R. :  Direct  and  Reflex  Accelerations  of  the  Mammalian  Heart,  Am.  J.  Physiol.,  Bost,, 

1899,  ii,  395. 
Garrey,  W.  E.:  Effect  of  Chemicals  on  the  Heart  Nerves,  Calif.  State  M.  J.,  San  Francisco, 

1907.    Some  Effects  of  Cardiac  Nerves  upon  Ventricular  Fibrillation,  Am.  J.  Physiol., 

Bost.,  1908,  xxi,  283. 


ALTERATIONS  IN  CARDIAC  RHYTHM.  143 

Henderson,  Y.  (with  the  collaboration  of  M.  McR.  Scarborough  and  F.  P.  Chillingworth) 
The  Volume  Curve  of  the  Ventricles  of  the  Mammalian  Heart,  etc.,  Am.  J.  Physiol.. 
Bost.,  1900,  xvi,  325. 

Lyon,  I.  P.:  Personal  communication. 

Pribram,  A.:  Wien.  med.  Presse,  1882.     Quoted  from  Bouveret. 

Dietlen,  H. :  Orthodiagraphische  Beobachtungen  ueber  Veranderungen  der  Herzgrosse 
bei  Infektionskrankheiten,  exsudativer  Perikarditis  und  paroxysmaler  Tachykardie, 
Miinchen.  med.  Wchnschr.,  1908,  lv,  2077. 

Nothnagel.    Quoted  from  Bouveret. 

Fairbrother,  H.  C:  A  Remedy  for  Paroxysmal  Tachycardia,  J.  Am.  M.  Asso.,  Chicago, 
1909,  liii,  300. 

Herz,  M.:  Ein  Kunstgriff  zur  Unterdriickung  der  Anfalle  von  Angina  Pectoris  und  paroxys- 
maler Tachykardie,  Wien.  klin.  Wchnschr.,  1908,  xxi,  803. 

Bensen:  Berl.  klin.  Wchnschr.,  1880. 


VI. 

X-RAY  EXAMINATION. 

The  discovery  of  the  X-rays  by  Rontgen  in  1895  introduced  a  new 
era  in  cardiac  diagnosis.  By  this  means  we  can  now  actually  see  the  heart, 
observe  its  outlines  with  accuracy,  and  note  the  changes  of  position  and 
of  contour  with  different  phases  of  respiration,  and  even  to  a  certain  extent 
the  changes  from  systole  to  diastole.  All  these  data,  when  obtained  with 
proper  precautions,  are  absolutely  accurate,  and  have  greatly  supplemented 
the  observations  made  by  percussion.1 

METHODS    OF    EXAMINATION. 

Most  of  the  facts  desired  in  the  study  of  the  circulatory  system  with 
the  X-ray  may  be  gained  by  means  of  inspection  with  the  fluoroscope, 
a  screen  of  barium  platinocyanide  or  calcium  tungstate  which  is  rendered 
luminous  wherever  the  X-rays  strike  it. 

A  tube  of  low  vacuum  ("soft  tube")  should  be  used,  one 
which  shows  the  bones  of  the  hand  black  without  re- 
vealing their  internal  structure,  and  the  tissues  of  the  hand  a 
fairly  dark  gray.  The  patient's  chest  wall  should  be  at  least  50  cm.  from 
the  screen.  Recently  the  usual  distance  has  been  increased  to  2  M.  (6 J 
ft.),  at  which  the  rays  are  almost  parallel. 

It  is  sometimes  best  to  interpose  a  lead  screen,  with  adjustable  opening,  between  the 
patient  and  the  tube  in  order  to  cut  off  all  the  rays  except  those  emanating  from  a  small 
part  of  the  anticathode,  thereby  securing  the  greatest  possible  definition  of  focus.  Indeed, 
Immelmann  found  greatest  definition  when  the  opening  in  the  lead  screen  was  only  1  cm. 
Often  a  lead  cylinder  (Albers-Schoenberg)  is  very  satisfactory.  It  is  also  important  that 
no  large  objects  be  placed  near  the  cathode,  as  rays  striking  these  may  also  generate 
secondary  rays  which  affect  the  fluoroscope  or  photographic  plate  and  thus  blur  the  outline 
of  the  original  image  (Walter).  For  securing  sharp  images  it  is  preferable  to  keep  a 
number  of  tubes  with  vacua  of  different  degrees  which  may  be  interchanged,  rather  than 
change  the  vacuum  in  each  tube.  Changing  the  latter  shortens  the  life  of  the  tube  by 
heating  the  platinum  target  and  causing  the  latter  ultimately  to  become  bent,  so  that  the 
rays  are  not  reflected  uniformly  from  its  surface. 

The  X-ray  image  is  a  true  shadow  formed  by  the  cutting  off  of  rays 
and  not  by  their  refraction,  and  the  shadow  is  magnified  in  proportion  as 
the  object  is  nearer  to  the  tube  or  farther  from  the  fluoroscopic  screen. 

1  Examinations  with  the  X-ray  require  a  very  special  technic,  for  which  the  student 
is  advised  to  consult  the  special  text-books  upon  the  subject,  especially: 

Albers-Schoenberg:  Die  Rontgentechnik,  Hamburg,  1906. 

Gocht,  H.:  Handbuch  der  Rontgenlehre  zum  Gebrauche  fur  Mediziner,  2te  Aufl., 
Stuttgart,   1903. 

Williams,  F.  H.:  The  Rontgen  Rays  in  Medicine  and  Surgery,  New  York,  1903. 

Beck,  C:  Rontgen-ray  Diagnosis  and  Therapy. 

Kassabian:  Rontgen  Rays  and  Electro-Therapeutics,  Phila.,  1909. 

i44 


X-RAY   EXAMINATION.  145 

In  fluoroscopic  examination  it  is  most  important  for  the  observer  to  accustom  his 
eyes  to  the  darkness  before  turning  on  the  current.  It  is  a  well-proved  physiological  fact 
that  the  longer  the  sojourn  in  darkness  the  greater  the  delicacy  of  vision.  Hence  the  exami- 
ner's vision  is  improved  by  closing  or  blindfolding  his  eyes  or  by  going  into  a  dark  room 
some  ten  or  fifteen  minutes  before  the  patient;  and  the  examining  room  should  be  lighted 
only  enough  to  permit  the  patient  to  undress  and  assume  the  proper  position.  The  exami- 
ner may  also  keep  his  head  under  a  dark  hood  or  wear  heavily  smoked  glasses  during  this 
time  so  as  to  accustom  his  eyes  to  the  darkness. 

In  looking  over  the  areas  of  light  and  shadows  each  region  should  be 
studied  carefully  and  in  detail,  the  size  and  shape  of  the  shadow,  the  clear- 
ness of  the  outline,  and  the  distribution  of  areas  of  half  shadows  as  well  as 
of  full  shadows.  Not  of  least  importance  are  the  so-called  pulmonary 
figures,  the  half-tone  shadows  of  pulmonary  vessels,  of  bronchial  glands, 
and  of  strands  of  adhesions.1  Not  only  the  full  shadows  but  especially 
these  half  shadows  should  be  examined  with  care,  for  an  interpretation 
not  apparent  at  first  may  become  clear  after  a  few  minutes'  observation. 

Radiographers  are,  moreover,  in  the  habit  of  looking  at  the  fluoroscope  through  half- 
closed  eyes  in  order  to  intensify  the  contrast.  This  may  be  further  intensified  by  the  use 
of  dark  glasses.  The  writer  has  also  found  it  very  useful  to  look  at  the  shadow  or  skiagraph 
through  a  biconcave  lens  which  at  once  sharpens  the  contours  and  intensifies  the  contrasts. 

Often  an  area  may  be  indefinite  during  quiet  breath- 
ing or  expiration  and  become  quite  definite  on  forced 
deep  inspiration,  or  it  may  become  so  by  simply  turning 
the  patient  so  that  the  rays  pass  through  his  body  in 
a  different  direction.  These  and  similar  precautions,  like  a  care- 
ful physical  examination,  reveal  the 
unsuspected,  and  distinguish  the 
skilled  examiner  from  the  unskilled. 

The  Cardiac  Shadow. — The  heart 
shadow  thrown  upon  a  screen  at  the 
front  of  the  chest  is  shown  in  Fig.  81a. 
It  will  be  noted  that  the  outline  of 
the  shadow  closely  resembles  the 
area  of  relative  dulness  on  percus- 
sion, except  that  the  former  extends 
upward  over  the  manubrium  sterni, 
where  it  is  due  to  the  presence  of 

the     latter    and    Of     the    great    Vessels  Fig.  81— Radiograph  of  normal  chest.     (After 

1         jfj-ii  j-Tii'  i         v.  Ziemmsen  and  Rieder.)     Tube  behind  the  chest 

and  not  ot  the  heart.    In  the  second      piate  in  front. 

left    interspace    the    shadow 

of    the    pulmonary    artery    is    seen,   and   in    the   second   right 

that    of    the    aorta.     Occasionally  a  small  prominence  is  seen  to  the  left 

of  the  sternum  arising  at  the  arch  of  the  aorta.     This  is  sometimes  mistaken 

for  an  aneurism,  but  if  the  patient  be  turned  a  little  it  will  be  seen  to  be 

due  to  the   curving  of   the  aorta  (Holzknecht). 

Oblique  Illuminations. — Much  can  be  learned  by  turning  the  patient 
about  and  examining  him  in  several  planes,  as  was  first  performed 
by  v.  Criegern  and  Holzknecht  (1.  c),  and  later  by  Rieder,  who  suggested  the 

10  '  See  chapter  on  Adherent  Pericardium. 


146 


DISEASES  OF  THE  HEART  AND  AORTA. 


following  cardinal  directions  (Fig.  81a)  :  (1)  dorso ventral ;  (2)  ventrodorsal; 
(3)  sagittal  from  right;  (4)  sagittal  from  left;  (5)  from  right  posterior  to 
left  anterior;  (6)  from  left  posterior  to  right  anterior;  (7)  from  left  anterior 
to  right  posterior;   (8)  from  right  anterior  to  left  posterior. 


PCAPHRAG'M  '.'.- 
"•      1. 
1 


i 


Fig.  81o. — X-ray  shadows  in  different  axes  of  the  body.  (Modified  from  Holzknecht.)  The 
arrows  show  the  direction  of  illumination  and  position  of  the  tube  corresponding  to  the  shadow. 
AO,  aorta;  PA,  pulmonary  artery;  LA,  left  auricle;  RA,  right  auricle;  LV,  left  ventricle;  RV,  right 
ventricle.    In  3  there  is  a  metal  sound  in  the  oesophagus. 


By  the  examination  in  these  planes  every  part  of  the  heart  can  be 
brought  into  view,  even  the  left  auricle,  which  escapes  observation  in  almost 
all  other  methods  of  examination  but  appears  quite  clearly  when  the  tube 
is  placed  at  the  back  or  behind  the  right  scapula.  The  oblique  and  trans- 
verse examinations  should  never  be  omitted. 


X-RAY  EXAMINATION. 


147 


THE    ORTHODIAGRAPH. 

The   shadow  of  the  heart  and  vessels  upon  the  screen  or  plate  is 
always    larger  than  the   objects  themselves.     In   order  to   obviate   this 

when  measuring  out  the  heart  F. 
Moritz  devised  an  instrument  known 
as  the  orthodiagraph  (Fig.  82). 


Fig.  82.- 


-A  simple  form  of  orthodiagraph. 
(After  Gillet.) 


Fig.  83. — Diagram  showing  the  use  of  the  ortho- 
diagraph. 1,  first  position;  2,  second  position;  P, 
pencil;   FLUOR,  fluorescent  screen. 


In  the  orthodiagraph  the  fluorescent  screen  and  X-ray  tube  are  fixed  upon  each  arm 
of  a  large  ^/-shaped  frame  in  such  a  way  that  the  patient  may  stand  or  he  between  the 
two  arms  of  the  U  and  the  rays  thus 
pass  through  his  body  to  the  screen. 
At  the  point  upon  the  screen  which  is 
exactly  opposite  to  the  centre  of  the 
anticathode  or  target  of  the  tube,  a 
small  hole  is  pierced,  and  a  skin  pencil 
is  fixed  in  place  here  so  that  the  site  of 
this  spot  can  be  marked  upon  the  body 
of  the  patient.  The  whole  [/-shaped 
frame  bearing  the  tube  and  fluoroscope 
is  movable  in  two  directions  by  any 
one  of  a  variety  of  mechanisms,  so  that 
the  perpendicular  ray  can  be  brought 
opposite  any  desired  point.  A  series  of 
points  corresponding  to  the  exact  con- 
tour can  thus  be  marked  off,  and  when 
these  are  joined  with  lines  the  exact 
outline  of  the  heart  is  repre- 
sented. As  shown  by  Fig.  83,  this 
furnishes  a  means  of  determining  the 
size  of  the  heart  or  any  organ  with 
absolute  accuracy. 

The  outlines  and  mobility  of  the  heart  thus  obtained  are  discussed 
on  page  160. 

It  is  also  possible  with  the  fluoroscope  to  watch  the  individual  con- 
tractions of  the  heart  and  to  note  the  changes  in  size  due  to  systole  and 


Fig.  84. — Orthodiagraphy  outline  of  normal  heart, 
showing  Moritz's  conjugates.  MR,  midline  to  right 
border  (greatest  distance);  ML,  midline  to  left  border; 
L,  oblique  longitudinal;  Q,  transverse;  numerals  indi- 
cate centimetres. 


148  DISEASES  OF  THE  HEART  AND  AORTA. 

diastole,  but  this  is  very  difficult  and  can  rarely  be  done  with  satisfactory 
accuracy.  On  the  other  hand,  the  contractions  of  the  auricles  can  be  seen 
with  considerable  definiteness,  and  dissociation  of  rhythm, 
heart-block,  can  often  be  diagnosed  in  this  way 
by   simple   inspection    (Kraus,    Gibson). 

PERMANENT  RADIOGRAPHS. 

For  obtaining  permanent  photographs  a  "  medium  soft "  tube  (Moritz 
scale  W  6  B  W  5)  is  used  in  connection  with  a  Wehnelt  electrolytic  inter- 
rupter and  an  induction  coil  with  proper  self-induction  yielding  a  40  to  60 
cm.  spark.  The  patient  is  laid  upon  a  table  with  the  tube  above  or  below 
him,  as  is  most  suitable  to  the  purpose  of  the  examination.  In  order  to 
absolutely  immobilize  him  it  is  well  to  support  the  shoulders  upon  sand 
bags.  He  may  also  be  examined  standing  by  immobilizing  the  shoulders 
to  prevent  blurring  of  the  picture.  Skiagraphs  of  the  chest  made  with  very 
short  exposures  have  proved  particularly  valuable,  since  they  give  greater 
definition  (Rieder). 

Teleroentgenography. — Recently  the  need  for  the  orthodiagraph  nas  been 
obviated  to  a  great  extent  by  taking  permanent  radiographs  at  a  distance  of 
150  to  200  cm.  from  the  patient,  in  which  the  rays  are  so  nearly  parallel  that 
the  shadow  of  the  heart  is  never  more  than  5  mm.  larger  than  the  heart  itself, 
and  the  individual  borders  are  not  displaced  more  than  the  thickness  of  an 
ordinary  chalk  line  (2  mm.)  (Koehler).  Such  radiographs  are,  of  course,  much 
more  objective  records  and  preserve  many  more  details  than  are  furnished  by 
the  orthodiagraphic  outlines,  and  are  in  this  respect  much  more  valuable,  and 
the  need  of  an  expensive  and  cumbersome  apparatus  is  also  removed. 

If  satisfactory  pictures  are  not  obtained  in  this  way,  it  may  be  necessary 
to  back  the  plates  with  an  "  intensifying  screen  "  (Verstarkungsschirm)  of 
calcium  tungstate,  etc.,  exactly  similar  to  the  screen  of  the  fluoroscope,  which 
intensifies  the  action  of  the  rays  upon  the  plate.  By  the  use  of  such  intensi- 
fying screens  it  has  been  possible  to  obtain  satisfactory  radiographs  of  the 
thorax  with  exposures  of  1/10  to  1/20  sec.  (Rieder  and  Rosenthal)  or  even 
1/100  sec.  (Dessauer).  Dessauer  has  found  that  these  can  be  made  if  the 
tube  is  strongly  illuminated  (anticathode  red)  before  the  plate  is  exposed, 
especially  if  an  unusually  large  anticathode  is  placed  in  the  tube.  The  expo- 
sure takes  place  through  a  slit  in  a  lead  disk  which  is  rapidly  rotated  by  a 
motor  in  front  of  the  plate. 

Weber  has  devised  an  apparatus  whereby  such  instantaneous 
photographs  may  be  taken  at  any  given  phase  of  the 
cardiac  cycle,  and  has  obtained  very  interesting  pictures  in  this  way. 

His  method  for  obtaining  this  instant  in  the  cycle,  which  depends  upon 
the  use  of  a  selenium  cell,  is  very  elaborate  and  cumbersome,  and  a  much 
simpler  and  more  satisfactory  solution  of  the  same  problem  can  be  obtained 
by  using  a  slight  modification  of  the  apparatus  devised  by  Hirschfelder  and 
Eyster  for  obtaining  a  series  of  induction  shocks  at  exactly  the  same  phase  of 
the  cardiac  cycle. 

This  apparatus  consists  of  two  parts,  the  first  being  a  sphygmograph  tambour  arranged 
to  give  an  electric  contact  when  its  lever  is  lifted  in  systole,  and  the  second  consisting  of  a 


X-RAY  EXAMINATION.  149 

clockwork  device  arranged  to  rotate  for  a  definite  period  after  the  sphygmograph  contact 
has  been  made,  after  which  it  sets  off  a  second  electric  contact  operating  either  the  X-ray 
coil  or  a  shutter  in  front  of  it  so  as  to  give  an  instantaneous  exposure  at  the  instant  desired. 

The  first  part  of  the  apparatus  differs  somewhat  from  the  original  apparatus  of  Hirsch- 
felder  and  Eyster  in  the  manner  in  which  the  contact  is  made,  for  in  their  experiments 
systole  was  recorded  by  the  downstroke  of  the  lever,  which  was  allowed  to  dip  into  a  pan 
of  mercury,  while  in  the  clinical  sphygmographs  systole  is  recorded  by  an  upstroke.  In 
order  to  use  the  clinical  sphygmograph  or  the  ordinary  tambour  for  this  purpose,  one  of 
the  bright  metal  parts  should  be  well  wrapped  with  the  end  of  an  elsewhere  insulated  copper 
wire  to  be  used  in  the  circuit.  The  second  contact  consists  of  a  piece  of  platinum  wire  or 
foil  which  is  bent  in  such  a  way  that  when  mounted  and  fastened  upon  the  sphygmograph 
by  means  of  thread  or  rubber  bands  the  sphygmograph  lever  will  just  touch  it  on  the  up- 
stroke and  leave  it  on  the  downstroke.  This  contact  should  be  insulated  from  the  metal 
parts  of  the  tambour  by  interposing  a  piece  of  paper,  fibre  or  rubber,  and  it  should  be  con- 
nected with  a  piece  of  insulated  copper  wire  so  that  the  upstroke  of  the  lever  may  close  a 
circuit  through  the  two  wires  leading  from  the  tambour,  while  the  downstroke  breaks  it. 

The  second  or  clockwork  part  of  the  apparatus  consists  of  a  set  of  wheels  driven  by 
a  spring  in  the  usual  manner.  One  of  these  wheels  bears  a  small  outrigger  which  is  caught 
by  the  lever  from  an  electromagnet  when  the  circuit  through  the  latter  is  open,  and  released 
when  the  lever  is  moved  by  closing  the  circuit.  When  this  magnet  is  connected  with  the 
wires  from  the  sphygmograph  tambour  this  represents  the  instant  of  systole.  Upon  the 
axle  of  the  same  wheel  or  a  second  wheel  of  the  clockwork  there  is  set  an  arm  bearing  a 
platinum  wire  which  is  just  long  enough  to  dip  into  a  small  pan  of  mercury  fixed  to  the 
base-board  but  insulated  from  it.  The  arm  is  adjustable  on  the  axle  so  that  the  arc  through 
which  it  moves  from  the  time  the  outrigger  is  released  until  it  reaches  the  mercury  may  be 
varied  at  will.  A  binding  post  is  made  to  connect  with  the  metal  work  of  the  clockwork 
and  another  to  connect  with  the  mercury  pan,  so  that  when  the  arm  dips  into  the  latter  a 
second  circuit  is  closed,  and  this  circuit  may  be  arranged  to  operate  the  X-ray  exposure. 

It  is  preferable  to  have  the  X-ray  tube  inclosed  in  a  metal  box  and  to  allow  the 
above-mentioned  contact  to  close  a  magnetic  circuit  operating  a  photographic  shutter  of 
metal  placed  in  front  of  the  tube.  Each  upstroke  of  the  sphygmograph  lever  thus  sets  the 
clockwork  in  motion,  giving  rise  to  an  electric  current  which  passes  through  the  latter  at 
any  desired  instant  later  in  the  cardiac  cycle.  This  exposure  may  be  repeated  an  indefinite 
number  of  times  always  at  the  same  instant  after  the  onset  of  systole,  so  that  the  summated 
exposures  upon  the  plate  have  the  same  effect  as  a  single  instantaneous  photograph  at  the 
same  instant,  only  much  more  intense.  By  taking  a  series  of  such  plates  at  successively 
later  instants  in  the  cardiac  cycle  a  series  of  pictures  which  are  practically  kinetoscopic 
can  be  readily  obtained. 

Rontgen  Kinematographs. — Levy-Dorn,  Eykman,  and  Dessauer  and 
Groedel  have  taken  kinematographic  pictures  of  the  heart-beat. 

In  Groedel!s  apparatus  designed  for  this  purpose  a  series  of  24  plates, 
each  provided  with  an  intensifying  screen,  are  pushed  one  after  another 
into  place  by  the  rotation  of  a  spiral,  one  turn  of  which  represents  a  dis- 
tance of  one  centimetre.  As  in  Dessauer's  instrument,  the  exposure  takes 
place  through  a  slit  in  a  lead  disk  which  is  rotated  by  the  same  belt  as  the 
spiral  and  at  the  same  speed.  The  changing  of  plates  occurs  automati- 
cally during  the  period  when  the  film  is  covered  by  the  disk,  the  exposed 
plate  being  shoved  into  a  padded  box  below  before  the  new  one  is  pushed 
into  place. 

Kinetoscopic  pictures  have  not  yet  come  into  general  use,  but  promise 
to  open  a  new  field  for  the  study  of  the  heart. 

Stereoscopic  Radiographs. — Still  better  also  than  the  study  of  single 
plates  are  stereoscopic  pictures,  which  can  be  made  by  taking 
two  pictures  with  the  tube  moved  6.0  cm.  laterally  between  exposures.  In 
order  to  secure  the  best  results,  the  two  exposures  should  occur  before  the 


150  DISEASES  OF  THE  HEART  AND  AORTA. 

patient  has  had  time  to  move,  and  hence  a  special  apparatus  should  be  used 
for  automatic  moving  of  the  tube  and  changing  of  plates.  The  plates  are  then 
viewed  in  the  Wheatstone  stereoscope. 

Stereoscopic  radiographs  do  not  have  the  flat  appearance  of  ordinary 
radiographs,  but  all  the  organs  stand  out  plastically,  showing  themselves  in 
perfect  perspective  and  thus  establishing  the  spacial  relations  of  each  shadow 
to  the  neighboring  organs.  It  becomes  easy  to  determine  whether  an  object 
is  located  in  the  anterior,  middle  or  posterior  portion  of  the  chest  and  whether 
an  object  like  a  tumor,  aneurism,  or  mass  of  glands  is  pointing  backwards 
or  forwards.,  By  obtaining  a  clearer  view  of  the  form  of  the  object  and  the 
relations  of  the  surrounding  shadows,  it  is  often  possible  to  determine  that  a 
certain  shadow  which  upon  the  single  plate  cannot  be  distinguished  from  a 
solid  mass  is  actually  made  up  of  conglomerate  smaller  masses,  and  thus 
mediastinal  tumors  and  fused  tuberculous  glands  can  often  be  distinguished 
from  aneurisms  with  much  greater  definiteness  than  is  possible  upon  the 
single  plate.  Similarly  the  plastic  appearance  causes  strands  of  adhesions 
to  stand  out  more  clearly  and  facilitates  their  differentiation  from  ordinary 
lung  figures.  In  some  cases  it  is  possible  even  to  differentiate  pleuritic  de- 
posits from  intrathoracic  structures  by  this  means.  So  great,  indeed,  are 
the  advantages  of  the  stereoscopic  over  the  ordinary  X-rays  that  in  all  doubt- 
ful cases  the  former  should  be  resorted  to,  and  the  last  word  upon  the  diagnosis 
has  not  been  said  until  this  has  been  done. 

BIBLIOGRAPHY. 

Rontgen,  W.  K.:  A  New  Form  of  Radiation,  Science,  N.  York  and  Lancaster,  1896,  N.  S. 

iii,  726  and  729. 
Barker,  Geo.  F. :  The  Rontgen  Rays.    Memoirs  by  Rontgen,  Stokes,  and  Thompson,  N.  Y. 

and  Lond.,  1899. 
Michelson,  A.  A.:  Theory  of  the  X-ray,  Am.  Jour.  Sc,  1896,  4th  ser.,  i,  312. 
Rowland,  H.:  Notes  of  Observations  on  the  Rontgen  Rays,  ibid.,  1896,  4th  ser.,  i,  247. 
For  details  regarding  the  secondary  rays  see : 
Walter,  B.:  Physikalisch  technische  Mitteilungen,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrah- 

len,  Hamb.,  1900,  i,  82. 
Faulhaber:     Ueber  eine  durch  Sekundarstrahlung  bedingte  Erscheinung  auf  Rontgen- 

platten,  ibid.,  1903,  vi,  93.    . 
Holzknecht,  G.:    Die  rontgologische  Diagnostik  der  Erkrankungen  der  Brusteingeweide, 

Hamb.,  1901.     Das  radiologische  Verhalten  der  normalen  Brustaorta,  Wien.  klin. 

Wchnschr.,  1900. 
Cotton,  W.:    Some  Principles  and  Fallacies  of  X-ray  Interpretation,  Practitioner,  Lond., 

1906,  Extra  No.  on  X-rays,  100. 
v.  Criegern:    Ergebnisse  der  Untersuchung  des  menschlichen  Herzens   mittelst  fluores- 

cirenden  Schirmes,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1899,  xvi,  302. 
Rieder,  H. :     Die  Untersuchung  der  Brustorgane  in  verschiedenen  Durchleuchtungsricht- 

ungen,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb.,  1902-03,  vi,  115. 
Moritz,  F.:     Ueber  die  Bestimmung  der  wahren  Grosse  von  Gegenstanden  mittels  des 

Rontgenverfahrens,  Munchen.  med.  Wchnschr.,  1900,  xlvii,  590,  902.    Ueber  ortho- 

diagraphische  Untersuchungen  am   Herzens,  ibid.,  1902,  xlix,  1.     Ueber  Tiefenbe- 

stimmungen  mittels  des  Orthodiagraphen  und  deren  Verkiirzungen  bei  der  Orthodia- 

graphie  des  Herzens  zu  ermitteln,  Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb., 

1904,  vii,  169. 
Levy-Dorn:     Schutzmaassregeln  gegen   Rontgenstrahlen  und  ihre   Dosirung,    Deutsche 

med.  Wchnschr.,  Berl.  und  Leipz.,  1903,  xxix,  921. 


X-RAY  EXAMINATION.  151 

For  numerous  forms  of  orthodiagraphs  of  Moritz  and  Albers-Schoenberg  (1.  c),  but  what 

seems  to  the  writer  to  be  the  most  convenient  and  simple  form  is  the  apparatus  de- 
scribed by : 
Gillet:    Ein  Orthorontgenograph  einfacher  Konstruction,  Forthschr.  a.  d.  Geb.  d.  Rontgen- 

strahlen,  Hamb.,  1906,  x,  114. 
For  the  examination  of  the  heart  cf.  also 
Moritz,  F. :    Einige  Bemerkungen  zur  Frage  der  perkutorischen  Darstellung  der  gesammten 

Vorderflache  des  Herzens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  lxxxvii,  276. 
Dietlen,  H.:    Ueber  Grosse  und  Lage  des  normalen  Herzens  und  ihre  Abhangigkeit  von 

physiologischen  Bedingungen,  ibid.,  1906,  lxxxviii,  55. 
Levy,  M.:     Ueber  Abkiirzung  der  Expositionszeit  bei  Aufnahmen  mit  Rontgenstrahlen, 

Fortschr.  a.  d.  Geb.  d.  Rontgenstrahlen,  Hamb.,  1897,  i,  75. 
Rieder,  H.,  and  Rosenthal,  J.:    Ueber  Moment-Rontgenaufnahmen,  Fortschr.  a.  d.  Geb. 

d.  Rontgenstrahlen,  Hamb.,  1900,  iii,  100. 
Rieder,  H.:    Neue  Ausblicke  auf  die  weitere  Entwicklung  der  Rontgendiagnostik,  Mun- 

chen.  med.  Wchnschr.,  1908,  lv,  381. 
Koehler,  A.:    Teleroentgographie  des  Herzens,  Deutsche  med.  Wchnschr.,  Leipz.,  1908, 

xxxiv,  186. 
Dessauer,  F.:  Instantaneous  Radiography  in  Less  than  1/100  of  a  Second;  a  New  Method 

of  Radiography,  Med.  Rec,  N.  Y.,  1909,  lxxv,  890;  and  ROntgen  Moment  Aufnahmen, 

Munchen.  med.  Wchnschr.,  1909,  lvi,  1075;  also  Rontgen  Aufnahmen  in  weniger  als 

1/100  Sekunde,  Ztschr.  f.  Elektrol.  u.  Rontgen.,  Leipz.,  1909,  xxv,  1095. 
Groedel,  F.  M.:    Die  Technik  der  Rontgen  Kinematographic,  Deutsche  med.  Wchnschr., 

Berl.,  1909,  xxxv,  434. 
Hirschfelder,  A.  D.,  and  Eyster,  J.  A.  E.:    Extrasystoles  in  the  Mammalian  Heart,  Am.  J. 

Physiol.,  Bost.,  1907,  xviii,  222. 
Weber,  A.:  Eine  Methode  zur  Darstellung  von  Herzmoment  Aufnahmen  in  verschiedenen 

Phasen  der  Herz  Revolution,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1910, 

xxvij  673. 


VII. 

PHYSICAL  EXAMINATION. 

While  it  is  impossible  to  enter  into  a  treatise  upon  physical  exami- 
nation, a  few  points  which  are  of  special  importance  in  cardiac  cases  may 
be  discussed. 

General  Appearance. — The  general  appearance  of  the  patient,  expres- 
sion and  color,  are  of  great  importance.  The  position  which  he  naturally 
assumes  in  bed,  the  presence  or  absence  of  dyspnoea  and  orthopncea,  the 
general  degree  of  nervousness  or  dulness  are  all  to  be  noted. 

The  typical  appearance  of  the  cardiac  patient  (cardiac  facies)  is 
characterized  by  an  anxious  expression,  bright  eyes  with  moist,  glistening 
conjunctivae,  cheeks  full  rather  than  sunken  as  in  the  abdominal  facies, 
and  as  a  rule  a  tinge  of  cyanosis  about  the  lips. 

There  are  two  main  types :  (1)  the  mitral  (or  mitrotricuspid)  facies,  with 
rosy,  flushed  cheeks,  dilated  capillaries,  and  cyanosis  (most  commonly  seen  in  mitral 
stenosis) ;  and  (2)  the  aortic  facies,  with  pale,  often  sallow,  rather  sunken  cheeks, 
bright  eyes,  moist  conjunctivae,  and  slight  cyanosis  of  lips  and  fingers.  To  these  might  be 
added  (3)  the  subicteric  facies  of  broken  compensation,  with  pallor,  subicteric  conjunctivae, 
and  cyanosis  of  the  lips. 

Nasopharynx. — The  tonsils  and  posterior  nasopharynx  should  always  be  carefully 
examined.  The  former  are  the  chief  portals  of  entry  for  the  germs  of  rheumatism,  while 
adenoids  and  affections  of  the  nasal  septum  may  of  themselves  induce 
cardiac  arrhythmia,  and  may  also  be  an  important  contributing  factor  in  the  attacks  of 
asthma  in  organic  heart  disease. 

Ophthalmoscopic  Examination. — The  eye-grounds  should  always  be  examined  when 
arteriosclerosis  (page  358)  or  congenital  heart  disease  (page  542)  is  suspected. 

Neck. — In  the  neck  especial  attention  should  be  directed  to  the  visible 
throbbing  of  the  carotids,  the  fulness  of  the  neck,  and  the  size  and  consist- 
ency of  the  thyroid  gland  (page  678),  the  presence  of  thrills  and  murmurs 
over  vessels  or  thyroid,  or  a  tracheal  tug  (page  643).  The  jugular  pulsation 
is  discussed  in  full  in  Part  I,  Chapter  IV,  page  71. 

Chest. — The  form  of  the  chest  is  of  considerable  importance,  not  only 
as  regards  kyphosis,  but  particularly  as  to  its  f  u  1  n  e  s  s  or  flatness  (see 
Part  III,  Chapter  II).  In  recording  this,  the  width  of  the  costal  angle 
should  be  noted,  and  the  general  obliquity  of  the  ribs  in  quiet 
expiration  should  be  designated  by  noting  the  vertebral  spines 
which  are  on  the  same  level  with  the  sternoxiphoid 
articulation  (normally  at  the  level  of  the  eighth  thoracic  spine) 
(page  699).  It  should  be  noted  whether  the  chest  in  quiet  breathing  ap- 
proaches more  nearly  to  the  position  of  expiration,  flat  chest,  or  to  that 
of  inspiration.  Pulsations,  bulgings,  heaving,  or  retractions  of  the  ribs  or 
interspaces,  as  well  as  the  presence  of  abnormal  shocks  and  thrills,  should 
of  course  be  noted. 

Abdomen. — In  the  abdomen  the  important  features  to  be  noted  are 
presence  or  absence  of  ascites,  enlargement  of  liver  (systemic 
152 


PHYSICAL   EXAMINATION. 


153 


stasis),  pulsation  of  the  liver,  systolic  impulse  (tricuspid  insuffi- 
ciency), systolic  retraction  (dilated  or  hypertrophied  right  ventricle),  the 
nature  and  the  time  of  epigastric  pulsation  (systolic  elevation  being  trans- 
mitted from  the  abdominal  aorta,  systolic  retraction  indicating  dilated 
hypertrophied  right  ventricle) .  A  palpable  spleen  of  cardiac  origin 
points  to  infarction,  septic  or  thrombotic.  When  aneurism  or  arterio- 
sclerosis is  suspected  the  course  of  the  abdominal  aorta  should 
be  mapped  out  by  deep  palpation  with  both  hands,  one  above  each  side  of 
the  aorta  and  that  vessel  between  them  (page  660). 

The  genitalia  should  of  course  always  be  examined  for  signs  of  gonor- 
rhoea and  lues, — urethral  smears  for  the  former  and  a  Wassermann 
reaction  for  the  latter  being  made  whenever  possible. 

Extremities. — Upon  the  extremities  the  presence  of  oedema  and 
arthritis,  acrocyanosis  or  pallor,  and  the  size,  consistency,  and 
uniformity  of  the  brachial,  radial,  femoral,  popliteal,  and  dorsalis  pedis 
arteries    are  the  chief  points  of  importance. 


THE    CARDIAC   IMPULSE. 

Mechanics  of  the  Cardiac  Impulse. — The  apex  itself,  as  shown  by 
Ludwig  and  Dogiel,  does  not  move  appreciably  up  or  down  during  systole; 
and,  as  Hesse  has  demonstrated,  the  transverse  diameter  of  the  heart 
shortens  more  than  the  longitudinal. 

The  chief  movements  which  lead  to  the  production  of  the  apex 
impulse  are  due  more  to  the  systolic  erection  of  the  heart  upon  the  great 
vessels  than  to  its  diminution  in  size. 

If  one  watches  the  exposed  heart  of  a  dog, 
cat,  or  rabbit,  it  is  seen  to  execute  two  move- 
ments in  systole:  (1)  the  general  contraction 
affecting  chiefly  the  transverse  diameter  of  the 
heart,  and  (2)  a  twisting  about  of  the 
apex  from  left  to  right  and  forwards. 
This  torsion  of  the  apex  is  the  resultant  of  the 
several  lines  of  traction  exerted  by  the  muscu- 
lature of  the  right  and  left  ventricles  upon  the 
base  of  the  aorta  and  pulmonary  artery,  and 
modified  by  the  pivoting  of  the  heart  against 
the  vertebral  column  and  by  the  shifting  of  its 
centre  of  gravity  owing  to  variation  in  its 
liquid  content.  The  tendency  of  this  move- 
ment is  to  push  the  apex  of  the  left  ventricle  against  the  chest  wall,  while  the  left 
wall  of  the  left  ventricle  and  the  right  (anterior)  wall  of  the 
right  ventricle  move  inwards  toward  the  septum.  Wherever  in 
man  these  walls  are  in  contact  with  the  chest  wall  these  inward  movements  give  rise  to 
retraction  of  the  interspaces  above  them.  The  surface  of  the  thin- walled  right  ventricle 
moreover  is  actually  pulled  inwards  during  systole,  so  that  there  may  actually  be  an 
indentation  of  its  surface  which  still  further  contributes  to  the  systolic  retraction. 

Protrusions  and  Retractions. — A  variety  of  protrusions  and  retractions 
of  the  interspaces  may  be  seen  to  occur  with  each  cardiac  contraction. 

Graphic  records  of  the  impulse  have  been  taken  by  means  of  the  polygraphs 
described  above,  the  receiving  funnel  being  placed  over  the  area  of  pulsation  exactly 
as   for   a   jugular   or   carotid  tracing.      Tracings  can  be  made   either  with  a  rubber- 


Fig.  85. — Movements  of  the  heart  leading 
to  the  protrusions  and  retraction  during  sys- 
tole.   Forces  shown  by  the  arrows. 


154 


DISEASES   OF   THE   HEART   AND    AORTA. 


covered  spring  tambour  like  that  used  for  the  carotid,  or  with  an  open  funnel ; 
the  former  exerting  pressure  upon  the  apex,  the  latter  merely  recording  the  com- 
pression or  rarefaction  of  the  air  in  the  funnel  due  to  the  impulse. 

The  writer  also  finds  that  a  funnel,  made  from  a  soft  rubber  stethoscope  tip  stoppered 
tightly  with  a  perforated  rubber  stopper  penetrated  by 
a  glass  tube  and  bearing  a  rubber  tip,  is  very  satis- 
f  factory  (Fig.  86). 

The  movements  seen  may  be  divided  as : 
(1)   Lifting    of   the    entire    precordium, 
which  results,  especially  in  flat-chested  individ- 
uals or  in  those  with   very  large  hearts,  from 
the  systolic  erection  of  the  heart  as  a  whole  as 
it  pivots  against  the  vertebral  column  behind 
and  pushes  against  the  chest  wall  in  front. 
This  is  usually  seen  in  hearts  which  from  any  cause  whatever  are 
beating  heavily,  though  it  is  most  marked  over  large  hearts. 

(2)  The  normal  type  of  apex  beat  consists  of  a  large  protrusion 
synchronous  with  and  lasting  throughout  the  duration  of  ventricular  systole 
(Fig.  88,  I,  s-d),  usually  preceded  by  a  small  presystolic  wavelet  (as),  due 


APEX 


CAROTID 


Fig.  86. — Rubber  funnel  for  car 
diographic  tracings. 


5cm  y-\ 


CAROT    KJl 


^hW~ 


c  d  c  a  cd    cd 
cd    cd   cd    cd 


D 

4th  LEFT 
'ERSPACE 

-^ 

—~s~ 

JUGULAR 

Pn^^v^l 

■j\ 

ir\r 

Fig.  87. — A,  tracing  from  the  apex  impulse  and  carotid  artery:  c,  time  of  carotid  wave;  d,  time 
of  dicrotic  notch.  Upper  line  gives  the  time  in  £  sec.  B.  cardiogram  obtained  over  a  normal  apex. 
C  and  D,  cardiogram  over  the  fourth  left  interspace  5  cm.  from  costal  margin  (systolic  retraction),  from 
the  same  individual  as  B. 


to  systole  of  the  auricles.  The  large  ventricular  wave  is  followed  by  a  fall 
in  early  diastole,  coincident  with  the  fall  in  intraventricular  pressure. 
After  this  fall  there  is  sometimes  a  small  upstroke  of  the  lever  (passive 
protrusion  of  the  apex  by  the  inrushing  blood)  which  may  terminate  in  a 
small  protodiastolic  wavelet  (p).     This  protodiastolic  wavelet  corresponds 


PHYSICAL  EXAMINATION. 


155 


to  the  shoulder  upon  the  cardiac  plethysmogram  at  the  end  of  ventricular 
filling  (page  11),  and  is  particularly  marked  in  cases  in  which  a  third  heart 
sound  can  be  heard  (Thayer). 

In  cases  with  hypertrophy  of  the  left  ventricle  the  protrusion  is 
usually  very  forcible  and  heaving  throughout  systole — dome-like  protru- 
sion, choc  en  dome   (Bard). 

Occasionally,  however,  especially  when  there  is  some  hypertrophy 
of  the  right  ventricle,  the  systolic  protrusion  may  not  last  throughout 
ventricular  systole,  but  may  be  represented  by  only  a  momentary  protru- 
sion, followed  by  a  retraction  during  midsystole  (Fig.  88,  III).  Such  a 
beat,  which  really  represents  the  algebraic  sum  of  the  systolic  protrusion 
over  the  left  ventricle  and  the  systolic  retraction  over  the  right,  may  be 


~1Hr 


III. 


IV. 


Fig.  88. — Various  forms  of  apex  tracings.  I.  Normal,  showing  presystolic  (auricular)  wave  a, 
systolic  plateau  s-d,  and  the  curve  of  ventricular  filling  d-p,  ending  in  the  protodiastolic  wavelet  p.  II, 
Normal  apex  beat  showing  only  systolic  elevation.  III.  "Mixed"  type  of  impulse  showing  an  elevation 
followed  by  a  retraction  during  the  period  of  systole.  IV.  Systolic  retraction.  Apex  formed  by  the 
right  ventricle.  V.  "Mixed"  type  of  apex  beat  showing  protrusion  during  auricular  systole  and 
retraction  during  systole  of  the  ventricle. 


termed  a  "mixed"  type  of  apex  beat.  In  other  mixed  types 
there  may  be  protrusion  during  auricular  systole  (presystolic  protrusion) 
followed  by  retraction  during  systole  of  the  ventricle  (systolic  retrac- 
tion) .  The  right  ventricle  plays  the  leading  role  in  the  production  of 
such  an  impulse. 

(3)  Systolic  retractions  over  the  entire  right  ven- 
tricle (third,  fourth,  fifth  left  interspaces  between  the  parasternal 
line  and  sternal  margin)  when  this  chamber  is  hypertrophied  or 
contracting  strongly,  sometimes  also  in  second  left  interspace 
(Mackenzie).  Occasionally,  especially  in  cases  of  mitral  stenosis,  the 
presence  of  a  systolic  retraction  of  the  interspaces  over  the  right  ventricle 
and  a  systolic  protrusion  over  the  apex  gives  the  cardiac  impulse  the 
wavy  appearance  of  a  peristalsis.  In  reality,  however,  the  two  move- 
ments are  synchronous.     It  is  not  a  peristalsis  but  a  see-saw  movement. 


15-6 


DISEASES   OF   THE   HEART    AND    AORTA. 


(4)  Systolic  impulse  in  the  second   right  interspace  in  aortic 
insuf f icien  cy  . 

(5)  Systolic  impulse  in  the  second  left  interspace  (pulmonic  area)  in 
pulmonaryinsufficiencyor  vigorous  contraction  of  the  right  ventricle. 

(6)  Systolic  retraction  at  the  apex  in  adherent  peri- 
cardium or  when  the  apex  is 
formed  by  an  hypertrophied 
right  ventricle. 

(7)  Systolic  retrac- 
tions in  the  interspaces 
beyond  the  apex  (left  axilla)  due 
to  negative  pressure  over  those 
areas  of  lung  produced  by  con- 
traction of  a  very  large  heart  or 
to   pleuropericardial    adhesions. 

(8)  Retraction  of  the 
xiphoid  process  or  ribs 
from  traction  of  costopericardial 
adhesions  during  systole 
(Broad bent's   sign). 

Fig.  89. — Areas  of  pulsation  and  retraction.       ?  ,  .       ° 

protrusion;     ^.retraction.    CAR,  carotid  artery;  J  UG,  (9)     byStOllC     impulses 

jugular  vein;  CEPH  cephalic  vein;  AO  aorta;  PA,  pul-  •         various     abnormal     sites 
monary  arterv;  RV,  right  ventricle;  APHD,  apex  with 

high  diaphragm;    AP,  apex;   LIV.TR.INS,   liver-pulsa-  due     to     aneurisms,      tumors,     Or 

tion  in  tricuspid  insufficiency;   LIV.  HYP.RV,  liver-  +rirT1imic,     oplprrrHp     qrfprips* 

retraction  with  hypertrophy  of  right  ventricle.  tOrtUOUS     SCierOtlC     arteries. 


PALPATION. 

Palpation  of  the  precordium  and  thorax  is  undertaken  with  a  view 
to  determine,  (1)  the  force  of  the  apex  impulse;  (2)  the  presence  and  force 
of  any  diffuse  heave;  (3)  the  intensity  of  the  shock  accompanying  the 
heart  sounds;  (4)  the  presence  and  distri-  \ 

bution  of  "thrills";    (5)  the  presence,  dis- 
tribution, and  character  of  other  pulsations. 

Thrills. — Corrigan  (1837)  and,  later,  Marey 
showed  that  thrills  may  be  imitated  by  producing  a 
constriction  in  a  rubber  tube  attached  to  a  water 
faucet.  It  will  be  seen  that  this  causes  the  stream  to 
assume  a  corkscrew  form,  giving  rise  to  eddies,  twists, 

and  nodes  below  the  constriction.  These  tend  to  produce  zones  of  constriction  and  dilatation 
in  the  tube  itself  and  thus  set  it  into  vibrations  which  are  palpable  as  thrills  and  audible  as 
murmurs.    Above  the  constriction  there  are  no  eddies,  hence  neither  thrills  nor  murmurs. 

The  thrill  is  best  transmitted  in  the  direction  of  the  stream  producing 
it.  It  disappears  when  the  constriction  becomes  too  great  or  the  pressure 
falls  too  low,  and  increases  with  the  force  of  the  stream  (blood-pressure). 


Fig.  90. — Eddies  producing  thrills  as 
illustrated  by  a  stream  of  water.  Arrows 
show  lines  of  force.  The  large  arrow  indi- 
cates the  pressure  at  the  point  of  palpation. 


PERCUSSION. 

It  is  of  the  greatest  importance  to  determine  the  exact  outline  of  the 
heart.  As  has  been  seen,  this  is  done  most  accurately  by  means  of  the 
orthodiagraph  (page  135),  but  under  ordinary  clinical  conditions  this  is 
not  available  and  the  cardiac  area  is  outlined  by  percussion. 


PHYSICAL  EXAMINATION.  157 

RELATIVE    CARDIAC    DULNESS. 

In  mapping  out  the  area  of  relative  cardiac  dulness  it  is  important 
to  begin  percussion  as  far  away  from  the  heart  as  possible,  and  then  to 
approach  the  heart,  marking  the  points  at  which  the  very  first  change  of 
note  can  be  recognized  as  the  heart  is  approached.  In  this  way  one  obtains 
an  absolutely  resonant  note  as  long  as  the  plessimeter  finger  is  over  lung 
tissue,  and  a  sharp  contrast  to  this  as  soon  as  one  percusses  over  the  borders 
of  the  heart;  whereas,  if  one  were  to  begin  percussion  over  the  heart  and 
percuss  outward  there  would  be  a  gradual  change  of  note, 
becoming  more  and  more  resonant,  until  it  finally  faded 
into  the  perfect  resonance  over  the  lung. 

Choice   of  Methods. — In  outlining  the  cardiac  area  one  has  the 
choice  of  several  methods: 

(1)  Direct   or  immediate  percussion  by  tapping  the  chest  wall 
directly  with  the  finger-tips  of  one  hand. 

(2)  Heavy   indirect  or  mediate  percussion. 

(3)  M  e  d  i  u  m  - 1  i  g  h  t   percussion. 

(4)  Lightest    audible    percussion    (threshold    percussion   of 
Ewald,  Goldscheider,  Curschmann  and  Schlayer). 

(5)  Palpatory  percussion  (Ebstein)  by  note  too  low  to  be  Fig.  91. — Gold- 
heard  at  all.                                                                                                                             scheider's  ortho- 

(6)  Orthopercussion    (Goldscheider)    (Fig.    91),   distal      Percusslon- 
phalanx  of  the  plessimeter  finger  held  perpendicular  to  the  chest  wall. 

(7)  Instrumental  percussion  with  a  mechanical  plessimeter,  the  blow  being 
struck  by  either  the  finger  or  a  hammer. 

In  selecting  the  method  of  percussion  it  should  be  borne  in  mind  that 
the  vibrations  of  heavy  percussion  are  readily  communicated  to  neighboring 
areas  of  lung,  while  those  of  the  lightest  percussion  are  readily  absorbed  by 
the  neighboring  lung  tissue  and  hence  are  best  transmitted  by  the  clear  lung 
tissue  in  the  axis  of  the  stroke.  The  resonations  of  the  lightest  strokes  pass 
through  the  entire  thickness  of  the  lung  (Goldscheider).  Moreover,  it  is  a 
well-known  law  of  sense-perception  that  the  softer  the  initial  sound  the  easier 
it  is  to  detect  variations  in  it.  Indeed,  de  la  Camp  goes  so  far  as  to  recom- 
mend light  direct  percussion  through  a  single  layer  of  blanket  laid  upon  the 
chest  as  the  most  accurate  method  of  outlining  the  cardiac  dulness. 

Moritz,  Dietlen,  de  la  Camp,  Goldscheider,  Curschmann  and  Schlayer, 
and  a  number  of  other  writers  have  compared  outlines  made  by  the  various 
methods  of  percussion  in  hundreds  of  cases  with  those  obtained  by  the 
orthodiagraph,  while  Simon  has  marked  out  his  outlines  by  percussion 
upon  the  intact  cadaver  with  pins  and  then  tested  his  accuracy  upon 
opening  up  the  thorax.  All  these  observers  are  unanimous  in 
advocating  very  light  percussion  for  outlining  the  left  border 
of  the  heart,  but  Moritz  prefers  a  rather  heavy  palpatory  percussion 
for  the  right  border. 

Moreover,  the  sensations  which  percussion  imparts  to  the  finger  are 
more  delicatelv  graded  for  a  light  stroke  than  for  a  heavy  one,  since  the 
pressure  of  a  heavy  blow  somewhat  dulls  the  sensibility  of  the  finger-tips, 
and  in  this  way  also  a  light  stroke  is  more  satisfactory.  The  oft-made 
claim  that  a  light  stroke  does  not  penetrate  deep  enough  for  mapping  out 


158 


DISEASES  OF  THE  HEART  AND  AORTA. 


N5>* 


the  right  border  of  the  heart,  though  seeming  plausible,  is  not  warranted  by 
experience.  On  the  contrary,  the  writer  has  observed  that  those  clinicians 
who  rarely  make  out  at  all  the  area  of  cardiac  dulness  which  lies  to  the 
right  of  the  midline  were  usually  those  who  used  heavy  percussion. 

Avoidable  Errors  in  Percussion. — The  exact  method  used  is  a  matter  of  individual 
preference  and  practice.  The  essentials  for  all  forms  are:  (1)  a  loose  wrist,  loosely  held 
finger-joints,  and  a  short  sharp  blow  with  immediate  elastic  recoil;1  (2)  firm  pressure  of 
the  plessimeter  finger  against  the  chest  wall,  especially  in  the  interspaces.  In  the  writer's 
experience  the  important  point  is  not  the  method  used  but  the  care  in  discriminating  the 
first  slight  differences  in  note  and  sensation.  The  errors  of  percussion  so  frequent  among 
students  and  even  experienced  physicians  are  far  more  frequently  due  to  in- 
ability to  detect  differences  in  note  than  to  inability  to  elicit 
them.  This  inability  to  detect  slight  differences  was  due  in  most  cases  to  a  precon- 
ceived notion  as  to  the  intensity  of  change 
obtainable.  The  observer  usually  expected  a 
greater  change  and  permitted  his  ear  to  neglect 
the  lesser,  although  once  his  attention  was 
called  he  was  perfectly  able  to  detect  it. 

Special  Methods  of  Percussion. — The 
method  of  choice  varies  somewhat  with  the 
purpose.  For  ordinary  purposes  very  light 
direct  percussion  is  quite  satisfactory,  or  ordi- 
nary threshhold  percussion  with  barely  audi- 
ble note.  Where  accuracy  is  important, 
as  in  determining  the  mobility  of  the  heart 
or  of  the  lung  borders,  Goldscheider's  or- 
thopercussion or  J.  O.  Hirschfelder's 
orthoplessimeter   is   preferable. 

Goldscheider  believed  that  orthopercus- 
sion was  so  delicate  that  dulness  was  given 
only  by  bodies  directly  in  the  axis  of  the 
plessimeter  phalanx  and  that  in  this  way  the 
plane  of  an  oblique  surface  could  be  detected,  but  experience  shows  that  this  is  rarely 
possible.  It  succeeds  much  more  frequently  when  the  orthoplessimeter  (Fig.  92)  is 
used;  so  that  a  resonant  note  may  be  obtained  when  the  shaft  is  pointed  parallel  to  the 
heart  surface,  a  dull  note  when  it  is  pointed  toward  the  heart. 

Unavoidable  Errors  in  Percussion  Outlines. — In  outlining  the  heart 
by  percussion  the  right  and  left  borders  present  different  problems.  The 
right  border  is  situated  deeply  and  recedes  at  once  from  the  chest  wall,  so 
that  it  represents  the  first  point  at  which  dulness  could  be  obtained.  The 
left  border  is  superficial  and  convex  and  the  convexity  sometimes  follows 
the  curve  of  the  ribs  in  the  left  axilla.  Accordingly  it  may  happen  that  in 
round  narrow  chests  or  in  persons  with  large  hearts  the  left  ventricle  may 
almost  fill  the  left  half  of  the  thorax.  The  curve  of  the  ribs  follows  the  wall 
of  the  left  ventricle  and  the  latter  may  remain  near  the  chest  wall  through- 
out the  axilla.  The  outer  border  of  dulness  may  thus  be  obtained  not  over 
the  apex  but  over  the  posterior  wall  of  the  left  ventricle.     In  persons 


Fig.  92. — Percussion  with  the  orthoplessi- 
meter. A.  J.  O.  Hirschfelder's  orthoplessimeter 
and  its  mode  of  application.  B.  Supposed  line  of 
transmission  of  the  percussion  impulse  from  the 
orthoplessimeter.    RES,  resonant  percussion  note. 


1  Some  persons  are  possessed  of  a  loose  wrist  at  once,  others  acquire  it  only  after 
long  practice.  For  the  latter  the  writer  recommends  the  following  exercise  practised  two 
to  five  minutes  daily:  Hold  the  wrist  as  loosely  as  possible,  then  vibrate  the  forearm  very 
rapidly  to  and  fro  from  the  elbow  until  the  hand  shakes  about  like  a  flail  upon  the  loose 
wrist  too  fast  for  the  eye  to  follow  its  movements.  The  improvement  in  percussion  fol- 
lowing this  exercise  is  very  gratifying. 


PHYSICAL  EXAMINATION. 


159 


Fig.  93. — The  heart  as  outlined  by  ordi- 
nary percussion,  by  orthopercussion  perpen- 
dicular to  the  measuring  tape,  and  by  ortho- 
diagraph. 


with  narrow  chests  or  much  enlarged  hearts  the  area 
of  dulness  on  percussion  extends  around  the  heart 
and  not  merely  across  the  transverse  diameter.  The 
transverse     diameter   corresponds   accu-  <C^ 

rately  to  the  point  mapped  out  with 
the  orthodiagraph.  Accordingly  there 
may  be  a  discrepancy  of  several  cen- 
timetres between  the  percussion  and 
orthodiagraph  estimations  of  the  dis- 
tance from  the  midline  to  the  left  bor- 
der. In  a  very  large  series  of  cases 
Moritz  found  his  percussion  (light  per- 
cussion for  the  right  border,  threshold 
percussion  for  the  left)  to  be  correct  for 
the  right  border  in  86  per  cent.,  for  the 
left  in  70  per  cent.  When  the  dulness 
reaches  far  around  the  axilla,  this  dis- 
crepancy may  be  reduced  several  centi- 
metres by  stretching  the  tape  out  to  the 
left  and  projecting  the  outer  border  of 
cardiac  dulness  perpendicularly  upon  it  and  measuring  this  projection.  In 
order  to  diminish  this  discrepancy  A.  D.  Hirschfelder  (Virginia  Medical 
Semi-Monthly,  1914)  has  devised  a  plessimeter  rod  attached  perpendicularly 
to  the  measuring  tape  which  acts  as  an  orthoplessimeter,  and  gives  a  fairly  true 
projection  of  the  cardiac  outline,  similar  to  that  given  by  the  orthodiagraph. 

DIAMETER    OF    THE    CARDIAC    AREA. 

In  mapping  out  the  area  of  cardiac  dulness  the  position  of  the  apex  is 
given,  designating  the  level  of  rib  or  interspace  during  quiet  respiration,  and 

the  number  of  centimetres  to  the 
left  of  the  midline  (Figs.  84  and 
94)  (ML).  The  level  of  upper 
border  at  the  left  sternal  margin 
is  given  and  also  the  distance  to 
the  right  of  the  midline  (MR) 
in  the  fourth  right  interspace. 
The  acuteness  or  obtuseness  o  f 
the  angle  formed  between 
the  hepatic  and  the  cardiac 
dulness  (cardiohepatic  angle, 
angle  of  Ebstein)  is  also  noted. 
In  addition  to  this,  Moritz  and 
Dietlen  call  attention  to  the 
importance  of  recording  the  two 
diagonal  diameters  of  the  heart 
(longitudinal,  L,  from  apex  to 
the  aortic  angle  of  the  dulness, 
and  transverse,  Q,  from  the  cardiohepatic  angle  to  the  upper  left  border, 
as  shown  in  Fig.  84).  Normal  figures  for  these  conjugates  according  to 
Dietlen  are: 


Fig.  94. — Areas  of  cardiac  dulness  and  flatness  in  a 
normal  man.  The  outer  fine  line  represents  cardiac  dul- 
ness; the  inner  heavy  line  represents  cardiac  flatness. 


160 


DISEASES    OF   THE    HEART   AND    AORTA. 


Height  of  individual. 

Men. 

Women. 

Cm. 

Feet  and  In. 

MR. 
Cm. 

ML. 
Cm. 

L. 
Cm. 

Q. 

Cm. 

Cardiac 
area. 
Qcm. 

MR. 

Cm. 

ML. 
Cm. 

L. 
Cm. 

Q. 
Cm. 

Cardiac 
area. 
Qcm. 

145-154 
155-164 
165-174 
175-187 

4.7—5. 
5.1—5.5 
5.5—5.9 
5.9—6.2 

3.5 
4.1 

4.2 
4.4 

7.9 

8.7 
8.8 
9.1 

12.5 

13.8 
14.1 
14.8 

9.7 

9.9 

10.3 

10.7 

95 
109 
116 
127 

3.5 
3.5 

3.8 

8.1 

8.4 

8.5 

12.7 

13.2 
13.4 

9.4 
9.7 
9.9 

93 
101 
105 

Dulness  in  Children. — In  children  the  heart  is  proportionately  larger  and  lies  more 
transversely  than  in  adults.  Sawyer  found  the  apex  outside  the  mammillary  line  in  63 
per  cent,  of  500  young  children.  Veith  has  shown  that  the  cardiac  shadow  in  children 
extends  exactly  twice  as  far  to  the  left  as  to  the  right  of  the  midline  (ML  :  MR  2:1). 

Changes  in  the  Relative  Dulness. — The  relative  proportions  of  the 
various  conjugates  undergo  quite  typical  changes  in  various  forms  of  heart 

disease.  In  weakening  of  the  right 
heart,  in  tricuspid  insufficiency,  and 
tricuspid  stenosis  the  conjugate  MR  is 
increased  (dulness  increased  to  the 
right) ;  in  hypertrophy  of  the  left  ven- 
tricle and  in  mitral  insufficiency,  dulness 
increases  to  the  left  (MR  increased), 
while  in  the  latter  condition  as  well  as 
in  mitral  stenosis  the  oblique  transverse 
diameter  (Q)  is  increased.  In  aortic 
disease  there  is  lengthening  of  the 
long  axis  (L). 

Cardiac  Flatness. — The  area  of  ab- 
solute dulness  or  cardiac  flatness  repre- 
sents the  portion  of  the  heart  which  is 
not  covered  by  lung  (Figs.  93  and  94). 
It  forms  a  triangle  which  varies  very 
much  in  size  and  bears  no  relation  to  the 
size  of  the  heart  (Schieffer  and  Weber). 
It  is  best  mapped  out  by  very  light  percussion,  beginning  over  in  the 
fifth  left  interspace  at  the  left  sternal  margin,  percussing  lateralward 
and  upward,  passing  from  the  absolute  flatness  to  the  area  of  impaired 
resonance  instead  of  in  the  opposite  direction.  By  this  procedure  the  tran- 
sition from  absolute  flatness  to  slight  resonance  occurs  suddenly,  whereas  on 
percussing  in  the  opposite  direction  the  change  of  note  occurs  gradually. 

Variations  in  the  Area  of  Flatness. — In  the  primitive  mammals  (dog 
and  cat)  the  heart  does  not  lie  in  close  apposition  to  the  chest  wall,  but 
is  slung  rather  loosely  between  the  folds  of  the  mediastinum  and  com- 
pletely covered  by  lung.  There  is  no  area  of  flatness.  This  same  condition 
is  met  with  in  many  otherwise  normal  persons,  especially  in  the  long  flat- 
chested,  and  in  those  who  have  extremely  movable  hearts  or  general  mo- 
bility of  all  the  viscera  (visceroptosis,  enteroptosis,  page  699). 

Entire  absence  of  cardiac  flatness  is  also  found  in  the  exact 
opposite  type  of  chest,  in  the  barrel-chest  patients  with  emphysema,  in 


Fig.  95.  —  Cardiac    outlines   in 
nine   years. 


child    of 


PHYSICAL   EXAMINATION. 


161 


whom  the  exaggerated  efforts  at  inspiration  have  caused  the  lungs  to  be 
sucked  in  gradually  between  the  heart  and  the  chest  wall. 

On  the  other  hand,  the  area  of  cardiac  flatness  is  often 
enlarged  in  persons  with  flat,  rhachitic,  or  tuberculous  chests.  In 
hypertrophy  of  the  right 
ventricle  the  area  of  flatness 
is  enlarged  and  the  right  border 
becomes  oblique,  extending 
downward  to  the  right  margin 
of  the  sternum,  often  interrupted 
by  step-like  protrusions  (Kroe- 
nig).  In  pericardial  effusion  it 
extends  well  into  the  fifth  right 
interspace. 

Changes  in  Size  of  the 
Heart. — As  seen  in  the  investi- 
gations upon  cardiac  volume, 
the  size  of  the  heart,  and  hence 
the  area  of  cardiac  dulness,  is 
subject  to  a  physiological  in- 
crease when  the  heart  is  slow 
and  decrease  in  size  when  it  is 
rapid  (Henderson,  see  page  9). 
This  decrease  in  size  is  especially 
noticeable  in  certain  cases  with 
rapid  hearts,  like  paroxysmal 
tachycardia  when  there  is  no 
heart  failure  nor  vasodilation 
(Hoffmann,  Dietlen).  An  in- 
crease in  size  may  be  associated 
with  a  slow  pulse  or  with  in- 
spiration, hypertrophy  of  the 
heart,  or  with  a  pathological 
dilatation.  The  physiological 
condition  should  first  be  con- 
sidered before  assuming  the 
pathological. 

Changes  in  Position  of  the 
Heart. — (1)  Upon  changes  in 
posture.  Normally  changes 
in  posture  are  accompanied  by 
considerable    changes    in    the 

position  of  the  heart.  The  apex  may  move  3-5  cm.  when  the  patient 
turns  from  one  side  to  the  other,  always  moving  towards  the  side  which 
is  lower.  On  standing  a  similar  but  less  marked  change  occurs.  Moritz, 
and,  later,  Dietlen  have  shown  that  the  area  of  the  cardiac  shadow  is  from 
ten  to  thirty  per  cent,  smaller  on  standing  than  on  lying  down.  The  latter 
observer  confirms  Erlanger  and  Hooker  in  stating  that  the  pulse-pressure, 
and  hence  the  systolic  output  of  the  ventricles.,  diminishes  correspondingly. 

11 


Fig.  96. — Diagrams  illustrating  the  movements  of 
the  normal  heart  on  change  of  posture  from  side  to  side 
(A),  and  in  the  various  phases  of  respiration  (B).  Solid 
black  line,  normal  cardiac  outline  in  quiet  breathing; 
dotted  line  (R),  cardiac  outline  with  patient  lying  on 
right  side;  broken  line  (£),  cardiac  outline  with  patient 
lying  on  left  side;  EXP  (horizontal  shading),  outline  in 
expiration;  INSP  (vertical  shading),  cardiac  outline  in 
inspiration.  The  movements  shown  in  these  figures 
represent  the  upper  limits  of  normal  mobility. 


162  DISEASES  OF  THE  HEART  AND  AORTA. 

The  diminished  filling  of  the  heart  is  due  also  to  the  fact  that  the  pressure 
under  which  the  blood  enters  it  in  diastole  (venous  pressure)  is  lower  upon 
standing  than  upon  lying  down. 

In  some  people  extreme  mobility  (6-8  cm.)  of  the  apex  is  found  (wan- 
dering heart) — a  condition  often  associated  with  cardiac  neurasthenia  and 
palpitation,  and  even  paroxysmal  tachycardia.  Changes  in  position  of  the 
diaphragm,  upon  expiration,  inspiration,  or  intestinal  flatulence,  also  affect 
the  position  of  the  heart,  especially  upon  standing,  so  that  in  expiration 
or  flatulence  the  apex  is  pushed  up  and  the  heart  lies  more  trans- 
versely, while  in  inspiration  the  apex  falls  and  the  heart  lies 
more  nearly  in  the  long  axis  of  the  body  (Fig.  96).  As  can  be  readily  shown 
with  Henderson's  cardiometer,  the  former  position  interferes  with  the  cardiac 
filling  and  hinders  the  circulation,  while  the  latter  position  facilitates  both. 
The  amount  of  change  of  position  of  the  apex  is  normally  about  1-2  cm. 

AUSCULTATION. 
CHARACTER   AND   TIME    OF   THE   HEART   SOUNDS. 

The  beat  of  the  heart  is  accompanied  by  two  definite  sounds  ordinarily 
likened  to  the  syllables  "  dub-lub  "  or  "ta-ta,"  the  first  sound  accompany- 

12  12 

ing  systole,  the  second  occurring  just  at  the  beginning  of  diastole. 

SPECIAL  METHODS  FOR  THE  STUDY  OF  HEART  SOUNDS. 

The  Telephone  Stethoscope. — S.  G.  Brown  has  devised  a  telephone  relay  by  means 
of  which  it  is  possible  to  intensify  the  telephone  currents  twenty-fold,  or  using  two  relays 
in  tandem  four-hundred-fold.     Such  instruments  may  prove  of  value  for  demonstrating 


CAROTID 


PHONOGRAM 


Fig.  97. — Graphic  records  of  the  heart  sounds.     (Kindness  of  Prof.  Einthoven.)    Each  vertical  division 

represents  .02  sec. 

heart  sounds  to  a  whole  amphitheatre,  or,  as  Barker  suggests,  for  enabling  permanent 
records  of  the  heart  sounds  to  be  made  upon  a  graphophone  for  use  in  medical  society 
demonstrations  or  in  the  teaching  of  physical  diagnosis. 

It  has  already  been  used  for  auscultation  of  the  heart  at  long  distance,  and  the  heart 
sounds  of  a  patient  have  been  heard  by  physicians  a  hundred  miles  off  (from  London  to 
the  Isle  of  Wight). 

Graphic  Methods  of  Recording  the  Heart  Sounds. — The  first  method  for  recording  the 
heart  sounds  was  introduced  by  Donders  (1856)  and  revised  by  Martius  (188S),  who  merely 
beat  the  time  of  the  sounds  upon  a  receiving  tambour  and  recorded  the  movements  of  the 
lever.  With  a  little  practice  it  was  possible  for  the  observer  to  time  the  beats  with  a  con- 
siderable degree  of  accuracy,  though  never  sufficient  to  be  absolutely  reliable. 

Huerthle  was  able  to  catch  the  sounds  upon  a  microphone  and  to  record  the 
duration  of  the  telephonic  currents  either  by  means  of  a  frog  nerve  muscle  preparation 


PHYSICAL  EXAMINATION. 
PLATE  XIV. 


163 


f^W^M 


Diagram  showing  the  connections  for  taking  graphic  records  of  the  heart  sounds  by  means  of  the 
Einthoven  galvanometer;  MICROPH,  microphone  suspended  upon  a  Julius  suspension;  GALV,  gal- 
vanometer; RHEO,  rheostat;  PHOTO,  photoregiatration  apparatus.  The  telephone  induction  coil  ia 
shown  upon  the  right  of  the  figure. 


B 


Record  showing  the  third  heart  sound  and  its  relation  to  the  venous  pulse.     (Redrawn  from  the  original 
curves  kindly  loaned  by  Professor  Eyster.)     Compare  with  Figs.  45  and  97. 


164  DISEASES  OF  THE  HEART  AND  AORTA. 

or  by  means  of  an  electromagnet,  but  his  method  never  became  practical.  H  o  1  o  - 
w  i  n  s  k  i  and  M  a  r  b  e  have  also  obtained  records  of  a  change  in  Newton's  rings 
and  of  the  vibrations  of  a  sensitive  flame  respectively,  but  none  of  these  have  been  of 
real  value. 

Einthoven  and  Geluk  were  the  first  to  make  really  satisfactory  records,  by  catch- 
ing the  sounds  from  a  stethoscope  upon  a  microphone  and  leading  the  currents  through 
a  capillary  electrometer  whose  movements  were  photographed.  Since  the  introduc- 
tion of  the  string  galvanometer  in  place  of  the  capillary  electrometer,  this  method 
has  passed  into  every-day  use,  and  excellent  records  of  normal  and  abnormal  heart 
sounds  have  been  obtained  which  throw  a  good  deal  of  new  light  upon  the  problems 
of  auscultation. 

The  heart  sounds  must  be  recorded  in  a  quiet  room,  in  which  the  microphone  must 
be  kept  absolutely  stationary,  free  from  the  slightest  vibrations.  In  order  to  do  this,  it 
must  be  clamped  firmly  upon  a  plate  which  is  suspended  from  the  ceiling  by  three  fine 
wires  (Julius  suspension)  and  made  stable  by  heavy  weights  (40-50  pounds) .  The  stetho- 
scope is  connected  with  the  microphone  by  means  of  a  long,  thin-walled  rubber  tube.  About 
two  feet  from  the  microphone,  the  rubber  tube  is  connected  with  one  arm  of  a  brass  Y  tube 
fixed  firmly  to  the  wall.  A  second  arm  of  the  Y  tube  is  connected  with  an  open  rubber 
tube,  whose  lumen  can  be  regulated  with  a  screw  clamp  in  order  to  prevent  mechanical 
vibrations  of  the  chest  wall  from  reaching  the  microphone.  The  third  arm  of  the  Y  is 
connected  with  the  tube  leading  to  a  small  (1J4  in.)  glass  funnel  or  stethoscope  bell,  which 
is  either  held  directly  on  the  thorax  or  fixed  in  a  special  ^-shaped  holder  against  which  the 
patients  may  lean  without  giving  rise  to  vibrations. 

The  tube  and  funnel  as  well  as  the  microphone  must  be 
absolutely  quiet  in  order  to  record  the  sounds,  free  from 
external    vibrations. 

The  microphone  itself  is  now  connected  with  the  primary  coil  of  a  telephone  circuit, 
the  secondary  of  which  passes  through  shunts  bearing  a  rheostat  and  the  string  galva- 
nometer. A  special  switch  must  be  employed  to  keep  the  galvanometer  out  of  the  circuit 
at  the  instant  that  the  primary  current  is  made  and  broken. 

A  galvanometer  which  gives  1  cm.  excursion  per  millivolt  (standard  delicacy  for  elec- 
trocardiograms) is  entirely  too  delicate  for  recording  the  heart  sounds,  and  the  thread 
must  be  either  very  much  tightened  or  the  smaller  form  of  galvanometer  used. 

Weiss  and  Frank  have  devised  instruments  of  a  differ- 
ent type,  in  which  no  microphone  is  used,  but  in  which  the 
vibrations  of  a  membrane  set  in  motion  by  the  heart  sounds 
are   magnified    and   recorded   photographically. 

O  .  Frank  places  a  small  mirror  upon  a  condom  membrane  stretched  across  the 
mouth  of  a  small  funnel.  A  beam  of  light  is  thrown  obliquely  upon  this  mirror  and  reflected 
upon  the  slit  of  a  photo-registration  apparatus.  The  funnel  is  connected  with  the  stetho- 
scope as  for  the  Einthoven  apparatus,  and  the  oscillations  are  photographed. 

Unfortunately,  Frank's  curves  represent  a  combination  of  phonogram  and  cardio- 
gram, and  are  therefore  not  entirely  satisfactory  for  many  purposes,  although  the  rapid 
vibrations  due  to  the  heart  sounds  are  so  characteristic  that  they  can  scarcely  be  confused 
with  the  much  slower  vibrations  due  to  the  heart's  movements. 

Weiss'  phonoscope,  which  is  a  much  more  delicate  instrument,  and,  accord- 
ing to  its  author,  more  sensitive  even  than  Einthoven's,  consists  essentially  of  a  closed 
chamber  containing  a  funnel  1  cm.  in  diameter.  The  mouth  of  the  funnel  is  covered  with 
a  film  of  soap-bubble,  in  the  centre  of  which  rests  an  L-shaped  order  of  capil- 
lary glass  tubes,  whose  movements  are  magnified  with  a  microscope  and  are  projected  upon 
a  photo-registration  apparatus.    The  soap  film  may  last  three  hours. 

Gerhartz,  who  has  made  use  of  the  same  apparatus,  finds  that  membranes  of 
collodion  may  be  substituted  for  those  of  soapsuds  and  are  much  more  permanent  and 
easier  to  use.    Condom  membrane  is  far  less  sensitive. 

Still  more  delicate  than  this  is  the  micrograph  of  Crehore  (page  76). 

Reproduction  of  the  Heart  Sounds. — Weiss  and  Joachim  have  successfully  repro- 
duced the  original  heart  sounds  from  the  cardiophonographic  curves  by  cutting  out 
the  curve  upon  a  piece  of  cardboard  and  passing  it  rapidly  between  an  arc  light  and  a 
photo-sensitive  selenium  cell.  Wherever  the  high  points  of  the  curve  cut  off  the  light 
the  conductivity  of  the  selenium  cell  changed  and  a  telephone  current  was  produced 


PHYSICAL  EXAMINATION.  165 

This  method  was  very  satisfactory,  but  it  is  necessary  to  make  use  of  a  selenium  cell 
of  very  low  resistance  (less  than  300,000  ohms).  The  resistance  of  the  ordinary  cells  is 
too  great  for  the  purpose. 

Clinical  Diagram  for  Heart  Sounds. — In  many  text-books  the  heart 
sounds  are  represented  graphically  in  various  ways,  but  it  seems  to  the 
writer  that  the  best  is  to  indicate  the  occurrence  of  the  sounds  directly  upon 
a  simple  diagram  which  indicates  the  relation  to  the  auricular  and  ventricular 
contractions,  as  shown  in  Fig.  98. 1 


CAUSES   OP   THE   HEART   SOUNDS. 

First  Sounds. — Harvey  states  that  "when  there  is  the  delivery  of  a 
quantity  of  blood  from  the  veins  to  the  arteries,  a  pulse  takes  place  which 
can  be  heard  within  the  chest."  Laennec  (1819)  was  the  first  to  describe 
the  character  of  the  sounds.  He  regarded  the  first  sound  as  due  to  ventric- 
ular systole,  though  he  thought  the  second  to  be  due  to  the  contraction 
of  the  auricle.  In  1836,  C.  J.  B.  Williams  and  a  committee  of  the  British 
Medical  Association  investigated  the  heart  sounds  experimentally.  He 
believed  that  the  first  sound  was  largely  of  muscular 
origin,  like  the  contraction  sound  of  skeletal  muscles,  because  it  could  be 
heard  upon  the  excised  heart  even  when  the  auriculoventricular  valves 


CARDIAC  CYCLE 

HEART  SOUNDS B ■ 


sJ~^^r^ 


Fig.  98. — Diagram  for  representing  the  heart  sounds  in  clinical  notes.  Upper  curve  represents 
the  events  of  the  cardiac  cycle,  the  small  auricular  contraction  followed  by  the  larger  ventricular  con- 
traction. Lower  line  represents  the  heart  sounds.  True  heart  sounds  are  represented  by  solidly  shaded 
blocks,  whose  height  indicates  their  intensity  and  whose  breadth  indicates  their  duration. 

were  held  open  with  the  fingers,  but  the  second  sound  could  not  be  heard 
unless  the  aortic  or  pulmonic  valves  closed.  This  view  was  substantiated 
by  Ludwig  and  Dogiel;  but  Sibson  and  Broadbent  found  that  in  the  exposed 
heart  of  the  ass  the  first  sound  begins  with  a  sort  of  rumble,  which  disappears 
when  the  blood  flow  is  shut  off  by  tying  the  venae  cavae.  This  rumble 
they  ascribe  to  the  movement  of  the  auriculo- 
ventricular   valves. 

Graphic  records  of  the  heart  sounds  by  Einthoven,  Flohil,  and  Battaerd 
have  shown  that  the  first  sound  in  man  begins  at  the  beginning  of  ventric- 
ular systole  and  lasts  .07  to  .10  sec.  It  is  loudest  at  its  very 
beginning,  is  decrescendo  in  character,  and  is 
almost  completed  before  the  aortic  valves  open, — 
i.e.,  before  the  heart  had  begun  to  pump  blood  into  the  aorta.  The  first 
sound  is  followed  by  the  short  pause,  which  usually  lasts  .15  to  .25  sec,  and 

1  Thus  in  cases  of  mitral  stenosis  (see  page  447)  the  first  sound  may  be  short  and 
tapping  in  character,  though  tracings  show  the  systole  to  be  of  duration  no  less  than  that 
met  with  in  the  absence  of  tapping  character  (Hirschf elder) . 


166  DISEASES  OF  THE  HEART  AND  AORTA. 

which  is  then  followed  by  the  second  sound.  Einthoven's  results  have  been 
confirmed  in  man  by  the  records  of  Weiss  and  Joachim,  Hess  and  Frank,  as 
well  as  by  Prof.  Barker,  Dr.  Bond,  and  the  writer.  In  the  dog,  R.  H.  Kahn 
has  shown  that  the  duration  of  the  first  sound  is  exactly  coincident  with  the 
period  during  which  the  intraventricular  pressure  is  rising,  while  the  dura- 
tion of  the  short  pause  is  exactly  coincident  with  the  systolic  plateau. 

Sahli  and  other  clinical  observers  believe  that  the  first  sound  at  the 
aortic  area  begins  later  than  that  at  the  apex  and  is  due  to  the  rush  of  blood 
from  the  ventricle  into  the  aorta;  and  the  graphic  records  of  Fahr  (Heart, 
1912-1913,  iv,  147)  show  that  the  first  pulmonic  sound  begins  .02  to  .04  second 
after  the  first  sound  at  the  apex. 

However,  the  first  sound  heard  on  listening  in  the  suprasternal  notch  is 
often  split;  and  it  is  possible  that  the  latter  portion  of  this  sound  is  due  to  just 
such  a  forcible  distention  of  the  aorta. 

The  valvular  element  of  the  sound  is  probably  brought  about  when  the 
valves  are  thrown  into  tension  by  the  ventricular  systole,  for  Fahr  has  shown 
that  the  first  sound  begins  with  the  rise  of  intraventricular  pressure,  about 
.01  second  before  the  summit  of  the  R  wave  on  the  electrocardiogram.  There 
is  no  evidence  that  the  normal  sounds  are  brought  about  by  eddy  currents 
like  those  which  produce  thrills  and  murmurs  nor  does  the  systole  of  the 
normal  auricle  take  part  in  the  production  of  the  first  sound,  though  Bridgman 
has  shown  that  it  may  cause  a  presystolic  sound  (Fig.  104). 

Hess  and  Frank  believe  that  the  movement  of  the  heart  within  the 
chest  and  perhaps  against  the  chest  wall  (systolic  erection)  may  be  an  impor- 
tant factor  in  the  production  of  the  first  sound.  This  might  explain  why 
the  heart  sounds  are  occasionally  inaudible  in  emphysematous  persons  in 
whom  the  organ  is  separated  from  the  chest  wall  by  a  layer  of  lung.  On 
the  other  hand  this  factor  is  shown  to  play  only  a  minor  role  by  the  fact 
that  the  first  sound  may  be  heard  in  its  normal  intensity  in  the  exposed  and 
even  the  suspended  dog's  heart. 

Second  Sound. — The  second  sound  has  been  shown  by  C.  J.  B.  Williams 
and  the  British  Commission  to  accompany  the  closure  of  the  aortic  and 
pulmonary  valves,  to  be  modified  when  these  valves  are  injured,  and  to 
disappear  when  they  are  held  against  the  vessel  wall.  It  lastsabout.05  second. 
It  is  loudest  when  the  blood-pressure  is  high,  when  the  valves  are  thicker 
and  .more  rigid  than  normally,  or  when  the  vessel  walls  are  more  elastic 
than  usual,  the  intensity  varying  at  different  times  of  life  and  under  patho- 
logical conditions. 

METHODS     OF     AUSCULTATION. 

Monaural  Stethoscope. — The  monaural  stethoscope,  introduced  by 
Laennec,  is  a  simple  wooden  tube  surmounted  by  a  fiat  disk  acting  as  an 
ear-piece  and  resonator.  The  tube  is  pressed  against  the  chest  and  the  ear 
laid  upon  the  disk,  so  that  the  observer  receives  at  once  the  sound  and  the 
thrill  in  the  wood  transmitted  directly.  Obviously  this  method  accentuates 
the  notes  of  low  pitch  which  are  nearest  to  the  essential  tone  of  the  instru- 
ment (and  constitute  most  of  the  normal  sounds),  as  well  as  those  of  relative 


GOOD 


PHYSICAL  EXAMINATION.  167 

loudness,  which  cause  it  to  vibrate  mechanically.  Hence  it  is  particularly 
adapted  to  the  detection  of  presystolic  and  other  rumbling  murmurs,  and  is 
the  method  used  almost  exclusively  outside  of  the  United  States. 

Binaural  Stethoscope. — In  the  United  States  the  binaural  stethoscope 
is  in  more  general  use.  This  consists  essentially  of  a  small  receiving  bell, 
which  is  placed  upon  the  chest  wall,  and  from  which  two  tubes  lead  off  to 
small  rubber  ear-pieces  which  fit  tightly  into  the  external  auditory  meatus. 
The  most  important  essentials  in  these  three  forms  are,  (1)  a  bell  composed 
of  various  materials — ivory,  wood,  celluloid,  or  hard  rubber — provided  with 
a  sufficiently  large  air  space  at  the  tip  (Emerson) ;  (2)  ear-pieces  perfectly 
fitting  the  ear  of  the  individual.  It  is  safe  to  say  that  more  errors  of  auscul- 
tation result  from  poorly  fitting  ear-pieces  than  from  real  inefficiency  on 
the  part  of  the  listener.  (3)  In  stethoscopes  in  which  the  ear-pieces  are  held 
in  the  ears  by  a  spring  this  should  not  exert  excessive  pressure  lest  it  produce 
sounds  within  the  ear  from  the  pressure  on  the  drum. 

There  are  three  main  forms  of  binaural  stethoscope:  (1)  those  with 
rigid  tubes  (Gannett's),  (2)  those  with  soft  rubber  tubes,  (3)  those  with  soft 
rubber  tubes,  flat  bells,  and  a  small  elastic  disk  of  metal  or  celluloid  to  act 
as  a  resonator  (Bowles).  Of  these  three  forms  it  may  be  said  that  the  rigid 
tubes  certainly  convey  the  sounds  somewhat  better,  but  this  is  often  more 
than  compensated  for  by  the  better  fitting 
of  the  ear-pieces  in  stethoscopes  with  soft  BAD 

rubber  tubes.  In  stethoscopes  with  disks 
certain  sound  waves,  and  particularly 
those  of  high  pitch  (soft  blowing  mur- 
murs), are  accentuated,  while  other  sounds 
may  be  relatively  suppressed.  Moreover, 
any  movement  of  skin  or  hair  over  the  Fig.  99.— choice  of  stethoscope  bells. 
disk  may  give  rise  to  a  sound  simulating 

a  friction,  and  this  source  of  error  must  be  carefully  excluded.  Hair  should 
be  moistened,  and  a  small  bell  should  be  used  with  perfect  approximation  to 
the  skin  throughout  its  circumference. 

Alteration  of  Sounds  by  Pressure. — Emerson  has  shown  that  many 
murmurs,  especially  presystolic  and  snapping  sounds,  are  diminished  or 
obliterated  by  pressure  with  the  stethoscope,  while  certain  others  are  inten- 
sified by  pressure,  and  that  this  is  dependent  upon  the  pitch  of  the  sound 
and  not  upon  the  site  of  its  production.  It  is  therefore  important  for  the 
observer  to  listen  carefully,  first  with  the  lightest  possible  pressure  upon 
the  stethoscope  and  then  with  gradually  increasing  pressure.  He  should 
do  this  consciously  and  as  a  matter  of  routine,  rather  than  allow  such  sounds 
to  escape  him  or  stumble  upon  them  by  accident. 

Moreover,  since  the  monaural  and  binaural  stethoscopes  each  intensifies 
different  sounds,  both  should  be  used  in  any  important  or  dubious  case  before 
the  examination  is  concluded. 

Differential  Stethoscope. — This  consists  of  an  ordinary  binaural  stetho- 
scope in  which  each  ear-tube  leads  to  a  separate  bell  or 
funnel.  If  one  bell  is  placed  over  the  mitral  area  and  the  other  over  the 
aortic,  the  observer  is  able  to  listen  with  one  ear  to  the  sounds  produced  at 


168  DISEASES  OF  THE  HEART  AND  AORTA. 

the  two  areas  at  the  same  time,  and  to  use  the  more  normal  sound  as  time 
marker  for  the  other.  By  squeezing  the  tube  or  lifting  the  bell,  it  is  possible 
to  diminish  either  sound  at  will. 

"  VALVULAR   AREAS  "    IN   AUSCULTATION. 

The  various  cardiac  sounds  are  best  heard  over  certain  definite  locations 
corresponding  more  or  less  to  the  structures  in  which  they  arise,  but  par- 
ticularly to  the  course  of  the  blood  current  and  to  their  mode  of  origin  (Fig. 
100).  Thus  the  sounds  produced  in  the  left  ventricle  are  best  heard  at  the 
apex;  those  produced  at  the  aortic  orifice,  though  produced  behind  the  ster- 
num, are  heard  just  to  the  right  of  it  in  the  second  interspace;  the  pulmonary 
sounds  are  carried  to  the  second  left  interspace  at  the  sternal  margin;  while 
the  sounds  from  the  right  ventricle  are  heard  over  the  entire  body  of  the 
sternum,  over  the  greater  part  of  the  area  of  absolute  dulness,  and  over  the 
base  of  the  ensiform  cartilage.  Abnormal  sounds,  murmurs,  etc.,  have, 
however,  a  different  distribution,  which  will  be  discussed  later. 

Normally  the  first  sound  at  the  apex  and  everywhere  else  below  the  third 
rib  is  louder  than  the  second  sound.  It  is  also  of  longer  duration  than  the 
latter  (.08  second  as  compared  to  .05).    Over  the  aortic  and  pulmonic  areas 

it  becomes  somewhat  fainter,  be- 

WJ^^~  ^B  gins  a  trifle  later,  and  is  of  longer 

^^^  ^^^j  duration  than  over  the  apex.  The 

^m  ^^  second  sound  is  then  louder  than 

V  .  V  ..  The  second  sound  at  the  sec- 

■  (/^~*v\  m\  ond  left  interspace  (pulmonic  sec- 

W  TTRVm\>*'  ■  ond)  is  usually  louder  than  that 

^— y~^-/  over  the  second  right  (aortic  sec- 

■  ond)  up  to  the  age  of  25  to  30, 

Hi  ■  when    the    latter    becomes    the 

HI  |  louder    (Cabot).1      This    varies 

W  §  km  greatly  in  different  individuals. 

B_  \  Mere  changes  in  blood-pressure 

n     inn    r™.  ..    i    i  »  are  n°t  sufficient  to  account  for 

hiG.  100. — The     valvular  areas. "  .  . 

all  these  conditions,  since  the 
pressure  in  the  pulmonary  artery  is  never  more  than  half  that  in  the  aorta, 
but  proximity  to  the  sternum,  greater  elasticity  of  the  walls,  etc.,  combine 
to  bring  about  the  relative  loudness  of  the  second  pulmonic  sound,  and 
therefore  any  further  increase  in  pressure  in  either  artery  alters  the  relation 
of  the  two  sounds  to  each  other,  increased  pulmonary  pressure  increasing 
the  pulmonic  second,  increased  general  blood-pressure  increasing  the  second 
aortic,  etc.  The  progressive  thickening  of  the  aortic  semilunar  valves  after 
the  age  of  30  also  contributes  to  the  intensity  of  the  sound. 

Other  Sites  for  Auscultation. — Boy-Teissier  has  also  recommended  auscultation  in  the 
suprasternal  notch,  pressing  the  bell  of  the  stethoscope  as  far  down  behind  the 
manubrium  as  possible.    In  this  way  he  states  that  he  can  hear  aortic  diastolic  murmur 

1  Directly  over  the  exposed  aorta  the  sound  is  louder  than  over  the  exposed  pulmonary 
artery.     (Thayer.) 


PHYSICAL  EXAMINATION. 


169 


Fig.  101. — The  propagation  of  the  heart  sounds  from  valves  to  chest  wall.  A,  course  of  the  sound 
■waves  within  the  heart.  B,  propagation  of  the  sounds  at  the  level  of  the  fourth  and  fifth  interspaces. 
C,  propagation  of  the  heart  sounds  at  the  level  of  the  second  interspaces 


170  DISEASES   OF   THE   HEART   AND    AORTA. 

not  otherwise  audible.  He  thinks  that  he  is  also  better  able  to  distinguish  the  character  of 
aortic  systolic  murmurs.  The  method  has  never  gained  general  usage,  and  the  writer  is 
unable  to  find  in  it  any  of  the  advantages  claimed  by  Boy-Teissier.  The  chief  value  of 
suprasternal  auscultation  is  found  in  persons  whose  heart  sounds  are  feeble  or  inaudible 
over  the  precordium.  It  must  be  borne  in  mind,  however,  that  the  mitral  murmurs  are  not 
well  transmitted  to  this  region,  and  that  the  first  sound  heard  there  is  frequently  redupli- 
cated or  split. 

Another  form  of  auscultation  not  in  general  use  is  the  auscultation 
through  the  stomach-tube,  introduced  as  for  a  tracing  from  the  left  auricle. 
This  method,  first  used  by  A.  Hoffmann  in  1892,  has  been  revived  by  Gerhartz,  but,  though 
it  might  throw  some  light  upon  the  nature  of  an  occasional  mitral  murmur,  it  is  in  general 
difficult  and  very  inconvenient  to  carry  out;  and  in  many  cases  at  least  the  murmurs  are 
no  better  heard  than  over  the  chest  wall.  Nevertheless  where  it  is  important  to  know 
whether  a  murmur  is  conducted  back  into  the  left  auricle,  a  positive  finding  by  this  would 
be  conclusive. 

EMBRYOCARDIA. 

Ordinarily  the  diastolic  pause  between  sounds  is  longer  than  the  sys- 
tolic period,  and  the  interval  between  the  second  sound  of  one  cycle  and 
the  first  sound  of  the  next  is  longer  than  the  interval  between  the  first 
and  second  sounds  of  the  same  cycle.  However,  when  the  heart-rate  is 
very  rapid,  the  diastolic  pause  may  become  shortened  to  about  the  same 
interval  as  that  between  the  first  and  second  sounds  (long  p  a  u  s  e  = 
short   pause),  so  that  the  sounds  succeed  one  another  at  uniform  inter- 


2  12  1 

Fig.  102. — Graphic  records  of  the  fetal  heart  sounds.     (After  Weiss  and  Joachim.) 

vals  like  the  ticking  of  a  clock.  This  rhythm  is  heard  normally  over  the 
fetal  heart  and  hence  has  been  termed  embryocardia  or  fetal  rhythm.  It 
also  occurs  in  adults  when  the  rate  is  very  rapid  (120  and  over),  and  hence 
under  conditions  in  which  the  heart  is  under  an  abnormal  strain  (see  page 
317),  as  in  fevers  with  high  temperature,  acute  heart  failure,  and  acute 
overwork  of  a  chronically  diseased  heart,  also  in  cases  of  paroxysmal  tachy- 
cardia and  allied  conditions.  Its  absolute  significance  is  simply  that  of  the 
rapid  heart-rate  to  which  it  corresponds. 

ACCESSORY   HEART   SOUNDS. 

REDUPLICATED  SOUNDS  AND  GALLOP  RHYTHMS. 

Reduplicated  Sounds. — Occasionally  one  or  the  other  of  the  two  normal 
heart  sounds  is  replaced  by  two  clear  sounds,  or,  in  other  words,  there  is  a 
reduplication.  This  reduplication  may  occupy  the  place  of  either  the  first 
or  the  second  sound,  and,  as  already  noted  by  Skoda,  it  may  seem  to  be 


PHYSICAL   EXAMINATION. 


171 


due  to,  (1)  splitting  of  the  normal  sounds  into  two  distinct  portions,  or 
(2)  pressure  of  an  accessory  sound  besides  the  normal  sound,  being  in  the 
latter  case  presystolic  (before  the  first  sound) ,  protodiastolic 
(shortly  after  the  second  sound) ,or  mesodiastolic  (in  mid-diastole) . 
The  relation  of  groups  1  and  2  to  one  another  and  to  the  cardiac  cycle  is 


shown  in  Fig.  103. 

Intraventricular  Pressure 

Volume  of  Ventricles 

Presystolic  Gallop 

Split  First  Sound 

Split  Second  Sound 

Protodiastolic  Gallop 


ra 


\. 


z\ 


an 


z 


TE-LUB        DUB 


mi 


JO 


K-LUBDUB 


II 


LUB       DUB-L 


S3 


MIL        ■   ■ 


I  UB      DUB — DA 


Fig.  103. — Diagram  illustrating  the  split  sounds  and  gallop  rhythms  and  their  phonetic  equivalents. 

As  to  the  causation  of  these  abnormal  sounds,  little  definite  is  known.  A  great  deal 
of  the  indefiniteness  which  permeates  the  enormous  literature  upon  the  subject  is  due  to 
the  failure  of  the  writers  to  distinguish  clearly  between  the  different  forms  with  which 
they  are  dealing.  The  presystolic  and  protodiastolic  forms  are  grouped  under  one  head 
regardless  of  their  relations  to  mechanism  or  etiology;  it  is  mainly  due  to  the  writers  of  the 
French  school  under  the  leadership  of  Potain  that  the  differentiation  has  reached  even  its 
present  stage  of  development.  L.  Bard,  of  Geneva,  has  recently  given  an  excellent  analysis 
of  the  subject  from  this  stand-point. 

According  to  Bard,  the  two  main  groups  of  accessory  sounds  are: 

(1)  The  presystolic  gallop  reduplication  (ta-tii-tat)  or  ta  ta  tat,  to  which  the  term 

1  2 

gallop  rhythm  should  be  limited,  most  commonly  met  in  nephritics  with  cardiac  hyper- 
trophy and  in  other  heavily  beating  hearts. 

(2)  The   protodiastolic   sound   ta  ta  ta  (lub-dub-da) ,  called   by  Bouillaud   bruit   de 

1  2 

rappel, — "sound  of  recall"  or  "diastolic  echo," — frequently  heard  at  the  apex  in  mitral 
stenosis.  Bard  thinks  that  the  above-mentioned  accessory  sounds  are  to  be  regarded  as 
merely  the  exaggeration  of  vibrations  normally  present  but  normally  inaudible. 

Split  Sounds. — The  sounds  (tlat-tat;  tat-tatl)  are  characterized  by  the 

12  12 

absolute  similarity  and  short  interval  between  the  two  portions,  and  may 
be  clue  either  to  slight  asynchronism  of  the  two  ventricles  (C.  J.  B.  Williams, 
1836,  Skoda,  Gibson,  1874)  or  slight  separation  of  two  parts  of  the  ven- 
tricular sound,  which  are  of  different  origin  but  ordinarily  fused. 

As  has  been  seen,  the  ventricular  sound  contains  both  a  valvular  (auriculo ventric- 
ular) and  a  muscular  element,  and  perhaps  also  an  element  due  to  the  stretching  of  the 
walls  of  the  aorta.  Bard  thinks  that  variation  in  either  the  muscular  or  the  valvular 
element  might  give  rise  to  their  separation  into  two  sounds.  The  question  of  asynchronism 
of  the  two  ventricles  which  arises  in  this  connection  is  one  which  was  long  without  an 
experimental  basis,  but  the  recent  observations  of  Stassen,  Kraus  and  Nikolai,  and  Hew- 
lett indicate  the  possibility  that  it  may  occur  clinically.  Stassen,  in  Fredericq's  labora- 
tory, has  recorded  asynchronous  contractions  of  the  two  ventricles  when  the  latter  were 
recovering  from  vagus  inhibition,  and  also  with  ventricular  extrasystoles  produced  during 
periods  of  vagus  inhibition.  The  writer  has  on  one  occasion  heard  a  split  first  sound  in  an 
animal  in  which  the  contractions  of  both  ventricles  were  being  recorded  with  myocardio- 


172 


DISEASES  OF  THE  HEART  AND  AORTA. 


graphs.  The  ventricular  contractions  were  slightly  asynchronous.  In  a  number  of  other 
instances  in  which  no  split  first  sound  could  be  heard  the  contractions  were  absolutely 
synchronous.    Eppinger  and  Stoerck  have  confirmed  these  observations  (see  page  106). 

The  splitting  of  the  first  sound  is  best  heard  over  the  base  and  body 
of  the  heart,  in  contrast  to  the  accessory  sounds  which  are  best  heard  at 
the  apex  (see  below).  As  to  the  splitting  of  the  second  sound,  this  likewise 
may  be  due  to  slight  asynchronism  of  the  two  ventricles,  or  to  the  fact  that 
even  without  this  the  semilunar  valves  may  not  close  at  exactly  the  same 
instant.  It  is  often  possible,  by  passing  the  stethoscope  along  the  second 
right  and  left  interspaces,  to  determine  which  second  sound  lags  behind. 

It  must  be  added,  however,  that,  as  Bard  himself  states,  no  accurate 
knowledge  of  either  the  split  sounds  or  the  accessory  sounds  can  be  gained 
until  they  are  registered  graphically  by  cardiophonographic  methods  along 
with  simultaneous  venous,  arterial,  or  cardiographic  tracings,  so  that  their 


APEX 


PHONOGRAM 

xhis  SECONDS 


PRE.     1     SYST.  A  2  B 


u  w  .um^fyty- ' 


.  r.  -*,1    *,   V"    >,Va    " 


-^ 


Pig.  104. — Graphic  records  of  presystolic  gallop  rhythm  and  split  pulmonic  second  sound.  A. 
PRE.,  presystolic  rumble;  SYST.,  systolic  murmur;  1,  first  heart  sound;  2  A,  B,  two  parts  of  split  second 
sound  (.04  sec.  apart).  (After  Weiss  and  Joachim.)  B.  Audible  auricular  sound  (presystolic  gallop  rhythm). 
Presystolic  sound  shown  by  arrows.  Protodiastolic  gallop  sound  shown  by  3.  (After  E.  W.  Bridgman, 
Arch.  Int.  Med.,  1914,  xiv,  474.) 


exact  relation  to  the  cardiac  cycle  may  be  determined.  So  rapid  is  the 
sequence  of  the  sounds  that  in  an  individual  case  the  differentiation  between 
split  and  accessory  sounds  is  often  difficult. 

Reduplication  of  the  First  Sound  from  Pericardial  Adhesions. — Reduplication  of  the 
first  sound  is  also  heard  in  a  number  of  cases  in  which  old  pericardial  and  pleural  adhesions 
are  found  at  autopsy  (Sewall),  which  may  be  easily  understood  to  give  an  abnormal  sound 
in  systole.  Just  how  commonly  this  group  occurs  has  not  been  determined  statistically, 
but  under  these  conditions  it  need  not  signify  any  disturbance  of  function. 

Presystolic  Gallop  Rhythm. — Exchaquet  (1875),  Johnson  (1876),  Kriege 
and  Schmall  (1891),  Friedrich  Miiller  (1906),  G.  C.  Robinson  (1908),  and  others 
have  thought  that  the  first  sound  of  gallop  rhythm  was  produced  by  the  auricu- 


PHYSICAL  EXAMINATION. 


173 


lar  systole,  a  view  revived  by  Sewall.  Moreover,  the  writer  has  been  able 
to  show  upon  the  excised  heart  that  when  the  ventricles  become  overfilled 
under  a  slight  positive  pressure  the  auriculoventricular  valves  may  open 
along  only  a  small  part  of  their  line  of  closure.  This  gives  rise  to  a  functional 
stenosis  at  the  point  at  which  they  open,  a  fact  which  may  play  a  role  in  the 
production  of  audible  vibrations.  As  far  as  the  time  of  occurrence  of  presys- 
tolic gallop  rhythms  is  concerned,  the  question  was  settled  by  the  graphic 
records  of  E.  W.  Bridgman  (Arch.  Int.  Med.,  1914,  xiv,  474).  Bridgman's  trac- 
ings show  a  small  wavelet  which  occurs  .07  sec.  before  the  first  heart  sound. 
He  encountered  this  wave  frequently  among  healthy  normal  school-boys. 

Many  of  the  conditions  under  which  presystolic  gallop  rhythm  is  en- 
countered, such  as  overstrain,  high  blood-pressure,  mitral  stenosis,  etc.,  are 
of  such  a  nature  as  to  indicate  that  the  sound  may  be  produced  when  both 
the  ventricles  and  the  auricle  are  overloaded  so  that  the  latter  is  stimulated 
to  very  forcible  contractions,  and  on  the  other  hand,  the  auriculoventricular 
valves  are  kept  closed  on  account  of  overloading  of  the  ventricle.  Indeed, 
R.  Offenbecher  (Arch,  exper.  Path.  u.  Pharmakol.,  1914,  lxvi,  1)  has  produced 
just  such  a  gallop  rhythm  experimentally.  He  did  so  by  producing  a  tempor- 
ary mitral  stenosis  in  animals  by  the  method  of  Hirschfelder,  and  gradually 
tightening  the  ligature  until  the  left  auricle  became  overloaded  and  began 
to  carry  out  contractions  of  increased  force.  At  this  stage  an  audible  sound 
was  present,  which  corresponds  closely  to  the  sound  recorded  graphically  by 
Bridgman. 

The  numerous  reviews  of  the  literature,  such  as  those  of  Obrastow,  Pawinski,  Robin- 
son, shed  no  further  light  upon  the  subject. 

Clinically,  the  presystolic  gallop  rhythm  is  usually  met  with  in  cases 
with  rapid  hypertrophied  hearts  which  are  under  a  slight  overstrain,  as  in  the 
classical  group  of  chronic  nephritis,  chronic  cardiac  disease,  aneurism,  cases 
with  arteriosclerosis,  exophthalmic  goitre,  mitral  stenosis,  and  acute  fevers. 

Protodiastolic  Gallop  Rhythm. 
Third  Heart  Sound. — The  role  of  the 
protodiastolic  sound  (bruit  de  rappel, 
diastolic  echo)  seems  to  be  more 
definitely  established.  Though 
already  heard  by  Bouillaud  in  1835, 
in  mitral  stenosis,  its  occurrence  was 
emphasized  by  Duroziez  (1874)  and  by 
Sansom  (1881),  who  term  it  the  "open- 
ing snap"  of  the  mitral  valve,  indi- 
cating that  it  was  brought  about  by  the  opening  of  the  stiffened  valve. 
Barie  (1893)  and  Thayer  (1906)  called  attention  to  its  occurrence  in  normal 
individuals.  In  1907  the  writer  observed  this  sound  in  a  normal  individual 
with  a  slow  and  vigorous  heart,  whose  venous  pulse  showed  a  peculiar  extra 
wave  (Fig.  106,  h)  which  follows  the  inflow  of  blood  into  the  ventricle 
(as  indicated  by  the  normal  v  wave,  Fig.  106,  page  174). 

The  writer  also  called  attention  to  the  fact  that  this  wave  bore  a  close  relation  to  the 
end  of  the  rapid  filling  of  the  heart  (or  diastole  proper)  upon  the  volume  curve  of  the  ven- 
tricles, and  that  Henderson  had  claimed  that  at  this  time  the  mitral  valves  and  tricuspid 
were  closed  by  the  elastic  recoil  of  the  heart  walls.    That  this  actually  takes  place  and  is 


Fig.  105.- 
sound. 


Graphic   record   of   the  third  heart 
(Kindness  of  Prof.  Einthoven.) 


174 


DISEASES   OF   THE   HEART   AND   AORTA. 


dependent  upon  a  high  venous  pressure  can  be  shown  on  the  dead  heart  by  pouring  water 
into  the  ventricles  from  a  beaker  after  the  auricles  have  been  cut  off  in  the  manner  devised 


Uf 

^[KrihMli- 

^S 

IMaL 

4:'Kf"i\ 

1    U 

,  P    A           c 

C   d        c   d 

— 

X   31               XV 

v  uu 

^^^^ 

^^^^ 

Fig.  106. — Jugular  and  carotid  tracings  from  a  normal  individual  with  a  well-marked  third  heart 
sound,  showing  a  large  h  and  a  smaller  preauricular  wave  (w).  ?  indicates  a  small  wave  in  middiastole 
following  the  h  wave,  occasionally  found  though  perhaps  an  artefact. 


by  Baumgarten  (1843).  If  the  water  is  poured  from  just  above  the  valves  they  merely 
float  out  a  little  toward  the  middle  of  the  orifice;  if  from  the  height  of  about  10  cm.  they 
float  into  apposition;  if  from  50  cm.  above  they  are  left  tightly  closed  when  the  flow  ceases. 
These  observations  have  been  confirmed  recently  by  C.  Lian  in  Francois-Franck's  labora- 
tory. Hirschfelder  also  suggested  that  this  clos- 
ure of  the  valves  may  be  sudden  and  vigorous 
enough  to  cause  a  sound.1  The  relation  of  this 
sound  to  this  portion  of  diastole  seemed  quite 
definite  by  comparison  with  a  graphic  record  of 
this  sound  made  at  about  the  same  date  by 
Einthoven  (Fig.  105),  which  shows  it  to  occur 
0.18  second  after  the  second  sound.  This  ex- 
planation has  also  been  supported  by  A.  G. 
Gibson  and  Professor  Thayer.  The  tracings  of 
Robinson,  who  was  investigating  the  subject 
from  a  different  stand-point,  have  also  shown 
the  constant  presence  of  the  h  wave  upon  the 
venous  tracings  accompanying  this  sound.  Rob- 
inson and  Thayer  have  also  shown  that  it  accom- 
panies a  wavelet  p  upon  the  cardiogram  in  early 
diastole  (Fig.  88,  I,  page  155),  probably  due  to 
the  filling  of  the  ventricles.  They  find  this  wave 
upon  the  cardiogram  in  almost  all  cases  of  pro- 
todiastolic gallop  rhythm,  and  regard  it  as  char- 
acteristic of  the  latter.  Thayer  has  demonstrated 
that  it  cannot  be  an  artefact,  since  it  is  often 
both  visible  and  palpable.  Ven- 
ous tracings  made  from  animals  by  Eyster  along 
with  the  volume  curves  of  the  ventricles  show 
that  the  foot  of  the  h  wave,  or  more  exactly  the 
trough  of  the  depression,  marks  the  end  of  the 
■  rapid  diastolic  filling,  and  his  graphic  records  of 
the  heart  sound  show  that  the  third  sound  occurs  at  this  instant.  The  sequence  of  events 
would  be  as  follows :  The  end  of  systole  is  marked  by  the  second  heart  sound  and  by  the 
fall  in  the  cardiogram.  The  tricuspid  and  mitral  valves  open  almost  instantaneously,  but 
a  period  of  about  tV  second  is  required  before  the  fall  of  pressure  is  transmitted  to  the  jugu- 
lar vein  and  the  pressure  begins  to  fall  (v-y  collapse) .     The  inrush  of  blood  into  the  ventricles 


VOL 


Fig.  107. — Forces  supposed  to  be  at  work 
in  the  production  of  the  third  heart  sound. 
Diastolic  closure  of  the  auriculoventricular 
valves.  Dotted  lines  indicate  the  direction 
of  inflow.  Black  arrows  indicate  the  recoil 
waves  tending  to  push  the  cusps  together. 


1  The  assumption  of  such  a  slapping  together  of  the  auriculoventricular  valves  at  the 
end  of  ventricular  filling  is  not  at  all  incompatible  with  the  fact  that  a  small  separation  (1-3 
mm.)  may  reappear  between  them  in  the  latter  part  of  diastole,  when  the  accumulation  of 
blood  in  the  auricles  has  become  sufficient  to  just  force  the  cusps  apart  (page  473). 


PHYSICAL   EXAMINATION.  175 

rapidly  distends  the  latter  until  they  reach  their  full  distention,  at  which  the  inflow  ceases  and 
the  cusps  of  both  mitral  and  tricuspid  valves  slap  together  (closing  slap  in  diastole). 
The  end  of  this  inflow  may  be  accompanied  by  a  slight  recoil  or  similar  movement  of  the 
ventricle,  giving  rise  to  the  small  wave  and  shock  noted  at  this  moment.  The  intensity 
of  this  recoil  is  probably  dependent  to  a  great  extent  upon  the  elasticity  (elastic  tissue) 
of  the  ventricular  walls;  hence  its  absence  in  old  persons.  Windle  and  Eyster  have  shown 
that  the  third  heart  sound  may  be  present  without  the  h  wave  or  the  h  wave  without  the 
third  sound.  This  is  not  surprising,  for  the  valves  may  slap  together  neither  suddenly 
enough  nor  hard  enough  to  cause  a  sound  though  they  may  cause  a  wave.  The  sound 
may  be  present  without  the  wave,  for  the  recoil  wave  may  be  damped  by  dilating  auri- 
cles; or  the  cusps  may  close  suddenly  along  the  greater  part  of,  but  not  the  entire  line  of, 
closure  and  give  a  sound  but  not  a  wave. 

A  'priori,  according  to  this  explanation  a  protodiastolic  sound  should 
be  heard  in  slow  hearts  because  in  them  the  ventricular  walls  are  distended 
to  their  full  extent  early  in  diastole;  in  cases  of  aortic  insufficiency  because 
of  the  high  intraventricular  pressure  which  tends  to  slap  the  cusps  of  the 
valves  together  early  in  diastole;  in  mitral  stenosis  owing  to  the  peculiar 
events  in  the  filling  of  the  ventricle  (vide  page  12),  and  perhaps  in  cases 
in  which  there  is  a  large  amount  of  residual  blood  in  the  ventricle  (dilata- 
tion) which  tends  to  diminish  and  shorten  the  period  of  inflow.  These 
represent  the  chief  conditions  in  which  it  is  actually  heard.  Thayer 
states  that  it  can  be  heard  at  the  apex  in  about  30  per 
cent,   of    normal   individuals   lying   upon   the   left    side. 

By  decades  its  frequency  was  as  follows;  First  decade  heard  in  58.9 
per  cent.;  second  decade  84.4  per  cent.;  third  decade  50.9  per  cent.;  fourth 
decade  42.3  per  cent.;  fifth  decade  14  per  cent.;  sixth  decade  and  after  0. 
It  seems  to  occur  in  practically  every  condition,  especially  in  cases  with 
slow  hearts,  and  seems  to  bear  no  definite  relation  to  cardiac  weakness. 

MURMURS. 

MECHANICAL   FACTORS    IN    THE    PRODUCTION    OF    MURMURS. 

As  has  been  seen  above  (page  156),  when  a  narrowing  occurs  in  the 
lumen  of  an  elastic-walled  tube  through  which  liquid  is  flowing,  eddies  are 
formed  which  set  the  walls  of  the  tube  into  vibration  and  give  rise  to  a  pal- 
pable thrill.  Accompanying  the  thrill  a  blowing  sound  known  as  a  "  mur- 
mur" may  be  heard  over  the  tube;  which,  like  the  thrill,  is  heard  much 
better  below  the  obstruction  than  above  it,  and  is  transmitted  in  the  direc- 
tion of  the  flow.  The  character  of  a  murmur  depends  upon  the  width  of 
the  orifice  at  which  it  is  produced,  upon  the  nature  of  the  walls  of  the 
orifice,  upon  the  velocity  and  tension  under  which  the  fluid  passes  through 
it,  and  upon  the  direction  in  which  the  flow  occurs. 

In  this  way  a  valvular  orifice  may  be  compared  to  the  larynx 
with  its  vocal  cords.  When  the  cords  are  lax  and  wide  apart,  the  air  moving  over  them  in 
even  forced  respiration  gives  no  sound;  when  the  cords  are  approximated  a  little  but  still 
held  loosely,  it  gives  a  whispered  "ch"  sound,  and  when  they  are  held  very  tense  true 
vocal  sound  is  heard.  Similarly,  no  sound  can  be  heard  over  the  excised  heart  when  the 
fluid  regurgitates  through  an  absolutely  patent  mitral  orifice  (Fig.  108) ;  if  one  of  the  chordae 
tendinete  be  stretched  and  the  regurgitation  takes  place  through  a  small  slit  whose  walls 

1  In  the  light  of  these  facts  it  is  difficult  to  comprehend  why  Windle  heard  the  third 
sound  in  only  2  per  cent,  of  his  cases. 


176 


DISEASES   OF   THE   HEART   AND    AORTA. 


are  flabby  (relative  insufficiency,  Fig.  108),  a  soft  low  blowing  murmur  will  be  heard  (the 
smaller  this  orifice  the  higher  pitched  and  more  distinct  the  murmur) ;  while  if  some  more 
or  less  hard  irregular  body,  like  calcified  vegetation,  is  situated  at  the  orifice,  this  acts  more 
or  less  as  a  resonator,  increases  the  sound,  and  may  even  give  it  a  roaring  or  a  squeaking 
(musical)  character.1 


Fig.  108. — Similarity  between  production  of  voice  sounds  and  the  production  of  murmurs.  (Kindness 
of  the  J.  Am.  M.  Asso.)  A,  B,  C,  vocal  cords  ;  D,  E,  F,  auriculo ventricular  valves;  G,  H,  I,  aortic  and  pul- 
monic valves.  A  (high  note),  D,  G,  small  leaks  producing  high-pitched  murmurs;  B  (low  note),  E,  H, 
larger  leaks  producing  low-pitcned  murmurs  ;  C,  F,  I,  very  large  leaks,  producing  no  murmurs. 

Occasionally  murmurs  become  so  loud  as  to  be  heard  several  feet  away 
from  the  chest  or  even  across  the  room.  Such  murmurs  are  usually  systolic 
in  time  and  are  often  due  to  calcified  vegetations,  arterial  plaques,  or  aortic 
or  mitral  stenosis.  As  in  the  larynx,  the  character  of  the  sound  produced 
at  a  valvular  orifice  is  due  not  only  to  the  size  and  shape  of  the  orifice,  but 
also  to  the  tenseness  of  the  walls  and  velocity  of  blood  flow  through  it,  and 
hence  is  largely  dependent  upon  the  height  of  the  blood-pressure.  All 
these  factors,  both  the  widening  of  the  leak  and  the  decreased  force  of  the 
beat,  explain  the  fact  that  as  the  heart  weakens  under  the  influence  of  the 
lesion  the  murmur  may  actually  disappear. 


CHARACTER    OF    MURMURS. 

Murmurs  may  be  roughly  divided  into  the  following  classes:  (1)  Direct  mur- 
murs best  transmitted  in  the  direction  of  the  blood  flow,  as  from  stenoses  or  calcified 
plaques;   (2)  Regurgitant  murmurs  due  to  a  flow  in  the  direction  opposite  to  the 

1  Musical  or  squeaking  murmurs  are  sometimes  due  to  the  presence  of  tense  mod- 
erator bands  stretching  across  the  ventricular  cavity  and  resounding  like  banjo  strings, 
although  usually  these  bands  do  not  cause  murmurs  at  all. 

Very  frequently  they  arise  in  dilated  right  ventricles  in  association  with  functional 
tricuspid  and  perhaps  functional  pulmonary  insufficiencies.  They  are  usually  systolic, 
but  sometimes  diastolic  in  time.     They  are  often  cardiopulmonary. 


PHYSICAL  EXAMINATION.  177 

usual  blood  flow  (as  in  mitral  and  aortic  insufficiencies);1  (3)  To-and-fro  "machinery" 
murmurs  which  occur  in  both  systole  and  diastole  in  congenital  heart  lesions;  (4)  Rum- 
bling murmurs. 

Of  these  1,  2,  and  3  are  more  or  less  blowing  or  roaring  in  character; 
while  the  rumbling  murmurs  are  devoid  of  this  character,  and  are  rumbling 
or  echoing,  more  like  a  series  of  heart  sounds  which  vary  in  intensity  (mitral 
stenosis,  Flint  murmur)  than  like  murmurs  due  to  the  passing  of  a  stream 
through  an  orifice. 

Brockbank  claims  that  these  may  be  produced  upon  a  model  by  means  of  a  stream 
flowing  through  a  conical  valve  from  apex  to  the  base  of  the  cone.  The  mechanism  of  the 
production  of  such  murmurs  is  still  very  obscure,  and  further  researches  are  necessary 
before  satisfactory  elucidation  can  be  given. 

Transmission  of  Murmurs  from  the  Auriculoventricular  Valves. — Regurgitations  at 
the  mitral  and  tricuspid  orifices,  however,  give  rise  to  systolic  murmurs  which  are  trans- 
mitted loudly  in  two  ways:  in  the  direction  of  the  regurgitant  stream,  and  also  in  a  direction 
exactly  opposite  to  the  latter.  In  the  cases  of  mitral  insufficiency  the  regurgitant  stream 
through  the  mitral  valve  strikes  the  posterior  wall  of  the  left  auricle  and  imparts  its 
vibrations  to  the  chest  wall  in  the  lower  left  interscapular  region.  In  this  area  a  systolic 
murmur  is  readily  heard  in  thin-chested  individuals,  but  even  in  them  it  is  not  so  loud  as 
the  systolic  murmur  heard  over  the  apex  and  in  the  left  axilla  near  the  apex,  which  is  con- 
ventionally accepted  as  the  characteristic  sign  of  mitral  insufficiency  and  which  is  heard 
in  many  cases  of  mitral  insufficiency  in  which  the  murmur  at  the  back  cannot  be  made  out. 
Similarly  in  tricuspid  insufficiency  the  regurgitant  stream  impinges  against  the  wall  of  the 
right  auricle,  which  is  distended  so  that  the  regurgitant  stream  should  strike  against  its 
wall  near  the  right  border  of  cardiac  dulness,  and  hence  the  murmur  should  be  heard  at 
its  maximum  far  to  the  right  of  the  sternum.  Though  a  loud  murmur  is  heard  in  this  area 
in  occasional  cases,  the  most  common  site  of  maximal  is  between  the  sternum  and  the 
parasternal  line  or  the  sternum  and  the  apex, — that  is,  over  the  right  ventricle.  In  both 
mitral  insufficiency  and  mitral  stenosis,  therefore,  the  murmur  is  conducted  loudest  for- 
ward over  the  ventricle,  though  the  blood  impact  of  the  regurgitant  stream  takes  place  in 
the  opposite  direction. 

No  explanation  for  this  apparently  paradoxical  condition  was  given  until  the  writer, 
in  1910,  suggested  that  the  vibrations  set  up  in  the  valves  by  the 
regurgitant  streams  might  be  propagated  along  the  chordae 
tendineae  and  the  papillary  muscles  to  the  walls  of  the  ven- 
tricles, and  thus  transmitted  to  the  chest  walls.  In  favor  of  this  theory  was  the  fact 
that  the  points  at  which  the  murmurs  of  mitral  and  tricuspid  insufficiency  are  heard  loud- 
est correspond  closely  to  the  insertions  of  the  anterior  papillary  muscles  in  the  walls  of  the 
right  and  left  ventricles.  At  the  writer's  suggestion  the  matter  was  subjected  to  experi- 
mental test  by  W.  T.  DeSautelle  and  E.  G.  Grey  (Arch.  Int.  Med.,  1911,  viii,  734).  These 
investigators  studied  the  intensity  of  the  murmur  produced  in  the  dead  pig's  heart  by 
the  passage  of  a  stream  of  water  allowed  to  flow  from  a  pressure  bottle  into  the  ventricles 
and  to  pass  out  of  them  through  a  leak  at  the  auriculoventricular  valves,  which  they  pro- 
duced either  by  cutting  the  cusps  or  by  sewing  upon  the  latter  "vegetations"  made  from 
masses  of  knotted  cord.  They  then  listened  over  the  entire  surface  of  the  heart  and  found 
that  the  murmur  was  maximal  over  the  insertion  of  the  valves  about  the  auriculoventricular 
ring  and  also  over  the  areas  which  corresponded  to  the  bases  of  the  papillary  muscles. 
When  the  papillary  muscles  were  cut  away  from  the  heart  wall,  the  murmur  over  these 
areas  became  greatly  diminished  in  intensity,  although  over  any  other  areas  on  the  walls 
removal  of  any  portion  of  its  thickness  tended  to  increase  the  intensity  of  the  murmur.  On 
the  other  hand,  they  found  that  when  they  sewed  the  base  of  a  papillary  muscle  which  had 
been  severed  from  its  normal  attachment  on  to  some  new  area  of  the  ventricular  wall,  and 
even  upon  the  interventicular  septum,  the  murmur  immediately  became  maximal  at  that 

1  Mitral  and  tricuspid  regurgitant  murmurs  may  be  transmitted  along  the  papillary 
muscles  (see  page  431). 
12 


178  DISEASES  OF  THE  HEART  AND  AORTA. 

point.  The  murmur  due  to  the  regurgitant  stream  was  thus  proved  to  be  carried  in  the 
direction  opposite  to  the  regurgitation  by  transmission  along  the  chordae  tendinese  and 
papillary  muscles. 

S.  Engh,  in  the  pharmacological  laboratory  of  the  University  of  Minnesota,  re- 
cently applied  the  same  method  to  the  study  of  the  incidence  of  regurgitant  streams  and 
the  conduction  of  murmurs  in  aortic  insufficiency  and  has  found  that  here,  too,  the  papillary 
muscles  conduct  the  murmurs. 

"accidental,"  "klemic,"  and  "cardiopulmonary"  murmurs. 

Murmurs  over  the  heart  without  the  presence  of  valvular  lesions  are 
so  common  that  autopsy  evidence  led  Laennec  to  the  erroneous  belief  that 
murmurs  (bruits  de  soufflet)  were  of  no  diagnostic  importance  whatever. 

Such  murmurs  are  designated  by  various  terms :  "Haemic,"  on  the 
assumption  that  they  are  always  due  to  anaemia,  hydrsemia,  or  other  changes 
in  the  quality  of  the  blood;  "Functional"  or  "inorganic,"  because 
they  are  not  associated  with  organic  lesion;  "Cardiopulmonary"  or 
"cardiorespiratory,"  on  the  assumption  that  they  arise  in  the  lung  above  the 
heart  and  not  in  the  heart  itself;  and  "Accidental,"  since  they  are  not  asso- 
ciated with  any  discernible  alteration  in  form  or  function.  These  terms  are  not 
mutually  exclusive;  but,  since  the  term  "functional"  has  been  used  to  desig- 
nate conditions  in  which  there  is  actual  leakage  owing  to  muscular  weakness, 
and  since  "inorganic"  should  include  both  "functional"  and  "accidental," 
the  term  "accidental"  appears  to  be  the  one  most  generally  useful.  Thus, 
one  murmur  may  be  said  to  be  an  accidental  murmur  of  hsemic  origin,  while 
in  another  case  the  accidental  murmur  may  be  of  cardiopulmonary  origin. 

Occurrence  of  Accidental  Murmurs. — Potain,  who  has  made  the  most  extensive  inves- 
tigations upon  the  subject,  found  such  murmurs  in  one-eighth  of  all  the  patients  seen  in  his 
hospital  service.  It  was  present  in  almost  all  his  cases  of  Basedow's  disease  (exophthalmic 
goitre).  In  chlorosis  the  frequency  was  50  per  cent.;  in  rheumatism,  measles,  and  scarlet 
fever,  20-25  per  cent.;  in  typhoid,  16  per  cent.;  in  pulmonary  affections,  5-10  per  cent. 
These  murmurs  were  common  in  subjects  in  the  first  three  decades  of  life,  reaching  maxi- 
mum frequency  at  the  age3  from  20  to  30,  and  gradually  decreased  in  frequency  after  the 
age  of  30.  For  description  of  the  murmurs  Potain  divided  the  precordium  into  the  follow- 
ing regions:  1.  About  the  apex  (apical  zone) ;  2.  Above  the  apex  (supra-apical) ;  3.  Lateral 
from  the  apex  (para-apical);  4.  In  front  of  the  infundibulum  and  conus  arteriosus  of  the 
pulmonary  artery  (pre-inf undibular) ;  5.  A  zone  between  the  pre-infundibular  region  and 
the  apex  (left  preventricular) ;  6.  An  area  behind  the  sternum  (sternal  region) ;  7.  A  region 
behind  the  xiphoid  (xiphoid  region).  The  murmurs  are  most  common  in  the  region  lying 
between  the  pulmonary  area  and  the  apex  (Potain's  left  ventricular  region), — that  is,  in 
the  region  above  the  right  ventricle  and  the  interventricular  septum. 

Character  of  Accidental  Murmurs. — T  hese  murmurs  usually 
are  soft  and  blowing,  and  often  seemrather  super- 
ficial. They  vary  greatly  when  the  patient  changes 
his  position.  Sometimes  they  are  best  heard  when  the  patient  is 
lying  down  and  diminish  or  disappear  entirely  when  he  stands  or  sits 
up;  sometimes  they  appear  only  when  the  patient's  position  is  vertical 
and  disappear  on  his  lying  down.  They  also  vary  with  the  phases  of 
respiration. 

Time  of  Accidental  Murmurs.  —  As  regards  their  occurrence  in  the 
cardiac  cycle,  accidental  murmurs  are  most  commonly  systolic  in  time, 
though  occasionally  diastolic.  Potain  calls  attention  to  the  fact  that  mur- 
murs may  occupy  either  the  whole  of  systole  (holosy st olic)  or  only 


PHYSICAL  EXAMINATION.  179 

a  portion  of  it.  The  latter  may  occur  only  at  the  very  beginning  of  systole 
(protosystolic),  so  that  they  accompany  or  replace  the  first  heart 
sound.  Or,  they  may  be  heard  in  midsystole  (mesosystolic),  in 
which  case  they  follow  the  first  sound  but  are  separated  from  the  second 
sound  by  the  short  pause,  which  is  then  somewhat  shorter  than  usual. 
Or,  they  may  occur  at  the  very  end  of  systole  (telesystolic)  and 
end,  without  interruption,  in  the  second  sound.  According  to  Potain, 
the  murmurs  of  mitral  and  tricuspid  insufficiency 
are  heard  throughout  the  entire  duration  of  systole, 
a  view  which  is  confirmed  by  the  graphic  records  of  Einthoven  and  Weiss 
and  Joachim.  The  accidental  murmurs,  however,  are  con- 
fined to  only  a  portion  of  systole.  Potain  believes 
that,  as  a  rule,  they  are  entirely  mesosystolic;  while 
Weiss  and  Joachim,  from  both  auscultatory  and  graphic  evidence  (Fig. 
110),  believe  that  they  also  accompany  and  modify  the  first  sound  though 
they  do  not  replace  it;  in  other  words,  that  they  occupy  both  the  proto- 
systolic and  the  mesosystolic  portions  of  the  systole. 

Sahli  states  that  accidental  murmurs  never  occupy  the  very  end  of 
systole  (telesystolic,  Potain;  prediastolic),  but  Potain  has  shown  that 
though  such  murmurs  are  rare  they  occur  occasionally. 

Accidental  diastolic  murmurs  are  also  rather  common,  and  may  occur 
either  in  the  aortic  region,  behind  the  sternum,  or  along  the  upper  left 
border  of  cardiac  dulness.  Occasionally  they  are  heard  at  the  apex.  They 
are  usually  short  superficial  puffs  following  a  well-marked  second  sound 
and  lasting  during  only  a  short  portion  of  early  diastole. 

Differential  Diagnosis  of  Accidental  Murmurs. — Potain  gives  the  following  points  in 
which  other  murmurs  differ  from  the  cardiopulmonary. 

1.  Pulmonary  Stenosis:  loud,  rough  holosystolic  murmur,  maximum  in 
second  left  interspace,  transmitted  toward  left  clavicle;  always  accompanied  by  a  thrill. 
The  accidental  murmur  is  soft,  often  mesosystolic,  devoid  of  thrill. 

2.  Pulmonary  Insufficiency:  diastolic  murmur  maximum  in  second  left 
interspace;  pulmonic  second  sound  absent  or  diminished.  The  accidental  diastolic  murmurs 
very  rarely  have  their  maximum  in  the  second  left  interspace. 

3.  Aortic  Stenosis:  rough  holosystolic  murmur,  maximum  in  second  right 
interspace,  propagated  toward  right  clavicle;  accompanied  by  thrill.  The  heart  is  hyper- 
trophied.  The  accidental  or  cardiopulmonary  murmur  in  this  region  is  more  superficial, 
soft,  and  changes  on  change  of  position. 

4.  Anaemia:  murmur  very  similar  to  that  of  aortic  stenosis,  but  the  thrill  is  less 
marked  and  the  heart  is  small  or  dilated  rather  than  hypertrophied. 

5.  Aortic  Insufficiency:  murmur  commences  exactly  at  the  beginning  of 
the  second  sound  and  almost  entirely  fills  diastole;  whereas  the  cardiopulmonary  diastolic 
murmur  follows  the  second  sound,  often  after  a  short  intervening  pause  (i.e.,  the  murmur  is 
mesodiastolic) .  Both  aortic  and  accidental  murmurs  are  of  wide  distribution,  embracing 
the  entire  precordium,  and  varying  greatly  with  change  of  position. 

6.  Patent  Septum  of  the  Ventricles:  holosystolic  murmur  loudest  at 
the  third  left  interspace;  rough,  always  accompanied  by  a  thrill;  whereas  the  accidental 
and  cardiopulmonary  murmurs  are  not. 

7.  Mitral  Insufficiency:  murmur  holosystolic,  usually  rather  rough,  maxi- 
mum at  the  apex.  The  cardiopulmonary  murmur  may  have  its  maximum  two  or  three 
centimetres  lateral  wards  from  the  apex;  and  this  is  usually  associated  with  a  systolic  retrac- 
tion at  the  apex. 

8.  Tricuspid  Insufficiency:  murmur  maximum  over  sternum  and  xiphoid 
process.  There  is  an  increased  area  of  flatness  (hypertrophy  of  ventricles).  This  murmur 
is  also  increased  by  leaning  forwards  so  as  to  throw  the  heart  against  the  chest  wall. 


180  DISEASES  OF  THE  HEART  AND  AORTA. 

Nature  and  Causation  of  Accidental  Murmurs, — The  facts  mentioned, 
above  apply  to  a  large  number  of  cases  in  which  murmurs  have  been  heard 
during  life,  but  in  which  no  leaks  and  no  lesions  of  the  heart  were  demon- 
strable at  autopsy. 

A  large  variety  of  factors  have  been  mentioned  to  explain  these  accidental  murmurs: 

Haemic  Murmurs. — Bouillaud  was  the  first  to  call  attention  to  the  fact  that  mur- 
murs were  more  readily  produced  in  the  less  viscous  blood  of 
anaemia  than  under  normal  conditions;  a  fact  which  was  subsequently 
verified  by  Cohnheim ;  but  Bouillaud  himself  realized  that,  though  ansemia  might  give  rise  to 
some  of  the  accidental  murmurs,  there  were  many  cases  in  which  it  could  not  be  a  factor. 
The  blood  counts  made  in  later  decades  have  entirely  substantiated  Bouillaud's  conserva- 
tism. However,  numerous  observers  from  Bouillaud's  time  to  the  present  have  adhered 
to  the  "haemic"  origin  of  the  accidental  murmurs.  Sahli  goes  so  far  as  to  state  that 
they  may  in  reality  be  only  venous  hums  transmitted  to  the 
ventricles,  though  he  does  not  explain  why  they  should  be  systolic  in  time.  Even 
though  this  explanation  is  inadequate,  it  is  certain  that  in  cases  of  grave  anaemia  such  trans- 
mitted murmurs  do  arise.  They  are  heard  very  loudly  over  the  aorta  and  second  right 
interspace,  but  are  loud,  rough,  and  superficial,  quite  different  from  the  gentle  blow  of  the 
usual  accidental  murmurs. 

Functional  Insufficiency  of  the  Auriculoventricular  Valves,  especially  of  the  mitral, 
was  supposed  by  Naunyn  to  be  the  chief  cause  of  the  accidental  murmur  in  the  pulmonary 
area.  Naunyn  believed  that  this  murmur  was  transmitted  from  the  left  auricle  directly  to 
the  pulmonary  artery  and  thence  to  the  chest  wall  in  the  pulmonary  area.  However,  in 
these  cases  the  murmur  may  not  be  heard  at  all  in  those  areas  in  which  the  definite  mitral 
and  tricuspid  murmurs  are  best  heard.  Functional  insufficiency  of  the  tricuspid  valve 
has  also  been  assumed,  but  this  is  rendered  improbable  by  the  fact  that  these  murmurs  have 
a  very  different  distribution  from  those  of  the  tricuspid  and  are  rarely  heard  over  the 
xiphoid  process.  In  dogs  the  writer  has  found  accidental  murmurs  very  common;  but, 
in  contrast  to  the  murmurs  in  tricuspid  or  mitral  insufficiency,  these  accidental 
murmurs  cannot  be  heard  over  the  right  or  left  auricle.  In  man 
also  they  are  not  heard  over  the  region  of  the  right  auricle,  even  when  the  patient  is  made 
to  lean  forward  and  the  walls  of  that  chamber  are  thus  pressed  against  the  chest  wall. 

Functional  Stenosis  of  the  Pulmonary  Artery  and  Infundibulum  has  been  assumed  by 
Luethje  in  order  to  explain  the  production  of  systolic  murmurs  in  the  pulmonary  area. 
It  is  true  that  the  pulmonary  artery  makes  a  sharp  bend  just  behind  the  second  left  inter- 
space; and  also,  as  Romberg  and  others  have  shown,  that  often  the  accidental  murmur  is 
increased  by  pressure  with  the  stethoscope.  Against  this  view  are  the  softness  of  the 
murmur,  the  absence  of  a  thrill,  and  the  fact  that  it  is  not  transmitted  toward  the  left 
shoulder,  but  is  well  heard  over  the  right  ventricle.  Moreover,  in  dogs  the  accidental  mur- 
mur may  persist  in  practically  every  position  in  which  the  heart  may  be  held. 

Eddy  Currents  within  the  Ventricles. — Hilton  Fagge  has  called  attention  to  the  fact 
that  eddy  currents  may  arise  within  the  ventricles,  as  the  blood  passes  between  the  papillary 
muscles  and  the  trabecular  carnae.  However,  W.  M.  Dunn  and  W.  S.  Bennett,  in  the  writer's 
laboratory,  have  studied  this  question  experimentally  upon  the  dead  pig's  heart  through 
which  a  stream  of  water  was  allowed  to  flow  from  a  pressure  bottle.  They  found  that  such 
a  stream  flowing  into  the  heart  from  the  right  auricle  and  out  through  the  pulmonary 
artery  gave  rise  to  just  such  a  murmur  over  the  conus  arteriosus,  but  that  this  murmur 
persisted  even  after  the  eddy  currents  were  altered  by  cutting  away  the  papillary  muscles 
and  the  columnar  carneae.  On  the  other  hand,  they  found  that  the  murmur  was  due  largely 
to  the  direct  impact  of  the  blood  stream  upon  the  walls  of  the  conus  and  that  a  similar 
stream  which  arose  in  the  left  ventricle  impinged  upon  the  septum  ventriculorum  just 
behind  the  infundibulum  and  was  transmitted  to  the  latter.  These  murmurs  were  loudest 
over  the  infundibulum  at  the  time  that  the  blood  stream  was  most  rapid  (i.e.,  in  midsystole, 
which  corresponds  to  the  instant  of  the  accidental  murmur)  and  it  was  most  intense  when 
the  viscosity  of  the  blood  and  the  peripheral  resistance  were  low.  All  these  factors  corre- 
spond to  conditions  which  seem  to  accompany  the  accidental  murmur  clinically,  but  though 
suggestive  they  cannot  be  accepted  as  a  complete  explanation  of  the  latter  without  further 
proof. 


PHYSICAL  EXAMINATION.  181 

Similar  to  this  view  is  the  old-time  assumption  that  accidental  blowing  as  well  as 
musical  murmurs  indicated  the  presence  of  a  moderator  band  across  the  chamber  of  the 
right  ventricle,  but  this  is  not  borne  out  by  autopsy  experience. 

Cardiopulmonary  Factors. — Laennec  in  1826  wrote:  "In  certain  persons  the  pleurae 
and  the  anterior  borders  of  the  lungs  extend  in  front  of  the  heart  and  cover  it  almost  entirely 
If  one  examines  such  a  person  when  his  heart  is  beating  more  forci- 
bly than  usual,  the  diastole  of  the  heart,  compressing  these 
portions  of  the  lungs  and  forcing  the  air  out  of  them,  alters  the 
breath  sounds  in  such  a  way  that  it  imitates  a  blowing  murmur  or  the  sound  of  wood  file. 
But  with  a  little  skill  it  becomes  easy  to  distinguish  this  sound  from  a  cardiac  murmur. 
It  is  more  superficial;  one  hears  the  normal  heart  sounds  be- 
low it;  and  it  disappears  almost  entirely  when  the  patient  is 
made   to   hold  his   breath  for  a  few  moments.''1 

Physiological  experiments  have  borne  out  Laennec's  claim  that  the  lung  moves  to  and 
fro  with  each  cardiac  cycle  (Buisson,  Voit,  van  der  Heul,  Landois,  Meltzer),  but  have  demon- 
strated that  the  most  sudden  movement  of  the  air  accompanies  the  rarefaction  of  the  air 
within  the  lung  during  systole,  rather 
than  its  extrusion  during  diastole.  m——mmm—mmmm— "  ~    HBHMH| 

The    cardiopulmonary   murmurs    I 
formed    the  subject  of  an  exhaustive 
study  from  1865  to  1894  by  Potain, 

many  of  whose  data  have  been  given  ^^B 

above.     Potain  controlled  the  findings 

by  auscultation  with  carefully  made  "*, i&i 

cardiograms  and  experimental  studies  f     u  ImfflfcY 

and  found  that:  (      M     l|j\  ■  tiiii 

1.  The  cardiopulmonary  murmurs         H  V^  J.j||  |  mm 
are    loudest    and    most     frequent   in        .  H                                   'Wiilljiy 

those  regions  (infundibulum  and  vicin-  Brae 

ity  of  the   pulmonary  artery)   where  .   ?,;. 

the  movement  of  the  heart  is  greatest.  |HS 

2.  They  occur   in   regions  '"B  | 

and    in    phases    of     the     car-    l.&ii]  I  | 

diac   cycle   at   which   the  car-        MM  I 

diogram    shows     retractions    \f^i  _ ______■■...'■ 

of     the     interspace     (areas  of 

negative  pressure  with  sudden  expan-  FlG-  109.-DiStribution  of  the  accidental  murmur. 

sion  of  the  lung). 

Hence,  the  systolic  murmur  is  most  common  over  the  infundibulum  and  right  ven- 
tricle, over  which  there  is  usually  a  systolic  retraction  (see  page  153  and  Fig.  89). 

If  the  retraction  (fall  in  the  cardiogram)  occurs  in  the  middle  of  systole,  the  murmur 
is  found  to  be  mesosystolic;  if  at  the  end  of  systole,  the  murmur  is  telesystolic;  if  the  fall  is 
in  diastole,  the  murmur  is  diastolic.  Indeed  Potain  encountered  several  cases  in  which 
the  form  of  the  cardiogram  changed  upon  alteration  of  the  position  of  the  patient;  and 
corresponding  to  the  period  of  greatest  retraction  the  murmur  over  the  area  changed  from 
mesosystolic  to  diastolic. 

This  is  a  surprising  confirmation  of  the  theory  of  cardiopulmonary  murmurs.  There 
can  indeed  be  no  doubt  that  cardiopulmonary  murmurs  are  frequent,  and  that  they  form 
a  very  considerable  proportion  of  "  accidental "  murmurs.  Besides  the  blowing  murmurs 
referred  to  above, it  is  probable  that  many  of  the  so-called  "musical"  or  "squeak- 
ing" murmurs  are  of  cardiopulmonary  origin,  and  are  really  piping  rales  produced  by  the 

1  "Chez  quelques  sujets,  les  plevres  et  les  bords  anterieurs  des  poumons  se  prolongent 
au-devant  du  cceur  et  le  recouvrent  presque  entierement.  Si  Ton  explore  un  pareil  sujet 
au  moment  oil  il  eprouve  des  battements  du  cceur  un  peu  energiques,  la  diastole  du  coeur 
comprimant  ces  portions  du  poumon  et  en  exprimant  l'air,  altere  le  bruit  de  la  respiration 
de  maniere  a  ce  qu'il  imite  plus  ou  moins  bien  celui  d'un  soufflet  donne  par  le  cceur  lui- 
meme:  il  est  plus  superficiel;  on  entend  au  dessous  le  bruit  naturel  du  cceur;  et  en  recom- 
mandant  au  malade  de  retenir  pendant  quelques  instants  sa  respiration,  il  diminue  beau- 
coup  ou  cesse  presque  entierement." 


182  DISEASES  OF  THE  HEART  AND  AORTA. 

to-and-fro  movement  in  the  lung  during  either  phase  of  the  cardiac  cycle.  Other  rales  of 
cardiopulmonary  origin  more  closely  resembling  the  sonorous  and  crepitant  rales 
of  respiration  are  also  very  common  along  the  margin  of  the  left  lung.  Moreover,  the  breath 
sounds  themselves  are  frequently  modified  by  the  cardiac  movements,  giving  rise  to  the  so- 
called  cog-wheel  type  of  breathing;  in  which  inspiration  is  interrupted  by  a  series 
of  small  clicks  and  pauses  coincident  with  and  due  to  the  effects  of  cardiac  contractions 
upon  the  air  in  the  lungs.  The  cog-wheel  type  of  breathing  is  often  associated  with  slight 
changes  in  the  overlying  lung  and  is  thus  often  a  premonitory  sign  of  pulmonary  tuberculosis. 

Differentiation  between  Cardiopulmonary  and  other  Accidental  Mur= 
murs. — However,  in  spite  of  the  frequency  of  cardiopulmonary  murmurs, 
it  is  probable  that  Potain  erred  in  ascribing  all  accidental  or  non-valvular 
murmurs  to  this  origin.  In  the  first  place,  many  such  murmurs  are  audible 
over  the  area  of  cardiac  flatness  several  centimetres  from  the  lung  borders, 
when  breath  sounds  which  are  of  equal  loudness  over  the  lung  cannot  be 


CAROTID 


PHONOGRAM 


Fig.  110. — Graphic  record  of  an  accidental  murmur.     (After  Weiss  and  Joachim.) 

heard  at  all  at  these  sites.  Secondly,  the  murmurs  can  be  well  heard  directly 
over  the  exposed  dogs'  hearts  when  the  lung  has  been  entirely  retracted, 
and  when  valvular  insufficiencies  and  stenoses  can  be  absolutely  excluded. 
For  the  present,  therefore,  it  must  be  admitted  that  there  are  still 
many  uncertainties  in  the  differentiation  between  cardiopulmonary  and 
other  accidental  murmurs.  The  diagnosis  of  the  former  must 
be  confined  to  murmurs  of  distinctly  superficial 
quality  which  are  heard  loudest  over  the  lung  bor- 
ders and  are  absent  or  much  diminished  over  the  area, 
of  cardiac  flatness,  and  which  vary  with  change  of  position. 
The  diagnosis  may  be  considered  as  rendered  probable  if  the  area  over 
which  the  murmur  is  heard  moves  toward  the  sternum  in  inspiration  and 
away  from  it  in  expiration,  corresponding  to  the  movement  of  the  marginal 
strip  of  lung.  If  the  reverse  is  the  case  and  the  area  of  intensity  extends 
lateralward  in  expiration  and  recedes  toward  the  sternum  in  inspiration, 
the  murmur  is  more  likely  to  arise  within  the  heart. 

Imitations  of  the  Heart  Sounds. — A  remarkably  accurate  method  for  imitating  the 
heart  sounds,  reduplications,  and  rough  or  blowing  murmurs  has  been  used  for  the  past 
three  years  by  the  writer's  colleague,  Dr.  Charles  W.  Lamed.  This  is  carried  out  by  placing 
the  palm  of  the  observer's  hand  tightly  over  his  ear,  and  then  tapping  upon  the  elbow 
with  the  finger  tips  of  the  other  hand.  The  blow  must  be  struck  with  loose  finger-joints. 
Its  force  can  be  varied  to  suit  variations  in  the  loudness  of  the  sound.  Dull  and 
distant  sounds  may  be  imitated  by  light  blows  of  the  finger  or  by  raising  the  palm  of  the 
hand  from  the  ear,  snapping  sounds  by  pressing  the  hand  tightly  upon  the  ear  and 
executing  a  sharp  stroke.     Blowing  murmurs  are  reproduced  by  a  gentle  stroking  of  the 


PHYSICAL  EXAMINATION. 


183 


elbow.  Dr.  Henry  Lee  Smith  has  modified  this  procedure  by  striking  the  blows  directly 
upon  the  back  of  the  hand,  instead  of  the  elbow,  a  method  by  which  sharper  and  more 
snapping  sounds  can  be  produced.  He  is  able  to  give  a  very  accurate  reproduction  of  the 
presystolic  rumble  and  snapping  first  sound  of  mitral  stenosis  by  bringing  all  the  four  fingers 
down  upon  the  knuckles  or  metacarpals  in  as  rapid  succession  as  possible,  a  manoeuvre 
which  is  best  executed  by  a  quick  pronation  from  the  elbow.  The  blow  struck  with  the 
index  finger  (snapping  first  sound)  should  be  somewhat  louder  than  the  rest. 

While  these  methods  are  excellent  for  demonstrating  to  one  student  at  a  time,  they 
cannot  be  used  for  demonstrating  to  a  whole  group  simultaneously.  For  this  purpose  the 
writer  has  resorted  to  the  somewhat  cruder  method  of  executing  the  same  taps  and  strokes 
upon  the  top  of  a  derby  or  even  a  soft  felt  hat.  This  imitation  is  not  quite  so  accurate, 
and  the  snapping  and  rumbling  quality  are  not  reproduced,  but  nevertheless  it  enables 
the  instructor  to  point  out  the  salient  features  to  all  and  to  illustrate  their  main  variations 
and  relations  to  the  events  of  the  cardiac  cycle. 


INTRAVENTRICULAR 
PRESSURE 


VOLUME   OF 
VENTRICLES 


MITRAL  SYSTOLIC 
AORTIC  SYSTOLIC 
AQ.RTIC  DIASTOLIC 
PRESYSTOLIC 


,/A 


L 


\ 


aO 


Fig.  111. — Diagram  showing  the  relation  of  the  more  common  simple  murmurs  to  events  of  the 
cardiac  cycle.  Solid  black  bars  indicate  the  heart  sounds.  Vertical  parallel  lines  reaching  to  the  base 
indicate  blowing  or  rough  murmur.    Wavy  vertical  lines  not  reaching  to  the  base  indicate  a  rumble. 

The  exact  method  for  the  reproduction  of  each  sound  or  murmur  can  thus  be  indi- 
cated schematically  by  designating  the  finger  to  be  used  (I  =  index,  M  =  middle,  R  =  ring 
finger,  L  =  little  finger)  and  the  accent  of  the  sound'.  Time  intervals  may  be  shown  by 
dashes,  and  rapid  succession  of  the  split  sounds  by  bracketing  the  corresponding  letters. 
Murmurs  are  indicated  by  stroke. 

Thus:  P — I  =  Normal  first  sound  at  the  apex;  I — 1'  =  Normal  first  sound  at  aorta; 
stroke  I'  =  Mitral  murmur;  I — (I'M)  =  Split  second  sound;  (IM — I)  =  Split  first  sound; 
(I-M' — I)  =  Presystolic  gallop;  I — P-M  =  Protodiastolic  gallop;  I  stroke  I  =  Mesosystolic 
murmur;  LRMP — I  =  Presystolic  murmur;  I — stroke  =  Diastolic  blowing  murmur  replac- 
ing second  sound;  I — I  stroke  =  Diastolic  murmur  following  the  second  sound;  LRMP 
stroke  I  =  Presystolic  systolic  murmur  of  mitral  stenosis;  Gentle  to-and-fro  rubbing  of 
skin  =  Pericardial  friction. 

Relations  of  the  Simple  Murmurs  to  Events  of  the  Cardiac  Cycle. — The  relations  of 
the  simple  cardiac  murmurs  to  the  contractions  of  the  cardiac  chambers,  as  well  as  to  the 
filling  and  emptying  of  the  ventricles,  is  shown  in  Fig.  111.  The  mechanism  of  their 
production  will  be  discussed  in  detail  in  connection  with  the  valvular  lesions  to  which 
they  correspond.  It  will  be  seen,  however,  that  the  mitral  systolic  murmur  begins 
coincidently  with  the  first  heart  sound  before  the  blood  flows  into  the  aorta,  and  that 
it  continues  throughout  systole;  that  the  aortic  systolic  murmur  follows  the  first  sound 
and  is  loudest  in  midsystole;  that  the  aortic  diastolic  murmur  is  loudest  in  early  diastole, 
when  the  filling  of  the  heart  and  the  regurgitation  are  most  rapid;  and  that  the  presys- 
tolic rumble  is  produced  by  the  inrush  of  blood  into  the  ventricles  during  auricular  systole. 


184 


DISEASES  OF  THE  HEART  AND  AORTA. 

SINGLE  MURMURS. 


Time. 

Character. 

Phonetic  l 
equivalents. 

Distribution. 

Clinical  condition. 

Presystolic 

Rumbling,  occasion- 

12           12 

ftat-ta;    trat-at;    tr- 

Apex   only,   lower 

Mitral    stenosis ;    tri- 

ally blowing 

r-rub-dub 

1            2 

precordium  be- 
tween parasternal 
line  and  sternum 

cuspid  stenosis. 

Blowing  or  roaring. 
Enters  into  or  re- 

shush-dub; jjje-dub; 
ssh-dub;    faf-tam 

Over  body  of  heart, 
at  apex  and  to  ax- 

Mitral insufficiency ; 
tricuspid   insuffi- 

places  as   well   as 

illa,  often  at  back. 

ciency. 

follows  first  sound. 

Over    lower    ster- 

Uniform or  decres- 

num  and  neighbor- 

cendo 

ing  precordium 

..    „  - 

Blowing  or  roaring; 

luzsch-dub;   taf-dub 

Loudest   over   2d 

Sclerosis    of    aorta; 

follows  first  sound; 

right     interspace ; 

aortic  stenosis;   con- 

has    a     crescendo 

thrill  also  in  ves- 

genital heart  lesion. 

character    in   mid- 

sels  of  neck.    Not 

systole  and  decres- 

so  loud  at  apex 

-    - 

cendo  in  late  sys- 
tole 

' 

Similar  in  character 

1                   2             12 

lujseh-dub;  taf-dub; 

2d    left    interspace 

Pulmonary     stenosis, 

' 

to    aortic    systolic 

1          2 

and  to  left  of  ster- 

congenital heart  le- 

murmur 

taf-tam 

num  (thrill) .  Else- 
where  over   chest 

sion,  aneurism. 

(thrill) 

Mesosystolic  or  tel- 

Soft    blowing,     uni- 

lupff-dub;     taf-tat; 

Over  entire  precord- 

Functional,  accident- 

esystolic   (predi- 

form    or     decres- 

1            2 

ium,   esp.  2d  and 

al,  or  ansmic  mur- 

astolic) 

cendo 

luff-dub 

3d  left  interspace. 
Varying    with 
change  of  position. 
Not    transmitted 
beyond  apex 

mur.  Ansemic  fever; 
neurasthenia  etc.  - 
sometimes  organ- 
ic (?). 

lupd-shsh;    tam-taf; 

At  2d  rib  near  ster- 

Aortic insufficiency. 

lup-dush;  lup-shsh 

nal  margin;  loud- 
est  over    sternum 
at  level  of  2d  left 
interspace  and  in 
the  latter  near  the 

1  '  - 

■  >    -    ■ 

sternal  margin 

At    2d    left    inter- 
space and   right 
sternal   margin; 
also    to  right  of 
sternum 

At  2d  left  interspace 
and  sternal  margin 

Pulmonary  insuffici- 
ency. 

With  no  other  marked 
signs  of  valvular  in- 
sufficiency. Abnor- 
mal murmur  (Potain, 
Graham,  Steele). 

At  apex  only 

cases  with  pericard- 

ial adhesions,  etc. 

1  These  phonetic  equivalents  most  closely  imitate  the  cardiac  sounds  when  the  consonants  are 
prolonged  as  much  as  possible. 


COMBINED  MURMURS. 


Time. 


Presystolic  (Flint 
murmur) ,  systol- 
ic, and  diastolic 


Character. 


Presystolic  rumble; 
systolic  blow;  di- 
astolic blow 


Phonetic 
equivalents. 


ftaftash;       tr-r-rub- 

2 

dush 


Distribution. 


Blow  loudest  at  2d 
right  and  2d  left  in- 
terspaces; at  apex 
and  out  in  axilla. 
Rumble  over  apex 
only 


Clinical  condition. 


Vegetation  at  aortic 
valve,  aortic  insuf- 
ficiency. Sometimes, 
but  not  necessarily, 
mitral  insufficiency, 
occasionally  also 
mitral   stenosis. 


PHYSICAL  EXAMINATION. 


185 


COMBINED  MURMURS  (Continued). 


Time. 


Character. 


Phonetic 
equivalents. 


Distribution. 


Clinical  condition. 


Systolic    and    di- 
astolic 


Same 


Systolic    and    dias- 
tolic blow 


taf-tash;  lush-dush; 

1  2 

shush-shush 


Same. 


Same. 


Irregularly  in  both 
systole  and  di- 
astole 


Accompanies  both 
heart  sounds  and 
both  breath 
sounds 


Soft,   superficial, 
scratchy 


slush  -  dush  ;   si  ush 

2 

dush-da 


Pleuropericardial . 


Crepitant;  small  ex- 
plosive rales 


2d  right  and  left  in- 
terspace, sternum, 
left  sternal  mar- 
gin, transmitted  to 
arteries 

Loudest  at  left  ster- 
nal margin;  thrill 
maximum  to  first 
and  second  left 
interspace 


Over  the  entire  pre 
cordium,  especial 
ly  over  the  area  of 
absolute  dulness; 
increased  by  pres- 
sure with  stetho- 
scope 

Over  relative  cardi- 
ac dulness  only; 
scratch  simultane- 
ous with  respira- 
tion as  well  as 
cardiac  cycle.  In- 
creased by  pres- 
sure with  stetho- 
scope 

Over  relative  cardi- 
ac dulness  only 


Aortic  insufficiency 
with  aortitis;  aortic 
stenosis. 


Pulmonary  stenosis 
and  insufficiency; 
open  ductus  arterio- 
sus; other  congeni- 
tal heart  lesions. 


Fibrinous  pericarditis, 


Pleuropericarditis. 


Emphysema.      Inter- 
stitial emphysema. 


VASCULAR    SOUNDS    AND    MURMURS. 

Arterial. — Besides  the  murmurs  transmitted  from  the  heart,  murmurs 
also  occasionally  arise  in  the  arteries  themselves.  A  systolic  murmur  and 
an  audible  first  sound  (pistol-shot  tone)  may  be  produced  by  pressure  with 
the  stethoscope  over  the  arteries,  but  without  exerting  a  definite  pressure 
it  may  often  be  found  accompanying  the  dilatation  of  markedly  pulsating 
arteries,  as  in  aortic  insufficiency  and  with  dicrotic  pulses,  etc.  The  eddies 
arising  in  an  aneurism  usually  give  rise  to  a  rough  or  blowing  systolic 
murmur  which  may  be  transmitted  for  a  considerable  distance  along  the 
arteries.  In  aortic  insufficiency  a  double  murmur  (sytolic  and  diastolic) 
may  be  heard  over  the  arteries  (Duroziez). 

Venous. — Sounds  over  the  regular  vein  have  long  been  heard  in  anaemias 
(Cohnheim,  Camac)  and  the  tracings  of  Weiss  and  Joachim  show  that  these 
are  present  throughout  the  cardiac  cycle.  Josue  has  shown,  however,  that  the 
normal  venous  pulse  imparts  a  sound  of  presystolic  gallop  rhythm  to  the 
stethoscope,  while  the  ventricular  types  of  venous  pulse  give  rise  to  single 
loud  sounds;  so  that  this  method  can  be  used  in  the  diagnosis  of  cardiac 
arrhythmias. 

In  accordance  with  these  findings,  an  auricular  extrasystole  is  accom- 
panied by  two  sounds,  a  ventricular  extrasystole  is  accompanied  by  one. 
loud  sound,  and  in  the  absolute  arrhythmia  of  auricular   fibrillation  there 


186  DISEASES  OF  THE  HEART  AND  AORTA. 

is  an  indefinite  series  of  single  distinct  sounds  occurring  irregularly,  not  inter- 
rupted by  any  series  of  double  sounds.  The  venous  sounds  of  Josue  are 
most  distinct  in  persons  who  have  a  high  venous  pressure  and  hence  most 
distinct  in  those  persons  whose  venous  pulse  cannot  be  well  studied  by 
inspection. 

It  is  evident  from  what  has  gone  before,  as  well  as  from  the  consensus 
of  medical  practice,  that  auscultation  furnishes  a  most  important  means 
of  diagnosis  of  cardiac  lesion.  It  is  equally  evident  that  each  abnormal 
sound  may  be  associated  with  any  one  of  several  clinical  conditions,  which 
must  be  still  further  differentiated  from  one  another,  not  only  by  the  mur- 
mur but  by  its  distribution,  transmission,  and  variations,  but  particularly 
by  the  other  methods  of  physical  examination,  graphic  methods,  and  X-ray 
examination. 

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Selling,  T.:  Untersuchungen  des  Perkussionschalles,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

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M  tiller,  Fr.:  Studies  in  Percussion,  paper  read  before  the  Johns  Hopkins  Hospital  Medical 

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Dietlen,  H. :  Ueber  die  Grosse  und  lage  des  normalen  Herzens  und  ihre  Abhangigkeit  von 

physiologischen  Bedingungen,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  lxxxviii,  55. 

Die  Perkussion  der  wahren  Herzgrenzen,  ibid.,  1906,  lxxxviii,  286. 
Simon,  A.:  Die  Schwellenperkussion  des  Herzens  an  der  Leiche,  ibid.,  1906,  lxxxviii,  246. 
Hoffmann,  A. :  Die  paroxysmale  Tachycardie. 
Dietlen,  H.:    Orthodiagraphische  Beobachtungen  ueber  Veranderungen    der  Herzgrosse 

bei  Infektionskrankheiten,   exsudative  Perikarditis  und  paroxysmale  Tachykardie, 

Munchen.  med.  Wchnschr.,  1908,  Iv,  2077. 
Williams,  F.  H. :  Rontgen  Rays  in  Medicine  and  Surgery. 
Sawyer,  J.:  Brit.  J.  Child.  Dis.,  1909,  525,  quoted  from  the  Arch,  des  malad.  du  cceur  et 

des  vaisseaux,  Par.,  1910,  hi,  385. 
Schieffer  and  Weber,  A.:  Die  Perkussion  der  absoluten  Herzdampfung  und  deren  Werth 

fur  die  Bestimmung  der  Herzgrosse,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1908, 

xciv,  466. 
Veith,  A.:  Ueber  orthodiagraphische  Untersuchungen  bei  Kindern  im  schulpflichtigen 

Alter,  Jahrb.  f.  Kinderh.,  Berl.,  1908,  lxviii,  205. 
Sahli,  H. :  Lehrbuch  der  klinischen  Untersuchungsmethoden. 
Harvey,  Wm. :  De  motu  cordis. 

Williams,  C.  J.  B.:  Rep.  Brit.  Assoc.  Adv.  Sc,  Lond.,  1836,  p.  269. 
Ludwig,  C,  and  Dogiel,  A.  S.:  Ber.  d.  k.  sachs.  Gesellsch.  math.  nat.  CI.,  Leipz.,  1869, 

xx,  89. 
Sibson  and  Broadbent:  In  Sibson's  Medical  Anatomy,  1869,  p.  89. 
Emerson,  C.  P. :  The  Effect  of  Pressure  of  the  Stethoscope  on  Intrathoracic  Sounds,  Bull. 

Johns  Hopkins  Hosp.,  Baltimore,  1908,  xix,  49. 


PHYSICAL  EXAMINATION.  187 

Smith,  A.  H. :  On  the  Use  of  the  Differential  Stethoscope  in  the  Study  of  Cardiac  Murmurs, 

Med.  Rec,  N.  Y.,  1895,  xlviii,  121,  and  Trans.  Asso.  A.  Phys.,  Phila.,  1896,  x,  86. 
Cabot,  R.  C. :  Physical  Diagnosis. 
Boy-Teissier :  L'auscultation  retrosternale  dans  les  maladies  cardio-aortiques,  Marseilles 

meU,  1892,  xxix,  303;  Rev.  de  med.,  Par.,  1892,  xii,  169. 
Hoffmann,  A.:  Ueber  cesophageale  Auskultation,  Centralbl.  f.  klin.  Med.,  Leipz.,  1892, 

xiii,  1017. 
Gerhartz,  H.:  Zur  Frage  des  Stethoskops,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1907,  xc,  501. 
Bard,  L.:  Du  bruit  de  galop  de  l'hypertrophie  du  cceur  gauche,  Sem.  med.,  Paris,  1906, 

xxvi,  229.    Also  De  la  multiplicity  anormale  des  bruits  du  cceur,  ibid.,  1908,  xxviii,  3. 
Kriege  and  Schmall:  Ueber  den  Galopprhythmus  des  Herzens,  Ztschr.  f.  klin.  Med.,  Berlin, 

1891,  xviii. 
M  tiller,  F.:  Ueber  Galopprhythmus  des  Herzens,  Munchen.  med.  Wchnschr.,  1906,  liii,  785. 
Marey,  E.  J. :  La  Circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Par.,  1881. 
Sewall,  H. :  On  a  Common  Form  of  Reduplication  of  the  First  Sound  of  the  Heart,  Contrib. 

Sci.  Med.  (Vaughan),  Ann  Arbor,  1903,  29;  also,  A  Common  Modification  of  the  First 

Sound  of  the  Normal  Heart  Simulating  that  Heard  with  Mitral  Stenosis,  Am.  J.  M. 

Sc,  1909,  cxxxviii. 
Robinson,  G.  C:  Gallop  Rhythm  of  the  Heart,  Am.  J.  M.  Sc,  Phila.,  1908,  cxxxv,  670. 
Chauveau,  H.:  Etude  cardiographique  sur  la  mecanisme  du  bruit  de  galop,  Thesis,  Paris, 

1902. 
Pawinski,  J. :  Die  Entstehung  und  klinische  Bedeutung  des  Galopprhythmus  des  Herzens, 

Ztschr.  f.  klin.  Med.,  Berl.,  1907,  lxiv,  70. 
Duroziez  and  Sansom:  Quoted  from  Bard. 
Hirschfelder,  A.  D.:  Some  Variations  in  the  Form  of  the  Venous  Pulse,  Bull.  Johns  Hopkins 

Hosp.,  1907,  xviii,  265. 
Einthoven,  W.:  Ein  dritter  Herzton,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907,  cxx,  31. 
Gibson,  A.  G.:  Upon  a  Hitherto  Undescribed  Wave  in  the  Venous  Pulse,  Lancet,  Lond., 

1907,  ii,  1380. 
Thayer,  W.  S.:  On  the  Early  Diastolic  Heart  Sound  (the  So-called  Third  Heart  Sound), 

Bost.  M.  and  S.  J.,  1908,  clviii,  713;  Further  Observations  on  the  Third  Heart  Sound, 

Arch.  Int.  Med.,  Chicago,  1909,  iv,  297. 
Eyster,  J.  A.  E.:  Studies  on  the  Venous  Pulse,  J.  Exper.  M.,  N.  Y.  and  Lancaster,  1911, 

xiv,  594. 
Potain:  La  Clinique  m^dicale  de  la  Charite,  Par.,  1894. 
Laennec,  Bouillaud,  Hilton  Fagge:  Quoted  from  Potain. 
Luethje:  Quoted  from  Brugsch  and  Schittenhelm,  Lehrbuch  klinischer  Untersuchungs- 

methoden,  Berl.,  1908. 
Buisson,  Voit,  van  der  Heul,  quoted  from  Meltzer,  S.  J.:  On  the  Nature  of  Cardio-pneu- 

matic  Movements,  Am.  J.  Physiol.,  Bost.,  1899,  i,  117.    Also,  Saunders,  G.:  Cardio- 
pulmonary Murmurs,  Edinb.  M.  J.,  1897,  N.  S.,  i,  522. 
Stengel,  A. :  The  Significance  of  Systolic  Murmurs  over  the  Apex  and  Base  of  the  Heart, 

Cleveland  J.  M.,  1898,  iii,  191;  and  Foshay,  P.  M.:  A  Case  of  Cardiopulmonary 

Murmur  Illustrating  the  Importance  of  Differentiation,  ibid.,  1901,  vi,  236. 
Putnam,  J.  J. :  The  Clinical  Associations  and  Significance  of  the  Cardiopulmonary  Murmur, 

Tr.  Ass.  Am.  Phys.,  Phila.,  1903,  xviii,  157. 
Brown,  S.  G. :  Abstracted  in  the  Scientific  American,  1910,  cii. 
Donders:  Quoted  from  L.  Hill,  Schafer's  Text-book  of  Physiology,  Edinb.  and  Lond., 

1900,  ii. 

Martius:  Graphische  Untersuchungen  ueber  die  Herzbewegung,  Ztschr.  f.  klin.   Med., 

Berl.,  1888,  xiii,  327,  453,  558. 
Einthoven,  W.,  and  Geluk,  M.  A.  J.:  Registrirung  der  Herztone,  Arch.  f.  d.  ges.  Physiol., 

Bonn,  1894,  Ivii,  617. 
Huerthle,  K.:  Ueber  die  mechanische  Registrirung  der  Herztone,  ibid.,  1895,  lx,  263. 
Holowinski,  A.:  Physikalische  Untersuchung  der  Herztone,  Ztschr.  f.  klin.  Med.,  Berl., 

1901,  xiii,  186. 

Einthoven,  W.,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A.:  Registrirung  der  menschlichen 
Herztone,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1907,  cxvii,  461. 


188  DISEASES  OF  THE  HEART  AND  AORTA. 

Marbe,  K.:  Registrirung  der    Herztone    mittelst    russender  Flammen,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1907,  cxx,  205. 
Roos,  E.:  Ueber  die  objective  Aufzeichnung  der  Schallerscheinungen  des  Herzens,  Ver- 

handl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1908,  xxv,  643. 
Frank,  O.,  and  Hess,  O.:  Ueber  das  Cardiogramm  und  den  ersten  Herzton.,  Verhandl.  d. 

Kong.  f.  innere  Med.,  Wiesbaden,  1908,  xxv,  285. 
Weiss,  O.:  Das  Phonoskop,  Mediz.  naturw.  Arch.,  Berl.  and  Vienna,  1908,  i,  437. 
Weiss,  O.,  and  Joachim,  G.:  Registrirung  und  Reproduktion  der  menschlichen  Herztone 

und  Herzgerausche,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxiii,  341. 
Hess:  Entstehung  der  Herztone,  Deutsche  med.  Wchnschr.,  Leipz.,  1908,  xxxiv,  1611. 
Kahn,  R.  H.:  Weitere  Beitrage  zur  Kenntniss  des  Elektrocardiogrammes,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1909,  cxxix,  291. 
The  whole  literature  is  reviewed  in  detail  by — 
Barker,  L.  F.:  Electrocardiography  and  Phonocardiography,  A  Collective  Review,  Johns 

Hopkins  Hosp.  Bull.,  Baltimore,  1910,  xxi,  358;  and  also  by — 
Weiss,  O.:  Das  Phonoskop  eine  Vonichtung  zur  Analyse  und  Registrirung  schwacher 

Schallqualitaten,  Med.  naturew.  Arch.,  Berl.  and  Wien,  1907,  i,  437. 
Weiss,  O.:  Die  Seifenlamelle  als  Schallregistrirende  Membran  im  Phonoskop,  Ztschr.  f. 

biol.  Techn.  u.  Methodik,  Strassb.,  1908,  i,  49;  Zwei  Apparate  zur  Reproduktion  von 

Herztonen  und  Herzgerauschen,  ibid.,  1908,  i,  126. 
Gerhartz,  H.:    Die  Aufzeichnung  von  Schallerscheinungen  ins  besondere  die  des  Herz- 

schalles,  Ztsch.  f.  exper.  Path.  u.  Therap.,  Berl.,  1908,  v,  105;  Herzschallstudien, 

Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxxi,  509. 


PART  II. 

i. 

PRIMARY  CARDIAC  OVERSTRAIN. 

It  has  long  been  known  that  heart  failure  may  arise  from  simple  over- 
strain of  the  heart  without  the  intervention  of  any  actual  cardiac  lesions. 
This  condition  usually  remains  acute  and  ends  in  rapid  recovery,  but  it 
may  also  become  chronic  and  reduce  the  patient  to  lasting  invalidism.  In 
its  worst  form  such  a  purely  functional  weakening  of  the  heart  may  result 
in  death. 

This  conception  was  first  introduced  by  Stokes  in  1854,  and  was  con- 
firmed later  by  studies  of  Clifford  Allbutt,  A.  R.  B.  Myers,  and  Peacock  in 
England,  and  da  Costa  in  America.  Their  articles  were  collected,  trans- 
lated into  German,  and  published,  along  with  an  excellent  monograph 
upon  the  subject,  by  Johannes  Seitz,  of  Zurich,  in  1875,  bringing  them  to 
the  cognizance  of  the  German  writers.  In  1886  v.  Leyden  added  important 
contributions.  In  1898  the  matter  was  subjected  to  clinical  experiment 
by  Theodor  Schott,  whose  conclusions  have  been  disputed  by  a  host  of 
later  and  more  careful  observers. 

The  most  interesting,  extensive,  and  complete  of  all  these  papers  are 
those  of  da  Costa,  based  upon  several  hundred  cases  occurring  among 
Union  soldiers  of  the  Civil  War.  His  experience  and  deductions  are  paralleled 
and  confirmed  by  those  in  the  great  European  war,  which  have  recently  been 
brought  together  by  Sir  James  Mackenzie,  Drs.  R.  M.  Wilson,  F.  J.  Poynton, 
P.  Hamill,  Alexander  Morison,  O.  Leyton,  Florence  Stoney,  R.  Bezly  Thome, 
Capt.  R.  W.  Mitchell,  and  Major  T.  R.  Bradshaw  before  the  Royal  Medical 
Society  (Proc.  Roy.  Med.  Soc,  Lond.,  1916,  ix,  Therap.  and  Pharmacol. 
sec.  27).  It  is  often  termed  disordered  action  of  the  heart 
(D.  A.  H.). 

CLINICAL  CASES. 

A  very  typical  case  of  Da  Costa's  series  is  illustrated  by  the  following 
history. 

Case  I. — Irritable  heart,  chiefly  from  hard  service;  recovery. 
— Wm.  Henry  H.,  private  68th  Pennsylvania  Vol.,  admitted  into  the  Turner's  Lane  Hospital 
in  Philadelphia,  November  2,  1863,  having  just  returned  from  a  furlough.  He  enlisted  in 
August,  1862,  at  the  time  in  good  health,  though  he  had  suffered  occasionally  from  rheu- 
matism. He  did  a  great  deal  of  hard  duty  with  his  regiment.  Some  time  before  the  battle 
of  Fredericksburg,  he  had  an  attack  of  diarrhoea;  after  the  battle,  he  was  seized  with 
lancinating  pains  in  the  cardiac  region,  so  intense  that  he  was 
obliged  to  throw  himself  down  upon  the  ground,  with  palpitation. 
These  symptoms  frequently  returned  while  on  the  march,  were  attended  with  dimness  of 
vision  and  giddiness,  and  obliged  him  often  to  fall  out  from  his  company  and  ride  in  the 
ambulance.  Yet  he  remained  with  his  regiment  until  J  u  1  y  4,  1863,  when  he  was  wounded 
at  the  battle  of  Gettysburg.  The  wound  healed  in  about  one  month;  but  the  cardiac 
symptoms  became  worse,  and  violent  palpitations  ensued  upon  the  slightest  exertion, 
sometimes  also  whilst  in  bed,  obliging  him  to  rise.      There  was  soreness  in  the  cardiac 

189 


190  DISEASES   OF   THE   HEART   AND    AORTA. 

region,  and  a  constant  dull  pain.  The  impulse  was  extended,  slightly  jerky,  96,  and  of 
irregular  rhythm,  some  beats  following  one  another  in  rapid  succession;  the  first  sound  was 
feeble,  the  second  very  distinct.  The  man  did  not  look  sick.  Height  5  feet  7  inches; 
measured  31  inches  around  the  chest  one  inch  below  the  nipple;  he  did  not  smoke;  chewed 
tobacco  in  moderation. 

The  patient  did  not  improve  under  aconite;  but  under  digitalis  the  impulse  became 
quiet  and  78,  and  on  March  23,  having  previously  done  duty  as  orderly,  he  was  detailed 
on  police  duty,  and  his  treatment  stopped.  The  heart  continuing  to  act  regularly, 
he  returned  to  his  regiment  May  3,  1864. 

Another  case,  quoted  from  v.  Leyden,  illustrates  the  various  phases 
of  the  malady  very  well. 

Case  II. — Carl  Timm,  butcher,  aged  30.  Family  history  negative.  Syphilis  ten  years 
before,  quiescent  for  several  years.  Otherwise  always  healthy.  Performed  military  service 
for  5  years  without  any  trouble.  In  the  fall  of  1880  became  a  butcher  in  the  Charite  Hospital 
where  he  had  to  lift  and  chop  sides  of  beef  weighing  200  lbs.  The 
first  symptoms  appeared  suddenly  on  the  afternoon  of  December  30,  1880,  during  an 
ordinary  day's  work,  when  he  felt  a  severe  pressure  in  the  pit  of  the  stomach, 
preventing  him  from  taking  a  deep  breath  and  causing  him  to  stop  in  his  work.  At  this 
time  he  noticed  palpitation  and  irregularity  of  the  heart.  For  several  days 
after  this  he  did  no  heavy  work  and  then  felt  well.  When  he  tried  to  do  heavy 
hf ting  again  the  same  pain  and  sensation  of  pressure  returned,  and 
though  he  continued  his  work  he  was  compelled  to  stop  for  breath  from  time  to  time.  On 
Feb.  17,  1881,  the  pain  became  very  intense  and  he  entered  the  hospital  on  Feb.  21. 

Physical  Examination. — Patient  is  a  very  well-built  young  man,  well  muscled,  well 
nourished  but  not  fat.  Complexion  florid  but  healthy  looking.  No  dyspnoea  or 
cyanosis.  Moderate  oedema  of  lower  extremities.  Patient  complains  only 
of  palpitation  of  the  heart.  The  pulse  is  strikingly  irregular  so  that  it  is  im- 
possible to  count.  The  radial  arteries  are  small,  blood-pressure  apparently  low.  The 
cardiac  impulse  is  intense,  vibratory,  and  very  irregular.  Apex  impulse  is  in 
5th  left  interspace  2  cm.  beyond  mam m.i  1 1  a r y  line,  well  marked, read- 
ily palpable.  Cardiac  dulness  begins  above  at  3d  rib,  extending  below  to  6th  rib,  and 
reaching  just  to  the  right  of  the  sternum.  Heart  sounds  are  feeble  and  unequal  but 
clear.  Lungs  clear.  Liver  and  spleen  are  not  enlarged.  Urine  500  c.c,  sp.  gr.  1023,  no 
albumin. 

Ordered  rest  in  bed,  ice-bag  over  heart,  infusion  of  digitalis  every 
2  hours.  Within  a  few  days  symptoms  and  oedema  had  subsided,  but  the 
irregular  heart  action  persisted.  By  March  20  he  was  well  enough  to  be  discharged,  with 
the  following  note:  Apex  beat  0.5  cm.  to  left  of  mammillary  line;  first  sound  at  apex 
loud  and  ringing,  second  sound  distant  but  clear;  pulse  irregular;  examination  otherwise 
negative. 

This  represents  the  first  stage  of  his  illness,  in  which  the  following 
features  are  noteworthy:  1.  A  very  strong  and  perfectly  healthy  young 
man  suffers  from  heart  failure  as  the  immediate  result  of  overstrain.  The 
first  attack  came  on  suddenly  while  at  work  and  passed  off  soon,  but  attacks 
recurred  whenever  the  patient  did  heavy  work,  and  he  was  compelled  to 
enter  the  hospital.  2.  Physical  findings:  heart  dilated  especially  in  the 
longitudinal  axis,  weak  apex  beat  (dilatation  of  left  ventricle),  great  cardiac 
irregularity.  3.  Relatively  rapid  improvement  after  rest  in  bed  and  digi- 
talis. 4.  The  heart  then  returned  to  almost  normal  size,  but  the  irregu- 
larity in  rhythm  persisted. 

Second  Stage. — Patient  returned  to  his  old  work  in  spite  of  warning, 
and  within  two  months  oedema  of  the  legs  had  again  set  in  and  he  was  confined  to 
bed  for  eight  weeks  more.  Returning  to  work  again,  he  could  perform  only 
very  light  labor,  and  very  soon  returned  once  more  to  the  hospital  for  seven  weeks, 
with  still  more  marked  oedema.    Once  more  these  disturbances  disappeared  after  rest  and 


PRIMARY  CARDIAC   OVERSTRAIN.  191 

digitalis,  but  thereafter  the  slightest  work  caused  palpitation  and  the  feeling  as  though 
there  were  a  tight  c  o  rd  about  the  chest.  He  also  felt  pain  in  the  region  of  the 
liver.  At  this  point  he  re-entered  the  hospital.  Pulse  180,  small,  irregular.  Face  flushed, 
no  cyanosis.  Expression  depressed.  Skin  normal;  cedema  of  feet  and  legs.  Gangrene  of 
big  toe  of  right  foot.  Respiration  a  little  rapid,  dyspnoea  only  on  exercise,  but  while  walk- 
ing he  often  stops  to  catch  his  breath.  Occasionally  he  has  attacks  of  dyspnoea  lasting 
about  10  minutes,  beginning  with  afeelirg  of  pressure  in  the  region  of  the  heart.  He 
then  feels  as  though  hot  liquid  were  pouring  from  the  heart  upwards  to  each  side  of 
the  neck. 

Physical  Signs. — A pex  beat  in  6th  left  interspace  in  anterior  axillary 
line,  soft  and  easily  compressed.  Heart  therefore  much  enlarged,  sounds  clear  and  fairly 
loud,  action  markedly  irregular.    Liver  enlarged  and  tender. 

Ordered  rest  in  bed,  digitalis,  morphine  at  night.  Patient  became  much  better 
within  twenty-four  hours,  pulse  then  68  per  minute.  The  attacks  of  dyspnoea  almost 
disappeared.  Urine  1300,  sp.  gr.  1020.  Within  six  days  all  cardiac  symptoms  had  dis- 
appeared. March  11:  Pulse  52.  Feels  well,  no  pain.  Apex  beat  in  5th  left  interspace 
3  cm.  beyond  mammillary  line,  moderately  forceful.  Heart  sounds  clear  but  irregular. 
He  still  occasionally  has  feeling  of  pressure  in  chest. 

Features  of  second  stage:  1.  Dilatation  of  heart  much 
more  marked  than  before.  2.  Very  rapid  and  very  irregular 
heart  action.  3.  Definite  attacks  of  pain  in  heart  and  feeling  of  pressure 
(anginoid  in  character) ,  with  radiating  pains  in  shoulder  and  arm.  4.  Swell- 
ing of  liver  (failure  of  right  heart).  5.  Return  to  almost  normal  under 
treatment,  diminution  in  size  of  left  ventricle.  6.  Intercurrent  affections: 
small  infarct  of  lung,  pressure  gangrene  of  great  toe,  recovered  from. 

Third  Stage. — Returned  to  the  hospital  in  July,  1885  (two  years  later).  He  has  been 
able  to  do  very  little  since  last  admission.  Now  much  emaciated,  face  thin,  ap- 
pears depressed.  Cheeks  and  lips  slightly  cyanotic.  Respiration  dyspnceic  and 
stertorous.     No  orthopncea.     Moderate  cedema  of  shins. 

Cardiac  impulse  seen  in  5th  to  7th  left  interspaces,  apex  beat  felt  in  7th  in  axillary 
line,  forcible.  Heart  rate  about  132,  irregular.  Cardiac  dulness  19  cm.  from  left  sternal 
margin.  (Upper  limit  of  cardiac  dulness  as  before  begins  at  3d  rib.)  Liver  readily  pal- 
pable. Sounds  loud,  more  or  less  short  but  no  murmur.  Did  not  remain  in  hospital,  but 
on  October  4,  1885,  was  brought  in  again  in  collapse.  Marked  cyanosis,  extremities  cold, 
cedema  of  legs  up  to  knees.  Heart  as  before,  sounds  still  clear.  Pulse  150.  Liver  a  hand's 
breadth  below  costal  margin.  Ordered  digitalis,  also  camphor  subcutaneously,  tea  with 
cognac.  At  midnight  collapse  more  marked,  very  marked  dyspnoea  and  cyanosis;  threw 
himself  to  and  fro,  groaned  loudly.  Pulse  not  palpable,  not  revived  by  camphor  or  ether 
injection.     At  2  a.m.  became  quiet;  stertorous  breathing  set  in  at  3  a.m.;  died  quietly  at 

3.15  A.  M. 

Autopsy. — Marked '  cedema  of  legs.  Both  lungs  slightly  retracted,  slightly  adherent 
over  apices.  Pericardium  distended,  little  fluid.  Heart  markedly  enlarged  (more 
than  twice  the  size  of  patient's  fist),  especially  in  the  longitudinal  axis.  Left  ventri- 
cle more  dilated  than  right.  Distance  from  insertion  of  pulmonary  artery 
to  apex  13  cm.,  to  right  border  of  heart  10  cm.  Length  of  left  ventricle  15  cm.  Little 
epicardial  fat.  Valves  normal,  aortic  valves  close  perfectly.  Papillary  muscles  well  devel- 
oped, some  trabeculse  flattened  and  undergoing  fibrous  changes.  A  fibrous  patch  is  seen 
on  the  interior  surface  of  the  left  ventricle.  Endocardium  otherwise  delicate,  showing 
some  yellow  areas  of  fatty  degeneration  of  the  endocardium  and  papillary  muscles.  Cut 
surface  of  heart  muscle  shows  cloudy  swelling.  Left  auricle  markedly  di- 
lated. Right  ventricle  appears  pale  with  spots  of  yellow.  Lungs,  cedema  of  bases. 
Liver,  markedly  enlarged;  definite  nutmeg  liver.  Kidneys,  large,  dark  red,  harder 
than  normal. 

Microscopic  examination  shows  extensive  fatty  degeneration  of  muscle-fibres,  but 
only  in  the  inner  layers.  No  interstitial  changes,  no  changes  in  blood-vessels 
or  nerves  of  the  heart.  Here  and  there  the  interstitial  strands  of  connective  tissue 
appeared  thicker  than  normal  but  without  cellular  infiltration. 


192  DISEASES  OF  THE  HEART  AND  AORTA. 

ETIOLOGY. 

In  Da  Costa's  200  soldiers,  well-marked  fever  preceded  the  overstrain 
in  17  per  cent.;  diarrhoea  (among  which  there  may  have  been  many  mild 
cases  of  typhoid  fever)  30.5  per  cent. ;  Sir  James  Mackenzie  and  Wilson  have 
found  that  in  90  per  cent,  of  the  cases  of  overstrain  in  the  British  Army  in 
France  the  underlying  cause  is  a  bacterial  infection.  Lewis  and  Tele  have 
frequently  found  staphylococci  and  streptococci  in  the  urine  of  such  cases. 
Poynton  finds  that  the  patients  are  often  adolescents  of  great  stature  with 
big  frames,  but  often  decidedly  anaemic,  cases  of  long  flat  chest  with  low  heart 
(bathycardia — see  page  697).  Florence'  Stoney  calls  attention  to  the  impor- 
tance of  incipient  Basedow's  disease.  In  short,  anything  that  weakens  the 
heart  and  lowers  its  tonicity  predisposes  it  to  dilatation  and  overstrain.  Over- 
strain is  very  frequent  among  miners,  metal  workers,  carriers  of  heavy  burdens, 
blacksmiths,  moulders.  Morton  Prince  calls  attention  to  the  development  of 
cardiac  dilatation  under  severe  mental  strain,  as  in  a  civil  service  examination. 
Anaemia  and  chlorosis  (Henschen),  apparently  mild  illnesses,  intestinal  dis- 
turbances, acute  alcoholism,  and  febrile  diseases  (Dietlen)  are  also  frequent 
causes.  Sexual  excess  is  an  important  factor,  especially  in  men;  but  its  effects 
are  usually  more  marked  in  hearts  already  weakened  from  other  diseases 
or  from  valvular  lesions  than  in  perfectly  healthy  hearts. 

Myers,  Allbutt,  and  Schott  have  shown  that  tight  belts,  uniforms, 
and  corsets  displace  the  heart  upward,  embarrass  its  action,  and  predispose 
to  overstrain.  Indeed  Myers  found  that  cavalry  soldiers  with  tight  belts 
suffered  more  from  long  rides  than  infantry  from  marching  the  same  dis- 
tance. 

SYMPTOMS,    SIGNS,    AND    CLINICAL    COURSE. 

The  chief  symptoms  are  dulness,  excitability,  nervousness,  loss  of 
sleep,  loss  of  appetite,  restlessness,  buzzing  in  the  ears,  vertigo,  muscae 
volitantes,  palpitation  of  the  heart,  usually  very  severe  and  often  asso- 
ciated with  a  feeling  of  pressure  or  constriction  over  the  chest.  This  may 
be  very  distressing,  but  does  not,  as  a  rule,  cause  the  patient  to  remain 
absolutely  still  nor  give  him  the  fear  of  sudden  death,  though  da  Costa 
mentions  cases  in  which  the  precordial  distress  was  great  enough  to  cause 
soldiers  to  fall  to  the  ground  in  the  midst  of  battle. 

Pain  over  the  precordium  and  the  left  shoulder,  occasionally  down 
the  arm,  increased  on  inspiration  and  on  coughing. 

Dull  headache,  dizziness,  especially  on  bending  over,  sleep- 
lessness, indigestion,  tympanites,  and  diarrhoea  are  common. 

The  patient  often  wears  an  anxious  expression  and  there  are  usually 
pallor  and  more  or  less  cyanosis.  Pulse  is  usually  small,  feeble,  rapid,  and 
often  irregular.  The  cardiac  impulse  may  be  barely  or  not  at  all  visible, 
but  on  percussion  the  area  of  relative  cardiac  dulness  is  usually  found  to  be 
enlarged  considerably  to  the  left  both  downward  and  upward,  and  often  also 
to  the  right  as  well.  This  corresponds  to  the  dilatation  of  the  left  ventricle 
and  of  both  auricles  (i.e.,  diameters  MR  and  ML,  Fig.  84,  are  much  increased). 

On  the  other  hand  Katzenstein  has  shown  that  in  just  these  cases  the  impulse 
may  be  exceptionally  strong  and  impart  a  heaving  to  the  whole 
chest,  even  though  the  heart  be  much  dilated,  failing,  and  devoid 
of  the  slightest  trace  of  hypertrophy.    A  systolic  retraction  is  usually  seen  over  the  greater 


PRIMARY  CARDIAC   OVERSTRAIN. 


193 


part  of  the  precordium  of  these  overworking  hearts  (Fig.  89),  corresponding  to  the  con- 
traction of  the  right  ventricle  (page  155).  Occasionally  in  rapid  and  irregular  hearts  this 
appearance  is  somewhat  puzzling  and  has  led  some  clinicians  to  dictate  notes  of  "  delirium 
cordis"  where  this  condition  was  not  present  at  all.1 

The  area  of  relative  cardiac  dulness  is  much  enlarged  (Fig. 
112),  especially  to  the  left,  both  downwards,  corresponding  to  the  dilata- 
tion of  the  ventricle,  and  upwards,  corresponding  to  the  auricle.  In  more 
severe  cases,  especially  with  marked  cyanosis,  the  dulness  is  enlarged 
also  to  the  right  from  dilatation  of  the  right  auricle.  Occasionally  this 
dilatation  may  have  passed  off  before  the  patient  has  been  seen  by  the 
physician  and  only  the  other 
symptoms  and  signs  persist,  but 
it  is  safe  to  assume  that  it  has 
been  present  at  an  earlier  stage 
of  the  disease. 

The  heart  sounds  may 
be  either  very  distant  and  feeble 
or  very  short  and  sharp,  corre- 
sponding to  the  two  types  of 
cardiac  impulse.  They  are  usu- 
ally unaccompanied  by  mur- 
murs, but  in  an  irregular  heart 
may  be  of  uneven  intensity. 
The  second  pulmonic  is  usually 
the  loudest  sound  heard.  The 
clearness  of  the  first  sound  is 
often  altered  by  a  reduplication, 
especially  in  rapid  hearts,  or  by 

the  presence  of  a  soft  blowing  systolic  murmur,  which  is  usually  loudest 
over  the  pulmonic  or  tricuspid  area,  but  occasionally  also  heard  to  the 
anterior  axilla.  These  sounds  do  not  always  but  may  sometimes  corre- 
spond to  the  presence  of  functional  insufficiency  of  the  mitral  valve 
(vide  page  422),"  in  other  cases  to  anaemia.  It  is,  however,  extremely 
difficult  or  sometimes  impossible  to  decide  absolutely  whether  such  an 
insufficiency  is  present. 

The  pulse  is  usually  rapid,  ranging  from  80  to  160  per  minute, 
small,  and  weak,  in  many  cases  irregular  in  both  force  and  rhythm.  In 
less  severe  cases  there  are  only  occasional  extrasystoles  (Schott) ;  in  the 
more  advanced  there  is  an  absolutely  irregular  rhythm  which  persists 
even  after  the  rate  slows.  There  is  often  persistent  tachycardia  without 
dyspnoea,  lasting  for  even  weeks  or  months. 

Clinical  Course. — In  some  cases,  however,  all  the  signs  and  symptoms 
of  overstrain  may  be  present  without  any  irregularity  whatever,  but  often 
associated  with  a  rapid  and  regular  pulse.  Occasionally  the  pulse  may  be 
regular  only  while  it  is  rapid,  but  becomes  irregular  as  the  rate  diminishes. 
In  many  cases  no  murmurs  or  other  signs  of  valvular  insufficiency  are 

1  The  term  delirium   cordis   is  used  rather  indefinitely  to  designate  conditions 
varying  between  extreme  irregularity  with  tachycardia  and  true  fibrillation  of  the  heart. 
The  onset  of  the  latter  is,  however,  not  consistent  with  the  existence  of  life. 
13 


Fig.  112. — Cardiac  dulness  in  v.  Leyden's  case  upon  his 
three  successive  admissions   (I,  II,  III). 


194  DISEASES   OF   THE   HEART   AND    AORTA. 

encountered,  while  in  still  others  a  relative  or  functional  insufficiency  of 
the  mitral  or  tricuspid  valve  results  from  the  cardiac  dilatation,  with  some 
embarrassment  of  the  heart  resulting  therefrom  in  addition  to  the  original 
failure.  Systolic  (functional)  murmurs  are  heard  in  these  areas,  and  the 
stasis  is  still  further  increased  by  the  regurgitation  of  blood.  The  cedema 
becomes  extreme,  hydrothorax  may  set  in,  and  death  soon  results.  As  in 
the  case  of  da  Costa's  patient  under  discussion,  the  progress  may  be  stayed 
somewhat  by  occasional  treatment  and  rest.  If  the  latter  is  sufficient  and 
the  disease  not  too  far  advanced,  the  patient's  life  may  be  saved. 

The  liver,  as  in  Case  II,  enlarges  when  the  condition  becomes  severe 
and  tricuspid  insufficiency  has  set  in.  Its  edge  is  then  smooth  and  varies 
in  consistency  from  being  rounded  and  so  soft  as  to  be  palpable  only 
with  the  side  of  the  index  finger  to  almost  board-like  hardness.  It  is 
always  smooth.  In  severe  cases  jaun-dice  may  be  present  and  the  liver  may 
pulsate. 

The  abdomen  is  often  distended  with  gas,  a  factor  which  contrib- 
utes largely  to  the  cardiac  discomfort  by  pushing  up  the  diaphragm.  In 
the  later  stages  of  heart  failure  ascites  may  be  present. 

The   genitalia  show  cedema  only  in  the  later  stages  of  the  disease. 

The  lower  extremities  are  often  cedematous,  the  swelling  first  mani- 
festing itself  about  ankles  and  shins. 

The  urine  during  the  period  of  heart  failure  is  usually  scant, — less 
than  900  c.c.  (30  ounces)  for  24  hours, — owing  to  diminished  rapidity  of  blood 
flow.  It  is  then  of  high  specific  gravity  (1020  and  over),  and  often  contains 
albumin  and  casts.  In  extreme  stasis  numerous  epithelial,  coarsely  and 
finely  granular,  and  hyaline  casts  are  seen  in  every  field  of  the  microscope. 

Blood.  The  blood  picture  may  vary  from  a  moderate  anaemia  to 
a  real  polycythemia,  dependent  upon  the  condition  of  the  patient  before 
the  over-exertion. 

The  sputum  may  be  scanty  and  mucous,  or  profuse,  frothy,  and 
albuminous,  dependent  upon  the  relative  strength  of  the  right  and  left 
ventricles.  In  rare  cases  haemoptysis  results  during  the  exertion  from 
engorgement  of  the  pulmonary  capillaries. 

Transitory  Cardiac  Dilatation. — A  particularly  instructive  series  of 
cases  studied  with  modern  methods  are  those  reported  by  Hornung  (1908). 
Among  1100  cases  which  he  watched  with  the  X-ray  during  the  past  seven 
years  he  has  met  with  a  number  who  usually  showed  perfectly  normal 
hearts  but  were  subject  to  acute  dilatation  after  overstrain.  This  was 
particularly  frequent  in  persons  who  had  used  alcohol  to  excess,  in  those 
who  had  recently  suffered  from  infectious  diseases,  and  in  anaemic  indi- 
viduals. The  attacks  of  dilatation  are  brought  on  by  fright, 
high  altitudes,  excitement,  over-exertion,  etc.  Sexual  ex- 
citement might  be  added  to  this  list.  Hornung  returns  to  the  old  view  of 
Seitz,  Allbutt,  and  v.  Leyden,  that  cardiac  overstrain  with  acute 
dilatation  is  much  more  common  than  might  be  supposed 
from  the  work  of  Moritz  and  his  pupils. 

For  a  long  period,  however,  he  may  be  expected  to  be  more  subject 
to  other  attacks  than  before,  although  by  care  he  may  remain  free  from 
them.     Just  how  long  this  susceptibility  may  last  varies  with  each  case, 


PRIMARY  CARDIAC   OVERSTRAIN.  195 

but  da  Costa  has  shown  us  that  after  carefully  sparing  the  patient  from  all 
severe  effort  for  weeks  or  even  months,  he  may  again  perform  even  such 
severe  efforts  as  are  entailed  on  cavalry  charges  and  forced  marches  without 
injury  and  may  lead  a  life  of  perfect  health. 

The  other  side  of  the  picture  is  shown  by  v.  Leyden's  case.  This  man 
returned  to  work  in  spite  of  the  discomfort.  The  latter  became  worse,  and 
after  bearing  it  for  three  months  he  entered  the  hospital  with  a  heart  already 
dilated  and  permanently  irregular,  and  with  well-marked  oedema  of  the 
limbs.  Definite  heart  failure  had  set  in.  From  this  he  recovered  under 
rest  and  treatment  with  digitalis.  His  heart  resumed  almost  normal  size, 
his  oedema  disappeared.  The  circulation  once  more  returned  to  almost 
normal,  but  one  permanent  injury  had  been  done  for  which  the  treatment 
was  of  no  avail.    The  heart  action  had  become  irregular  and  remained  so. 

The  commencement  of  permanent  absolute  irregularity  in  rate  (pulsus 
irregularis  perpetuus)  (see  Part  I,  Chapter  IV)  at  this  stage  is  a  very  com- 
mon occurrence  in  overstrained  hearts,  and  seems  to  be  one  of  the  most 
important  factors  in  determining  the  subsequent  course  of  the  disease  (see 
page  191).  When  the  irregularity  persists  it  adds  its  own  mechanical  effects 
on  the  circulation  to  those  already  present  and  increases  the  overstrain. 

When  a  life  of  strenuous  muscular  work  is  continued  by  such  a  patient 
the  result  is  inevitable.  Strain  follows  strain,  and  the  condition  brought 
about  by  the  first  failure  is  exaggerated  with  each  successive  day's  work. 
The  attacks  of  pain  and  pressure  in  the  thorax  (anginoid  attacks)  increase 
in  severity  and  frequencj^.  The  heart  dilates  more  and  becomes  corre- 
spondingly weaker.  Blood  stagnates  in  the  veins,  first  in  the  more  depend- 
ent portions,  causing  oedema  of  the  ankles,  shins,  thighs,  genitalia,  then 
enlargement  of  the  liver  and  ascites  from  stasis  in  the  portal  system,  finally 
oedema  of  the  face  and  arms.  The  heart  dilates  still  more;  the  mitral  and 
tricuspid  orifices  no  longer  close.  After  each  attack  he  is  less  vigorous 
than  before,  and  greater  care  must  be  taken  to  avoid  exertion.  For  the 
manual  laborer  such  a  life  may  be  at  once  impossible  and  intolerable,  but 
the  litterateur,  the  scholar,  the  scientist,  and  the  man  of  affairs  may  be 
saved  for  years  to  a  life  of  quiet  but  none  the  less  useful  activity  in  spite  of 
a  considerable  degree  of  cardiac  break-down. 

DIAGNOSIS. 

The  diagnosis  of  primary  overstrain  of  the  heart  is  not  always  simple. 
It  is  always  a  question  not  of  whether  the  heart  has  been  overstrained  but 
of  whether  this  weakening  is  primary,  and  whether  the  heart  was  perfectly 
healthy  before  the  effort  was  made.  If  the  heart,  muscle,  or  valves  were 
in  any  way  diseased  before  the  effort,  the  overstrain  may  be  considered  as 
secondary  to  that  lesion.  Accordingly  the  diagnosis  rests  upon  the  pre- 
vious history,  upon  the  nature,  duration,  and  sequelae  of  previous  infec- 
tious diseases,  upon  the  degree  of  arteriosclerosis,  and  upon  the  general 
health  of  the  patient  before  the  onset  of  the  trouble. 

Latent  myocarditis,  fatty  degeneration,  and  arteriosclerosis  are  par- 
ticularly difficult  to  exclude.  A  mild  grade  of  myocarditis  may  have  given 
no  symptom  whatever  in  daily  life,  but  become  apparent  when  exercise 
is  violent.    A  mild  grade  of  arteriosclerosis  is  practically  universal  among 


196  DISEASES   OF  THE   HEART  AND  AORTA. 

persons  past  middle  age,  but  if  considerable  efforts  had  been  made  without 
symptoms  of  cardiac  insufficiency  these  may  be  disregarded.  When  symp- 
toms of  heart  failure  occur  suddenly  in  a  robust  individual  during  or  after 
some  intense  muscular  or  nervous  effort,  acute  cardiac  dilatation  and  over- 
strain may  usually  be  diagnosed  with  certainty,  but,  like  hysteria  among 
the  nervous  diseases,  it  should  be  arrived  at  only  after  a  process  of  careful 
exclusion. 

BIBLIOGRAPHY. 

Stokes,  W.:  Diseases  of  the  Heart  and  Aorta,  Dublin,  1854. 

Allbutt,  T.  Clifford:  The  Effect  of  Overwork  and  Strain  on  the  Heart  and  Great  Blood- 
vessels, St.  George's  Hosp.  Rep.  (Lond.),  1870,  v,  23. 

Da  Costa,  J.  M.:  On  the  Irritable  Heart;  a  Clinical  Study  of  a  Form  of  Functional  Cardiac 
Disorder  and  its  Consequences,  Am.  J.  M.  Sci.,  Phila.,  1871,  lxi,  17.  Medical  Diagnosis, 
Phila.,  1864.  Also,  Observations  upon  Heart  Diseases  in  Soldiers,  etc.,  Mem.  U.  S. 
Sanitary  Commission,  Washington,  1867,  ch.  x,  p.  36. 

Maclean,  W.  C. :  On  the  Diseases  of  the  Heart  in  the  British  Army  and  the  Remedy,  Brit. 
M.  J.,  Lond.,  1867,  i,  161. 

Myers,  A.  R.  B.:  Etiology  and  Prevalence  of  Diseases  of  the  Heart  among  Soldiers,  London, 
1870. 

Peacock,  T.  B.:  Lectures  on  Diseases  of  the  Heart,  Med.  Times  and  Gaz.,  Lond.,  1873, 
ii,  1,  57,  113,  169,  221,  319,  349.  On  Some  of  the  Causes  and  Effects  of  Valvular  Dis- 
eases of  the  Heart,  Lond.,  1865. 

Seitz,  Joh.:  Die  Ueberanstrengung  des  Herzens,  Berl.,  1875.  (A  monograph  by  the  author 
containing  translations  of  the  articles  of  Allbutt,  da  Costa,  and  Myers.) 

V.  Leyden,  E.:  Ueber  die  Herzkrankheiten  in  Folge  von  Ueberanstrengung,  Ztschr.  f. 
klin.  Med.,  Berl.,  1886,  xi,  105. 

Schott,  Th.:  Zur  acuten  Ueberanstrengung  des  Herzens  und  deren  Behandlung,  Wies- 
baden, 1898. 

Hornung:  Beitrage  zur  Frage  der  acuten  Herzerweiterung,  Berl.  klin.  Wchnschr.,  1908, 
xlv,  1769. 

Henschen,  S.  E.:  Ueber  die  Herzdilatation  bei  Chlorose  und  Ansemie,  Mitth.  a.  d.  med. 
Klin,  zu  Upsala,  1898,  p.  27. 

Katzenstein,  J.:  Dilatation  und  Hypertrophic  des  Herzens,  Munchen,  1903. 


II. 

PATHOLOGICAL  PHYSIOLOGY  OF  EXERCISE,  CARDIAC  OVER- 
STRAIN, HEART  FAILURE,  AND  COMPENSATION. 

PHYSIOLOGY    OF   EXERCISE. 

It  is  evident  from  the  foregoing  examples  that  muscular  efforts  which 
lead  to  cardiac  overstrain  are  in  themselves  merely  the  exaggeration  of 
ordinary  exercises.  To  understand  these  effects  it  is  necessary  first  to 
understand  those  of  ordinary  exercise. 

McCurdy  has  classified  exercises  as — 

1.  Exercises  of  speed,  like  running,  chest  weight  exercises,  etc.,  in  which 
the  individual  movements  require  little  effort,  but  the  main  effort  lies  in  the  rapidity  with 
which  they  are  repeated. 

2.  Exercises  of  endurance,  as  in  long-distance  running,  prolonged  walk- 
ing, forced  marches,  etc.,  in  which  the  movements  are  neither  difficult  nor  especially 
rapid  and  the  element  of  strain  sets  in  only  with  the  onset  of  fatigue. 

3.  Exercises   of   strain,    as  lifting  heavy  objects,  wrestling,  etc. 

Exercises  of  Speed. — The  cases  of  cardiac  overstrain  reported  by  All- 
butt  and  da  Costa  represent  overstrain  from  exercises  of  endurance ;  those 
by  v.  Leyden  and  Miinzinger  represent  exercises  of  strain. 

Masing,  Erlanger  and  Hooker,  Dawson  and  Eyster,  and  Gordon 
have  investigated  the  effect  of  exercises  of  speed  such  as  rapid  weight- 
lifting,  running,  etc.,  upon  man.  The  three  last  named  have  found  that 
in  individuals  in  training,  whose  circulation  is  least  affected,  mild  exercise 
causes  either  no  change  or  else  a  fall  of  blood-pressure.  Tangl  and 
Zuntz  also  found  this  in  horses  and  a  similar  period,  though  of  short 
duration,  in  dogs  running  on  a  tread-mill. 

In  all  muscular  work  an  increased  amount  of  C02  is  given  off  from  the 
muscles  and  acts  as  a  hormone 1  which  sets  into  play  the  following  physio- 
logical mechanisms: 

1.  Vasodilation  in  the  muscles,  diverting  four  or  five  times  as  much  blood  through 
this  channel   (Chauveau  and  Kaufmann). 

2.  Acceleration  of  the  heart,  at  first  through  diminution  in  the  vagus  action,  and  in 
the  later  stages  of  prolonged  severe  exercise  chiefly  through  stimulation  of  the  accelerators 
(Hering,  Bowen). 

3.  Vasoconstriction,  especially  in  the  splanchnic  vessels,  which  tends  to  counteract 
the  effect  of  the  vasodilatation  in  the  muscles. 

4.  Stimulation  of  the  augmentor  fibres,  and  perhaps  also  of  the  heart  muscle,  directly, 
causing  an  increased  force  of  contraction  (higher  maximal  pressure)  and  an  increased 
systolic  output  (higher  pulse-pressure).  Stimulation  of  the  augmentor  fibres  also,  as  a 
rule,  causes  increased  cardiac  tonicity. 

1  Hormone,  a  substance  generated  in  one  part  of  the  body  which  circulates  in  the 
blood,  reaches  and  sets  into  activity  another  organ,  thus  playing  the  role  of  a  "chemical 
messenger."  (Cf.  Starling,  E.  H.:  On  the  Chemical  Correlation  of  the  Functions  of  the 
Body,  Lancet,  Lond.,  1905,  ii,  391,  423,  501,  579.) 

197 


198 


DISEASES   OF   THE    HEART   AND    AORTA. 


The  heart  of  the  trained  athlete  is  habitually  throwing  out 
an  amount  of  blood  suited,  not  to  the  needs  of  the  moment,  but  to  the 
needs  of  the  periods  of  exercise  to  which  he  has  accustomed  himself.  The 
systolic  output  is  above  normal  when  the  exercise  (and  hence  the  increased 
production  of  C02)  is  slight.  The  heart  is  thus  able  to  take  care  of  the 
excess  C02  production  in  exercise  without  increasing  its  output;  and  hence 
the  vasodilatation  in  the  muscles  is  the  only  factor  influencing  the  blood- 
pressure.  When  the  exercise  becomes  severe  the  other  mechanisms  begin  to 
play  a  role. 

In  normal  but  not  trained  young  men  Masing  found 
that  upon  lifting  and  lowering  a  weight  with  the  feet  the  blood-pres- 
sure (maximal)  and  pulse-rate  rose  at  once  to  a  con- 
stant height,  where  they  remained  until  the  exercise 
ceased.     They  then  fell  almost  immediately  to  the  original  level.     The 


EXERCISE  EXERCISE 

Fig.  113. — Alterations  of  blood-pressure  due  to  rapid  lifting  of  light  weights  with  the  feet.     (After  Masing, 
Deutsches  Arch.  f.  klin.  Med.,  vol.  lxxiv.)    A.  Noimal  young  man.    B.  Man  aged  68. 

writer  has  found  that  the  minimal  pressure  rises  also,  but  less  than  the 
maximal,  the  pulse-pressure  being  increased.  In  middle-aged  persons 
Masing  found  that  the  pressure  rose  higher,  and  on  cessation  of  the  exercise 
required  several  minutes  to  reach  the  original  level;  while  in  very  old  persons 
the  rise  was  still  greater  and  neither  pressure  nor  rate  returned  to  normal 
for  a  considerable  period.    The  response  is  proportional  to  the  effort. 

When  exercise  is  continued  in  normal  young  persons  and 
the  organism  readapts  itself  to  the  effort  (the  "second  wind"  setting  in), 
blood-pressure  and  pulse-pressure  again  fall  to  a  fairly  constant  level 
(Dawson  and  Hatfield).  This  probably  explains  why  the  heart-rate  of 
well-trained  Marathon  racers  is  sometimes  slow  at  the  finish.  In  animal 
experiments  it  finds  its  analogy  in  the  improved  cardiac  action  observed 
as  a  result  of  clamping  the  thoracic  aorta,  and  represents  the  response  of 
the  heart  to  a  strain  which  is  not  excessive. 

The  weaker  the  individual  or  the  more  severe  the 
exercise  the  more  prominent  become  factors  2,  3,  and 
4,  the  greater  the  rise  of  b  1  o  o  cl-p  r  e  ss  ur  e  and  the 
greater  the  pulse-rate.  The  slowness  at  which  conditions  return 
to  normal  is  more  or  less  proportional  to  the  exertion  and  the  fatigue. 

It  is  also  true  that  for  a  given  amount  of  exercise  performed  in  a  given 
time  the  amount  of  C02  formed  is  least  when  it  is  done  with  least  effort 
by   trained    individuals  and  increases  when  the  effort  becomes  marked. 


PHYSIOLOGY  OF   EXERCISE. 


199 


Zuntz  and  Schumburg  have  shown  upon  German  soldiers  that  a  certain 
short  march  used  up  only  554.8  calories  of  energy  when  the  subjects  were 
fresh,  but  required  635.5  calories  when  they  were  fatigued.  This  is  prob- 
ably due  to  the  fact  that  with  the  increase  in  effort  accessory  muscles  are 
called  into  play,  many  of  which  contract  and  give  off  C02  without  mate- 
rially improving  the  execution  of  the  exercise. 


Fig.  114. —  Effect  of  walking  on  a  level  on 
patient  with  badly  broken  compensation.  (After 
Cabot  and  Bruce,  Am.  J.  M.  Sc,  cxxxiv.) 


Fig.  115. — Effect  of  prolonged  exercise  upon 
the  blood-pressure  of  men  in  various  degrees  of 
muscular  strength.  The  arrows  indicate  the  point 
at  which  symptoms  of  exhaustion  set  in.  COM- 
PENSATED, compensated  heart  lesions;  FAIL- 
ING, broken  compensation  with  heart  failure.  Up- 
per margins  of  bands,  systolic  pressures;  lower, 
diastolic. 


Exercises  of  Endurance.  — ■  The  point  at  which  an  exercise  of  speed 
becomes  converted  into  an  exercise  of  endurance  is  more  or  less  relative 
and  depends  chiefly  upon  the  condition  and  the  training  of  the  individual. 
The  most  typical  exercises  of  endurance,  the  forced  march,  the  long-dis- 
tance runs  (Marathon  races),  and  long-distance  bicycle  races,  have  been 
carefully  studied  by  Zuntz  and  Schumburg,  Blake  and  Larrabee,  Dietlen 
and  Moritz,  and  R.  T.  Abercrombie.  In  these  exercises  the  least  changes 
occur  in  the  best-trained  individuals  in  whom  the  amount  of  effort  put 
forth  is  least  or  least  prolonged. 

The  pulse-rate  of  the  men  who  finished  in  the  Marathon  races  at  Boston  showed  sur- 
prisingly little  increase,  the  greatest  rise  during  the  race  of  1900  being  from  76  before  to 
144  after;  but  the  average  rate  after  the  race  was  103  (Blake  and  Larrabee).  There  was 
frequently  a  moderate  grade  of  irregularity.  Zuntz  and  Schumburg  found  similar  effects. 
The  blood-pressure  after  the  race  was  usually  found  to  be  a  trifle  lower  than  before  the 
8tart3  though  it  varied  greatly  in  different  individuals.  J.  Barach  has  recently  obtained 
similar  results  with  the  Erlanger  apparatus  upon  another  set  of  trained  Marathon  racers; 
although  the  orthodiagraph  showed  dilatation  of  the  heart  in  all.  Quite  different  are 
the  results  in  long-distance  races  run  by  amateurs.  Dr.  R.  T.  Abercrombie  has  recently 
made  a  careful  study  of  the  condition  of  contestants  in  a  twenty-mile  road  race  before 
and  immediately  after  the  race.  Before  the  race  the  average  blood-pressures  with  the 
Erlanger  apparatus  were:  maximal  120-130,  minimal  75-80;  pulse-rate  80.  Immediately 
after  the  race  the  pulse  was  in  almost  every  instance  too  feeble  to  be  counted,  as  were 
also  the  heart  sounds;  and  neither  these  nor  the  blood-pressure  could  be  satisfactorily 
estimated  until  one-half  hour  after  the  finish,  when  the  pulse-rate  was  usually  about  120 
per  minute,  the  maximal  pressure  about  75-100  mm.  Hg.     The  heart  sounds  were  still" 


200 


DISEASES  OF  THE  HEART  AND  AORTA. 


rapid  and  feeble.  Nevertheless  all  of  these  men  felt  quite  well,  and  were  able  to  enjoy  a 
cold  plunge  immediately  after  the  examination.  Within  an  hour  after  the  finish  they 
were  all  feeling  quite  active.  The  blood-pressure  was  usually  found  to  be  lower  than  be- 
fore the  start,  but  this  varied  greatly  in  individual  cases.1 

Not  all  the  results  of  endurance  tests  are  as  mild  as  these.  During  the  amateur 
athletic  contests  in  the  United  States  the  past  five  years  there  have  been  several  cases  of 
permanent  heart  failure  following  directly  upon  overstrain  in 
long-distance  runs.  As  in  Da  Costa's  series,  the  persons  whose  hearts  were  injured 
were  usually  boys  under  twenty  who  were  poorly  trained  and  whose  hearts  were  not  fitted 
for  the  strain  put  upon  them. 

As  regards  the  metabolism  during  such  exercise,  Zuntz  and  Schumburg,  and  also  A. 
Loewy  and  L.  Zuntz,  found  that  both  the  amount  of  CO2  given  off  per  minute  and  the 
respiratory  quotient  were  markedly  lessened  (C02  falling  from  802.3  c.c.  to  743.0  c.c.  per 
minute;  respiratory  quotient  falling  from  0.855  to  0.780)  at  the  end  of  the  exertion,  though 
the  O2  used  was  unchanged.  This  is  due  to  formation  of  intermediate  oxidation  prod- 
ucts, sarcolactic  acid,  /8-oxybutyric  acid,  etc.,  the  pressure  of  whose  salts  may  add  to 
the  fatigue.  Ryffel  (Heart,  1913-1914,  v,  45)  has  found  that  this  acidosis  results  in  a  con- 
tinued low  CO2  content  of  the  alveolar  air  and  is  the  cause  of  the  continuance  of  dyspnoea 
for  some  time  after  the  exercise  ceases. 


cise. 


Corresponding  to  the  variations  in  rapidity  of  blood  flow,  the  urine 
is  increased  in  amount  during  mild  exercise,  decreased  during  severe  exer- 
After  boat  races  and  after  the  Marathon  races  it  often  contains 

albumin,  casts,  and  even  traces  of 
blood,  probably  as  a  result  of  stasis 
or  high  pressure  in  the  renal  veins 
and  capillaries. 

Exercise  of  Strain. — The  effect  of 
exercises  of  strain,  lifting,  etc.,  is  totally 
different.  McCurdy,  Bruck,  and  others 
have  shown  that  these  exercises  cause 
a  far  greater  rise  of  blood-pressure  than 
do  the  exercises  of  speed;  and,  on  the 
other  hand,  the  pulse-rate  does  not  rise 
rapidly  but  is  at  first  either  slowed  or 
unchanged.  The  rise  in  blood-pressure 
is  greater  in  arteriosclerotics,  old  per- 
sons, and  weak  individuals  for  the 
same  amount  of  work  than  in  well- 
developed  normal  individuals.  In  per- 
sons already  suffering  from  broken 
compensation,  on  the  other  hand,  the 
heart  absolutely  fails  to  respond  with 
increased  effort,  and  may  be  so  greatly 
weakened  by  the  strain  that  the  blood- 
pressure  may  fall. 
All  the  factors  which  are  called  into  play  by  the  hormone  action  of  C02 
in  exercises  of  speed  and  of  endurance  are  also  acting  in  exercises  of  strain; 
but,  since  the  latter  are  usually  intermittent  or  of  short  duration,  their 
effects  are  at  first  overshadowed  by  others  which  are  more  intense. 

1  O.  S.  Lowsley  (Am.  J.  Physiol.,  1911,  xxvii,  446)  has  found  that  the  more  severe 
the  exercise  the  longer  the  systolic  pressure  remains  subnormal  after  it  is  over. 


Fig.  116. — Rise  of  blood-pressure  during 
Valsalva's  experiment  and  during  exercise. 
Normal  individual.  (Schematic,  after  Bruck.) 
ARTERJOSCLER,  curve  of  blood-pressure  in 
man  with  arteriosclerosis  performing  the  same 
exercise. 


PHYSIOLOGY  OF  EXERCISE.  201 

In  carrying  out  any  exercise  involving  muscu- 
lar strain  the  individual  involuntarily  closes  his 
glottis  and  executes  an  attempt  at  forced  expira- 
tion. The  result  of  this  is  a  tremendous  increase  in  intrathoracic  pressure, 
which  hinders  the  outflow  of  blood  from  the  right  ventricle  as  well  as  the 
inflow  into  the  right  auricle. 

The  result  of  these  two  factors  is  dilatation  of  the  right  ventricle  and  stasis  in  the 
systemic  veins,  which  is  still  further  shown  by  the  cyanosis  of  the  face  and  distention  of  the 
veins  that  accompany  all  such  exercises  even  in  trained  athletes.  The  venous  stasis  is 
further  increased  by  the  sudden  squeezing  out  of  blood  from  the  large  masses  of  skeletal 
muscles,  which  are  being  forcibly  contracted  simultaneously,  as  well  as  from  the  vessels  of 
the  splanchnic  area. 

The  high  pressure  within  the  lungs  stimulates  the  sensory  endings  of  the  vagus,  which 
in  turn  reflexly  stimulate  the  motor  nucleus  of  the  vagus  and  the  vasomotor  centre  in  the 
medulla  and  cause  both  slowing  of  the  pulse  and  rise  of  blood-pressure.  The  general  result 
is  the  same,  but  less  marked  when  the  Valsalva  experiment  only  (forced  expiration  with 
glottis  closed)  is  carried  out,  and  depends  very  largely  upon  this  factor. 

SIZE    OF   HEART  AFTER   EXERCISE. 

Diminution  in  Size  in  Healthy  Hearts. — Examined  with  the  X-ray 
the  auricles  are  seen  to  dilate  greatly,  but  the  ventricles  do  not,  as  a  rule, 
show  any  dilatation  whatever.    This  again  is  a  question  of  tonus,  and  here 


Fig.  117. — Semi-schematic  drawing  showing  variations  in  size  of  the  heart  of  a  long-distance 
bicycle  rider,  as  the  result  of  a  very  long  race;  reconstructed  from  the  orthodiagraphic  outline.  A.  Before 
the  race.  B.  Immediately  after  the  race,  showing  the  great  diminution  in  size  of  the  heart.  C.  Four 
weeks  later.     (After  Moritz  and'Dietlen,  Munchen.med.  Wchnschr.,  1908,  lv.) 

also  the  latter  factor  seems  to  determine  whether  dilatation  shall  set  in  or 
not.  All  exercises  when  sufficiently  severe  lead  to  dilatation  of  hearts  whose 
myocardium  has  suffered  injury,  especially  during  the  course  of  infectious 
diseases  (da  Costa,  Zuntz  and  Schumburg,  de  la  Camp,  Moritz  and  Dietlen) 
or  during  the  first  few  weeks  following  them.  On  the  other  hand,  Schott  has 
claimed  to  have  seen  cardiac  dilatation  in  healthy  wrestlers  and  bicycle  riders 
as  a  result  of  short  wrestling  bouts.  This  fact  has  been  disputed  by  a  number 
of  observers  who  have  carefully  controlled  the  more  or  less  subjective  find- 
ings of  percussion  by  outlining  the  heart  with  the  orthodiagraph. 

The  following  exercises  have  been  studied:  bicycle  riding,  by  Mendelsohn,  Albu, 
Beyer,  Schieffer,  Dietlen  and  Moritz;  marching,  by  Zuntz  and  Schumburg,  Albu  and 
Caspari,  Balders,  Heichelheim  and  Metzger;  football  playing,  by  F.  Pick  and  by  Selig; 
ski  running,  by  Henschen;  wrestling,  by  Levy-Dorn,  Selig,  Mendl  and  Selig;  swimming, 
by  Kienbock,  Selig  and  Beck. 

The  results  of  these  observations  quite  uniformly  confirm  those  of 
de  la  Camp  in  showing  that  exercise,  even  to  the  point  of  exhaustion  and 


202  DISEASES   OF   THE   HEART   AND   AORTA. 

fainting,  does  not  bring  about  cardiac  dilatation  in  otherwise  healthy  men. 
In  most  cases  the  X-ray  and  orthodiagraph  show  an  actual  diminution  in 
the  volume  of  the  heart 1  (see  Fig.  117).  De  la  Camp  also  found  that  healthy 
dogs  could  run  upon  a  tread-mill  until  they  dropped  from  exhaustion  with- 
out causing  dilatation  of  the  heart;  whereas  the  hearts  of  dogs  which  had 
been  poisoned  with  phosphorus  and  which  were  in  a  state  of  mild  fatty 
degeneration  dilated  greatly  from  the  same  exercise. 

Dilatation  and  Myocardial  Injury.  —  On  the  other  hand,  Hornung, 
who  has  watched  the  course  of  1100  cases  of  weak  heart  with  the  X-ray, 
states  that  in  such  persons  acute  dilatations  (demonstrable  with  the  ortho- 
diagraph) are  very  common  as  the  result  of  slight  overstrain.  It  may 
require  comparatively  little  strain  to  bring  this  about.  For  example,  he 
cites  the  case  of  a  woman  with  a  weak  heart  who  acquired  a  dilatation  by 
taking  a  short  cut  instead  of  a  gradual  ascent  while  climbing  a  hill  (OerteFs 
Terrainkur).  The  dilatation  lasted  for  several  days  and  gradually  passed 
off.  Persons  whose  hearts  are  in  this  labile  equilibrium  are  liable  to  have 
repeated  attacks.  But  the  cardiac  condition  rarely  stands  still.  It  grad- 
ually becomes  either  better  or  worse,  according  to  the  treatment  and  the 
mode  of  life  of  the  patient. 

Thoracic  and  Abdominal  Constriction  as  a  Factor  in  Cardiac  Over= 
strain.  —  A  high  diaphragm  due  to  tight  belts  or  corsets  is  one  of  the  most 
important  factors  which  predispose  to  cardiac  overstrain.  This  was  already 
shown  by  A.  R.  B.  Myers  in  1867.  Myers  observed  that  certain  cavalry 
regiments  in  the  Indian  Army  were  particularly  subject  to  cardiac  over- 
strain and  to  chronic  cardiac  disease,  even  more  so  than  the  infantry  regi- 
ments which  were  doing  more  arduous  work  under  the  same  conditions  of 
climate  and  diet.  He  noticed  that  the  uniforms  of  this  cavalry  regiment 
were  very  tightly  belted  and  had  tight  cuirasses  compressing  the  chest. 
Upon  experimentation  he  found  that  the  men  in  this  regiment,  when  not 
wearing  their  uniforms,  were  quite  as  strong  as  those  of  other  regiments 
in  the  service.  He  also  found  that  the  same  men  were  able  to  withstand 
much  greater  exertion  in  the  same  uniforms  if  only  the  belts  were  worn 
looser.  This  has  been  shown  with  somewhat  greater  exactness  by  Th. 
Schott.  Schott  demonstrated  with  the  orthodiagraph  that  wrestlers  could 
withstand  much  greater  exertion  before  the  onset  of  acute  dilatation  or  of 
cardiac  symptoms  if  they  wore  no  belts  than  if  they  were  tightly  belted. 
This  is,  of  course,  not  surprising,  and  is  simply  another  way  of  demonstrat- 
ing the  every-day  experience  of  most  healthy  women  that  they  can  do 
more  work  without  a  corset  or  with  a  loose  one  than  when  wearing  one 
that  is  tightly  laced. 

The  reason  for  this  is  twofold.  The  belt  interferes  with  the  respira- 
tory movements  of  the  abdomen  and  diaphragm,  and  hence  diminishes  the 
rhythmic  alternation  of  positive  and  negative  pressures,  of  force-pump  and 
suction-pump  action,  in  one  of  the  largest  of  the  vascular  reservoirs,  thus 

1  The  syncope  (cerebral  anaemia)  under  these  conditions  is  probably  due  to  the  exactly 
opposite  condition,  diminished  cardiac  filling  and  hence  diminished 
cardiac  output;  arterial  anaemia  due  to  rapid  pulse-rate  in  a  heart  whose  tonicity 
is  increased.  (This  condition  is  fully  discussed  in  the  chapters  on  Paroxysmal  Tachycardia 
and  Miscellaneous  Heart  Diseases.) 


PHYSIOLOGY  OF   EXERCISE. 


203 


diminishing  the  rapidity  of  blood-flow.  Moreover  the  viscera  are  pushed 
back  and  the  diaphragm  is  pushed  upward  by  the  belt,  and  this  causes  the 
heart  to  assume  a  more  transverse  position,  in  which  kinking  of  the  great 
veins,  the  aorta,  and  the  pulmonary  artery  sets  in,  and  both  the  filling  and 
the  emptying  of  the  heart  are  impeded.  This  mechanism  is  readily  demon- 
strated upon  the  exposed  heart  of  the  living  animal.  A  comparatively 
slight  upward  or  downward  displacement  of  the  heart  from  its  natural  posi- 
tion may  cause  tremendous  fall  in  blood-pressure  and  interference  with 
the  work  of  the  heart. 

PHYSIOLOGICAL   FACTORS    BRINGING    ABOUT    DILATATION. 

The  diminution  in  the  size  of  the  heart  which  was  found  so  uniformly 
by  the  above-mentioned  observers  seems  to  be  due,  in  part,  to  diminished 
filling  of  the  ventricles  when  the  heart  is  rapid,  but  chiefly  to  the  fact  that 
the  cardiac  tonicity  was  increased  by  the  strain.1  This  clinical  observa- 
tion has  its  analogue  in  experimentation  on  animals.  0.  Frank  has  shown 
that,  other  things  being  equal,  a  moderate  increase  in  intraventricular 
pressure  acts  as  a  stimulus  and  causes  an  increase  in  the  force  of  the  next 
beat.     If  the  pressure  is  raised  further  it  reaches  an  optimum;  but  if  it 


VOL. 


T  + 


B.  P. 


jHMMHHMttl 


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mmmm^Sm, 


Fig.  118. —  Effect  of  strain  upon  the  dog's  heart  whose  tonicity  is  good.  Volume  curve  (VOL.) 
and  blood-pressure  curve  (B.P.)  of  an  animal  whose  heart  is  in  good  condition.  Descending  thoracic 
aorta  clamped  at  the  moment  indicated  by  the  arrow.  Momentary  dilatation  followed  by  a  diminution 
in  size.  The  heart  becomes  smaller  than  before  the  clamping.  Tonicity  is  increased  (T  +).  Blood- 
pressures  maximal  and  minimal  are  also  increased. 

becomes  too  high  the  force  of  contraction  becomes  much  weaker  than  if 
there  were  no  load  at  all.  There  is  a  similar  effect  upon  cardiac  tonicity. 
Hirschfelder  has  shown  that  if  the  thoracic  aorta  of  the  dog  is  clamped  the 
ventricles  at  first  dilate  rapidly  and  the  systolic  output  diminishes.  If  the 
heart  is  in  good  condition  the  systoles  soon  begin  to  increase,  the  excess 
of  blood  is  pumped  out  of  the  ventricular  cavities  in  systole,  and  on  the 
other  hand,  in  spite  of  the  high  pressure  in  the  veins,  less  blood  enters  the 
ventricles  than  before. 

2  It  is  possible  that  acapnia  (page  49)  may  play  a  role  under  these  conditions. 


204  DISEASES   OF   THE   HEART    AND    AORTA. 

The  amount  of  blood  which  enters  the  ventricles  depends  upon  two 
factors:  1.  As  Howell  and  Donaldson  have  shown  for  the  excised  heart, 
and  Roy  and  Adami  for  the  dog's  heart  in  situ,  it  is  more  or  less  propor- 
tional to  the  venous  or  intra-auricular  pressure.  2.  Roy  and  Adami, 
Hirschfelder,  Cameron,  and  others  have  shown  that  it  is  also  dependent 
upon  the  cardiac  tonicity,  being  greater  when  tonicity  is  low  (dilatation) 
and  least  when  tonicity  is  high.  It  is  therefore  evident  that  a  heart  whose 
tonicity  is  high  will  withstand  a  comparatively  high  venous  pressure  with- 
out dilating,  whereas  when  the  tonicity  is  low  it  readily  overfills. 

Several  factors  contribute  toward  diminishing  the  strength  of  an  over- 
filled heart:  1.  With  the  increase  of  the  cubical  contents  and  the  internal 
surface  of  the  ventricles  the  mechanical  work  necessary  to  exert  a  normal 


VOL. 


B.  p. 


SEC. 

Fig.  119. — Volume  curve  of  a  dog  whose  cardiac  tonicity  is  low.  Clamping  the  aorta  is  followed 
by  permanent  dilatation  and  only  a  slight  momentary  increase  in  blood-pressure.  The  systolic  output 
is  diminished,  owing  to  inability  of  the  heart  to  force  the  usual  quota  of  blood  against  the  increased 
resistance. 

pressure  is  increased  (Roy  and  Adami).  2.  In  the  dilated  heart  the  blood 
flow  through  the  coronary  arteries  and  hence  the  nutrition  of  the  cardiac 
walls  is  diminished  (Hyde) .  Moreover  the  dilatation  of  the  ventricles  may 
or  may  not  be  permanent,  dependent  upon  the  tonus  of  the  heart  muscle 
(Hirschfelder,  Cameron).  If  the  latter  is  low  the  dilatation  remains  and 
increases,  whereas  if  it  is  high  the  increased  pressure  acts  as  a  stimulus. 
It  is  usually  a  high  venous  pressure  which  keeps  the  heart  dilated  and  a 
low  tonicity  which  permits  it  to  remain  so. 

Not  the  least  of  the  factors  which  lead  to  diminished  tone  and  dilatation 
is  the  acidosis  mentioned  on  page  200,  for,  as  Cameron  has  shown,  the  slightest 
trace  of  acid  can  bring  on  these  results.  The  observations  of  Zuntz  and  Schum- 
burg  and  of  Lewis,  Ryffel,  Wolf,  Cotton  and  Barcroft  show  that  acidosis 
results  from  such  overstrains  and  that  it  may  play  a  major  role  in  rendering 
a  heart  more  susceptible  to  all  the  mechanical  factors  that  overtax  it. 

EFFECT   OF   THE    STRAIN   UPON   THE    HEART. 

The  response  of  the  heart  to  a  muscular  exertion  which  just  fatigues 
may  be  of  three  grades:  1.  The  heart  becomes  smaller  or  the  cardiac  out- 
lines are  unchanged — tonicity  high  (normal  hearts).  2.  There  is  a  transitory 
dilatation  (after  acute  infections  and  in  hearts  with  myocardial  or  some  other 
cardiac  disturbance).  3.  The  overstrain  leads  to  permanent  injury  of  the 
heart,  often  with  permanent  arrhythmia  (chronic  cardiac  overstrain,  myo- 


PHYSIOLOGY  OF  EXERCISE. 


205 


cardial  changes).  These  three  conditions  find  their  analogues  in  the 
effects  of  clamping  the  thoracic  aorta  upon  the  volume  of  the  ven- 
tricles (Fig.  119). 

As  has  been  seen  in  the  cases  quoted  above,  the  repetition  of  the  strain 
is  quite  as  important  a  factor  in  heart  failure  as  is  the  overstrain  itself. 
Even  a  heart  with  extremely  low  tonicity  will,  in  most  cases,  recover  and 
gradually  return  to  normal  volume  after  the  strain  has  been  removed,  but 
during  the  period  when  it  is  still  dilated  it  is  much  more  susceptible  to  a 
further  overstrain.  On  the  other  hand,  after  a  sufficient  period  of  rest  it 
regains  its  former  volume  and  still  later  its  former  tonicity,  and  once  more 
reaches  its  original  strength.  That  this  is  probably  the  case  in  man  also  is 
shown  by  the  fact  that  Poynton  did  not  regard  an  occasional  overstrain 


Fig.  120. — Effect  upon  the  volume  of  the  dog's  heart  produced  by  clamping  the  descending  tho- 
racic aorta.  Ascent  of  curve  =  diminution  in  volume;  descent  =  dilatation.  1,  normal  and  vigorous  heart; 
2,  slightly  weakened  heart  with  diminished  tonicity;  3,  very  weak  heart  with  much  diminished  tonicity. 

as  of  any  special  significance  in  boys,  provided  it  were  followed  by  a  period 
of  sufficient  rest.  Such  overstrains,  however,  are  not  to  be  lightly  disregarded 
in  spite  of  the  claims  of  Meylan  that  not  a  single  case  of  cardiac  disease 
occurred  among  the  Harvard  oarsmen  from  1852  to  1892,  though  albuminuria, 
hematuria,  and  signs  of  overstrain  were  frequent  just  after  the  races.  More 
recent  studies  by  Bardeen  (Jour.  Am.  Med.  Assoc,  1913,  lxi,  1657)  have 
not  proved  so  optimistic  and  have  established  so  much  proof  of  permanent 
injuries  that  the  University  of  Wisconsin  has  placed  a  ban  upon  intercollegiate 
boat  races. 

One  of  the  most  important  factors  in  determining  the  end  result  is  the 
period  of  rest  after  the  overstrain.  When  the  subject  rests  after  the  strain 
his  heart  regains  its  strength  and  tonicity  and  usually  returns  to  normal. 
But  in  v.  Leyden's  case  and  other  cases  of  permanent  heart    failure,    the 


206  DISEASES  OF  THE  HEART  AND  AORTA. 

heart  was  still  dilated  at  the  time  of  renewed  strain.  This  condition  seems  to 
determine  the  border-line  between  heart  failure  and  recovery. 

The  border-line  conditions  may  therefore  be  summarized  as  follows: 
Dilatation  of  the  heart  during  or  after  exercise  represents  a  pathological, 
though  not  a  very  infrequent,  condition  in  which  the  heart  has  overstepped 
its  limits.  The  condition  usually  recedes  and  leaves  no  traces  unless  the 
heart  is  again  overstrained  while  still  in  a  dilated  condition. 

As  regards  the  anatomical  changes  induced  by  the  condition  of  over- 
strain, Roy  and  Adami  have  shown  that,  when  the  dog's  heart  begins  to 
fail  after  clamping  the  aorta,  stasis  occurs  in  the  coronary  veins  and  the 
heart  muscle  becomes  cedematous.  This  oedema  is  especially  marked  in 
the  regions  which  are  richest  in  connective  tissue,  the  auricles  and  the 
auriculoventricular  valves.  They  believe  that  when  the  strain  is  con- 
tinued the  oedema  is  replaced  by  infiltration,  the  infiltration  by  connective 
tissue,  and  that  fibrous  myocarditis  results.  Indeed,  a  fibrous  myocarditis 
(cardiosclerosis)  is  a  common  autopsy  finding  in  cases  of  long-continued 
cardiac  overstrain  in  which  there  has  been  no  severe  infectious  disease  to 
account  for  the  lesion.  On  the  other  hand,  Fleisher  and  Loeb  and  Pearce 
have  found  exactly  the  stages  mentioned  by  Roy  and  Adami  in  animals  in 
the  various  stages  of  adrenalin  myocarditis  (see  page  316). 


BROKEN   CARDIAC   COMPENSATION. 

As  long  as  the  heart  is  able  to  maintain  a  certain  velocity  of  blood 
flow  throughout  the  circulation,  the  latter  may  be  said  to  be  compensated; 
but  when  the  blood  stagnates  to  such  a  degree  as  to  give  rise  to  the  signs 
and  symptoms  of  stasis,  compensation  may  be  said  to  be  broken. 

There  are  two  forms  of  broken  compensation.  When  the  blood  stag- 
nates in  the  systemic  veins  from  failure  of  the  right  side  of  the  heart,  the 
condition  may  be  termed  broken  systemic  compensation; 
when  stasis  occurs  in  the  lungs  because  the  left  side  of  the  heart  is  not 
acting  as  strongly  as  the  right,  broken  pulmonary  compensation 
results.  Each  of  these  two  forms  brings  with  it  a  characteristic  group  of 
symptoms:  The  broken  systemic  circulation  (usually  designated  simply  as 
"  broken  compensation  ")  manifests  itself  in  the  signs  and  symptoms  which 
are  seen  in  tricuspid  insufficiency — breathlessness,  cyanosis,  oedema,  begin- 
ning in  the  feet  and  legs,  enlargement  of  the  liver,  and  systolic  pulsation 
of  the  liver  and  veins,  etc.  Broken  pulmonary  compensation  is  accom- 
panied by  the  signs  and  symptoms  of  an  acute  severe  mitral  insufficiency — 
intense  respiratory  disturbance,  dyspnoea,  cough,  occasionally  pulmonary 
hemorrhage,  and  the  sputum  containing  the  characteristic  cells  of  passive 
congestion  (Herzfehlerzellen). 

Broken  Systemic  Compensation. — From  the  physiological  stand-point, 
the  cardinal  features  of  broken  systemic  compensation  are  dilatation  and 
weakening  of  the  right  ventricle,  dilatation  and  paralysis  of  the  right 
auricle,  increase  in  C02  and  decrease  in  02  in  the  venous  blood,  functional 
insufficiency  of  the  tricuspid  valve,  rise  in  venous  pressure  (often  to  as 
high  as  20  mm.  Hg)  (Fig.  121,  III).  The  signs  are  cyanosis,  engorgement 
and  systolic  pulsation  of  the  veins,  enlargement  of  the  liver,  oedema  of  the 


BROKEN   CARDIAC   COMPENSATION. 


207 


feet  and  legs,  and  sometimes  venous  stasis  in  the  medulla,  vasoconstriction, 
high  blood-pressure,  and  dyspnoea  of  medullary  origin. 

Broken  Pulmonary  Compensation. — The  characteristics  of  broken  pul- 
monary compensation  are  dilatation  and  weakening  of  the  left  ventricle, 
dilatation  and  usually  paralysis  of  the  left  auricle,  rise  of  pressure  and 
stasis  in  the  pulmonary  veins,  engorgement  of  the  pulmonary  capillaries, 
and  "erection"  of  the  lung  tissue  (v.  Basch)  (Fig.  121,  IV) v  Welch  has 
shown  that  when  the  stasis  is  very  intense,  pulmonary  oedema  sets  in. 
V.  Basch  and  his  pupils  have  applied  this  idea  to  the  milder  pulmon- 
ary manifestations  and  have  shown  that  a  moderate  erection  of  the  lung 
tissue  brings  on  cardiac  dyspnoea  and  leads  to  bronchitis  and  cough.  His 
pupil,  Kauders,  has  shown  that  the  position  of  the  diaphragm  is  affected 
reflexly  by  the  amount  of  blood  in  the  lungs,  congestion  causing  the 
diaphragm  to  descend,  depletion  causing  it  to  ascend.  It  is  thus  usually 
lower  than  normal  in  mitral  lesions,  higher  in  pulmonary  and  tricuspid. 


NORMAL 


ii 

BROKEN 
PULMONARY 

COMPENSATION 


III 

BROKEN 

SYSTEMIC 

COMPENSATION 


IV 

FAILURE  OF 
BOTH 

VENTRICLES 


Fig.  121. —  Diagram  showing  changes  in  the  circulation.  I,  normal;  II,  broken  pulmonary  com- 
pensation; III,  broken  systemic  compensation;  IV,  both  compensations  fail;  stases  in  lungs  and  veins. 
AO,  pressure  in  the  aorta,  PA.     (Compare  with  Fig.  26.) 


V.  Basch  also  believed  that  the  congestion  of  the  lungs  causes  the  elastic- 
ity of  the  lungs  to  diminish  and  to  become  so  rigid  as  actually  to  diminish 
the  respiratory  expansion,  but  the  experiments  of  D.  Gerhardt  have  thrown 
doubt  upon  this  phase  of  his  conclusions.  As  regards  the  changes  of  pres- 
sure and  the  distribution  of  the  blood,  however,  v.  Basch's  conclusions 
have  been  confirmed,  not  only  by  Gerhardt  in  Germany  but  by  W.  G. 
MacCallum  and  McClure  in  America. 

In  badly  weakened  hearts  both  forms  of  broken  compensation  may 
be  present,  sometimes  features  of  one,  sometimes  of  the  other,  predomi- 
nating. 

Functional  Valvular  Insufficiency  in  Broken  Compensation. — Although 
it  has  not  been  absolutely  proved,  it  seems  almost  certain  that  the  occur- 
rence of  broken  compensation  from  acute  dilatation  is  accompanied  by  a 
functional  insufficiency  of  the  tricuspid  or  the  mitral  orifice  which  may 
be  of  transitory  duration.  Indeed  this  functional  insufficiency  of  the  tri- 
cuspid valve  in  heart  failure  is  much  more  common  than  organic  lesion  of 


208  DISEASES   OF   THE   HEART   AND    AORTA. 

the  valve,  and  in  long-standing  cases  is  accompanied  by  actual  stretch- 
ing of  the  tricuspid  orifice  (T.  W.  King,  G.  A.  Gibson,  Mackenzie,  Keith). 

T.  W.  King,  in  1837,  demonstrated  that  such  functional  insufficiencies 
occur  at  the  triscupid  valves,  and  even  that  they  were  dependent  upon  the 
tonicity  of  the  ventricular  fibres ;  since  the  valves  which  had  been  in- 
sufficient a  few  hours  after  death  held  water  perfectly  after  rigor  mortis 
had  set  in  (quoted  in  full  on  page  498).  These  observations  have  been 
confirmed  and  extended  by  G.  A.  Gibson,  Francois-Franck,  Mackenzie, 
Friedreich,  Marey,  Hirschfelder,  Keith.  Hering  demonstrated  the  same 
phenomenon  for  the  mitral  valve  in  rabbits,  but  found  that  in  dogs  the 
mitral  valve  did  not  leak  even  after  clamping  the  aorta.  Stewart  and  the 
writer  have  been  able  to  demonstrate  the  occurrence  of  such  an  insuffi- 
ciency of  the  mitral  valve  when  the  aorta  was  clamped,  in  dogs  whose 
aortic  valves  had  been  rendered  insufficient.  In  man  Morton  Prince  and 
Broadbent  have  noted  the  presence  of  transitory  mitral  systolic  murmurs 
(sometimes  transmitted  to  the  axilla)  in  men  who  were  being  subjected 
to  the  strain  of  civil  service  examinations,  and  in  cases  with  similar  signs 
Minkowski  has  obtained  tracings  from  the  oesophagus  which  have  the  form 
characteristic  of  mitral  insufficiency. 

In  the  earlier  stages  of  cardiac  overstrain  the  dilatation  of  the  auricles 
is  a  more  or  less  passive  phenomenon  which  exerts  little  influence  upon  the 
circulation,  but  in  the  more  severe  stages  it  may  play  a  leading  role. 

Auricular  Fibrillation  and  Arrhythmia  in  Cardiac  Overstrain. — Condi- 
tions which  affect  tonicity  and  filling  of  the  ventricles  have  a  still  greater 
effect  upon  the  tonicity  and  filling  of  the  auricles.  It  was  demonstrated  by 
Ludwig's  pupils,  Waller  (1878)  and  v.  Frey  and  Krehl  (1890),  that  when 
the  ventricles  began  to  fail,  the  auricles  soon  became  overloaded  with  blood 
and  ceased  to  contract  visibly  when  the  pressure  reached  15-20  mm.  Hg. 
As  a  rule  this  does  not  affect  the  cardiac  rhythm,  but  Hirschfelder  has  shown 
in  dogs  that  when  this  is  brought  about  by  narrowing  the  mitral  orifice,  an 
absolute  irregularity  (disorderly  rhythm)  may  set  in  without  any  coordinate 
contractions  carried  out  by  the  auricles. 

The  contractions  of  the  auricles  under  these  circumstances  do  not  give  rise  to  any 
(a)  waves  upon  the  venous  pulse,  which  is  of  the  ventricular  type;  a'jd  when  the  latter 
furnished  the  sole  criterion  of  cardiac  activity  it  was  believed  that  these  chambers  were 
either  not  contracting  at  all  or  were  merely  originating  impulses  without  active  contrac- 
tions, as  Biedermann  had  shown  for  skeletal  muscle.  Lewis  has  shown  with  the  electro- 
cardiograph that  the  latter  occasionally  takes  place  (P  wave  present  upon  the  electrocardio- 
gram with  (a)  wave  absent  from  venous  pulse)  while  the  pulse  remains  regular,  but  when 
irregularity  sets  in  there  are  either  extrasystoles  or  auricular  fibrillation.  The  latter,  and 
especially  the  finer  type  of  auricular  fibrillations,  represent  the  more  severe  forms  of  cardiac 
failure. 

Arrhythmia.— Whatever  may  be  the  origin  of  the  arrhythmia  it  is  very  common  in 
severe  overstrains.  This  not  infrequently  arises  in  the  course  of  valvular  lesions  as  well,  as 
Mackenzie  has  proved.  The  case  cited  on  page  448  gives  an  example  of  such  an  irregularity 
arising  during  such  an  attack  and  subsiding  a  few  days  later  after  rest  and  digitalis.  Five 
days  later  the  rhythm  became  regular  and  the  auricles  were  contracting  once  more.  When 
the  overstrain  is  more  protracted  the  auricular  contraction  may  remain  absent  for  weeks 
and  even  months,  and  most  frequently,  if  it  has  persisted  for  a  considerable  length  of  time, 
permanent  changes  set  in  in  the  musculature  of  the  sinus  region  (Keith,  Schonberg),  and 
regularity  is  never  regained.  The  pulse  has  become  permanently  irregular  (pulsus  irregu- 
laris perpetuus,  arrhythmia  perpetua).    As   has   been  seen  on    page  127,  the  arrhythmia 


BROKEN   CARDIAC   COMPENSATION.  209 

itself  slows  the  blood  stream  and  the  diseased  condition  of  the  sinus  prevents  the  heart 
from  compensating  for  this  by  a  greater  number  of  contractions.  The  velocity  of  the 
circulation  is  thus  self-limited.  Only  a  certain  amount  of  C02  per  minute  can  be  taken  care 
of  and  any  excess  brings  on  overstrain. 

Changes  in  Venous  Pressure. —  Changes  in  pressure  in  the  systemic 
veins,  which  show  how  well  the  right  ventricle  is  pumping,  often  afford 
an  excellent  index  of  the  break  in  systemic  compensation,  rising  from 
normal  pressure  of  5-10  cm.  H20  to  a  height  of  20  or  25  cm.  It  usually 
rises  when  the  patient's  condition  becomes  worse  and  falls  as  improvement 
sets  in  (Hooker  and  Eyster). 

The  arterial  pressure,  on  the  other  hand,  is  affected  by  too  many 
factors  to  show  characteristic  changes.  It  may  be  kept  up  until  shortly 
before  death,  by  asphyxia  of  the  medullary  centres  and  resultant  vaso- 
constrictor and  augmentor  stimulation;  or,  on  the  other  hand,  when  this 
mechanism  is  not  brought  into  play,  the  arterial  pressure  may  be  low  and 
the  pulse  may  be  small  and  weak. 

CARDIAC  FAILURE  WITH  A  SMALL  HEART. 

There  is  another  form  of  failure  of  the  circulation  which  sometimes 
occurs  as  the  result  of  exertion,  even  in  trained  athletes.  This  form  is 
accompanied  by  pallor,  a  small  rapid  pulse,  and  sometimes  even  by  syncope. 
However,  as  Dietlen  and  Moritz  have  shown,  it  is  not  accompanied  by  a 
dilatation  of  the  heart,  but,  on  the  contrary,  the  latter  is  smaller  than 
normally.  It  is  a  failure  of  the  rest  of  the  circulation  rather  than  of  the 
heart. 

It  must  be  admitted  that  this  condition  has  not  attracted  much  attention,  and  but 
little  can  be  said  of  the  mechanisms  involved.  The  pallor,  small  pulse,  and  small  heart, 
however,  are  features  which  are  also  common  to  the  condition  of  shock  and  the  cardiac 
neuroses.  In  these  conditions,  the  important  mechanical  factors  are  the  accumulation  of 
blood  in  the  dilated  abdominal  veins,  giving  rise  to  a  low  venous  pressure,  the  diminished 
filling  of  the  heart,  and  consequently  the  diminished  output  into  the  aorta.  The  symp- 
toms are  symptoms  of  "arterial  anaemia." 

The  causal  factor  in  bringing  about  this  condition  may  be  dilatation  of  the  veins. 
In  the  case  of  exercise  this  veno-  and  vasodilatation  may  result  either  reflexly  from  dis- 
turbed digestion,  or,  perhaps,  as  Henderson  suggests  for  somewhat  similar  conditions,  it  may 
set  in  when  the  rapidity  of  breathing  exceeds  that  necessary  to  aerate  the  blood,  even  to 
meet  the  increased  needs  of  the  body.  Under  these  conditions  C02  leaves  the  lungs,  and 
hence  also  the  blood,  a  little  too  rapidly,  acapnia  results,  and,  as  its  first  effect,  allows  the 
veins  to  dilate  (see  page  49).  The  blood  thus  stagnates  in  the  veins.  As  a  matter  of  fact, 
Kraus,  Zuntz  and  Schumburg,  and  also  A.  Loewy  have  shown  that  at  this  stage  of  exercise 
less  C02  is  given  off  from  the  lungs  than  before,  and  the  respiratory  quotient  C02is  lessened. 
They  believe  that  oxidation  is  less  at  this  stage  and  hence  less  C02  is  present  in  the  blood. 
In  other  words,  from  a  totally  different  stand-point,  and  years  before  Henderson's  experi- 
ment, it  was  rendered  probable  that  a  state  of  acapnia  is  present  at  the  stage  of  fatigue 
in  exercises  of  endurance,  and  therefore  that  the  mechanism  which  he  observed  to  be  active 
in  acapnia  is  largely  responsible  for  this  form  of  circulatory  failure. 

FUNCTIONAL   TESTS   OF   CARDIAC   EFFICIENCY. 

It  is  evident  from  the  facts  discussed  above  that  the  most  important 
question  in  the  functional  study  of  heart  failure  is  to  determine  accurately  the 
border-line  between  fatigue  and  overstrain,  to  distinguish  between  the  nor- 
mal and  the  pathological.     Various  tests  have  been  devised  for  this  purpose. 

14 


210  DISEASES   OF   THE   HEART   AND    AORTA. 

1.  Postural  Change  in  Pulse=rate. — The  rise  in  the  pulse-rate  which  oc- 
curs when  the  patient  stands  after  lying  down  is  of  some  importance.  Under 
normal  conditions  the  acceleration  is  not  more  than  twenty  beats  per  minute,  the  average 
acceleration  for  normal  individuals  being  seven.  However,  this  depends  upon  many 
factors,  one  of  which  is  the  length  of  time  during  which  the  patient  has  lain  down,  his  state 
of  mental  excitement  or  quiet,  etc.  The  psychic  element  plays  a  particularly  important 
role  in  this  test. 

2.  Contraction  of  Antagonistic  Muscles.  —  Herz  has  introduced  another  procedure, 
the  self-checking  or  self-antagonizing  test  (Selbsthemmungsprobe) .  He 
counts  the  pulse  over  a  period  long  enough  to  assure  a  reasonably  constant  rate  per  minute. 
The  patient  is  then  made  to  sit  down  and  very  slowly  flex  and  extend  the  right  forearm, 
putting,  all  the  while,  his  full  attention  upon  the  movement,  but  contracting  simultaneously 
the  flexor  and  extensor  muscles  of  the  arm,  and  attempting  to  antagonize  his  own  move- 
ment with  as  much  force  as  possible.  This  converts  the  exercise  into  a  mild  exercise  of 
strain.  Herz  states  that  in  normal  individuals  this  causes  no  change  in  pulse-rate, 
while  in  those  with  feeble  hearts  the  pulse-rate  is  slowed  5-20  beats  per  minute.  (Per- 
haps this  is  due  to  the  more  vigorous  expiratory  effort  which  accompanies  this  procedure 
in  persons  with  diseased  hearts.)  Cabot  and  Bruce  have  repeated  Herz's  observations, 
and  find  that  they  are  correct  in  at  least  a  certain  number  of  cases,  but  they  are  unwilling 
to  subscribe  to  his  general  rule.  The  writer  also  has  found  a  number  of  perfectly  strong 
and  healthy  individuals  who  give  Herz's  pathological  reaction. 

3.  Rise  of  Blood=pressure  on  Constricting  the  Femoral  Arteries.  —  Marey  (1881) 
demonstrated  that  in  normal  individuals  the  blood-pressure  rose  when  both 
femoral  and  both  brachial  arteries  were  compressed.  Katzenstein  found  that  on  com- 
pressing both  femoral  arteries  alone,  in 

Blood-pressure  Pulse-rate 

Normal  individuals Rose    5-15  mm Fell. 

Compensated  cardiac  lesions Rose  15-40  mm Unchanged  or  fell. 

Slight  cardiac  insufficiency Unchanged Unchanged  or  rose. 

Very  weak  hearts Fell Fell. 

Hoke  and  Mende  and  others  have  repeated  Katzenstein's  observations,  and  find  that, 
though  these  results  hold  true  in  general,  the  method  is  unreliable  as  a  test  and  in  bad 
cases  is  too  dangerous  for  use. 

4.  Rise  of  Blood=Pressure  upon  Exercise. — Masing,  Graupner,  Baur  and  Graupner 
Cabot  and  Bruce  have  called  attention  to  the  fact  that  rise  of  blood-pressure  occurs  during 
exercise.  Baur  found  that  riding  a  stationary  bicycle  with  a  brake  caused  a  rise  of  5  to  10 
mm.  Hg  in  normal  individuals,  but  a  fall  of  5  to  20  mm.  Hg  in  weak  hearts. 

5.  Duration  of  Change  of  Pulse=Rate,  Blood=Pressure  and  Symptoms  after  Exercise. — 
The  animal  experiments  of  Hirschfelder  and  Cameron  cited  on  page  204  show  that  dilata- 
tion and  change  of  blood-pressure  may  occur  temporarily  under  the  influence  even  of  a 
strain  that  acts  almost  at  once  as  a  stimulus.  In  strong  hearts  they  are  only  transitory, 
in  weak  hearts  they  are  of  long  duration.  In  harmony  with  these  findings  O.  S.  Lowsley 
(Am.  J.  Physiol.,  1911,  xxvii,  446)  has  studied  the  duration  of  after  effects  of  exercise. 
He  found  that  after  severe  exercise  the  blood-pressure  fell  and  remained  low  not  more  than  an 
hour  and  a  half  in  normal  persons.  In  persons  whose  hearts  were  weaker,  however,  the 
fall  of  blood-pressure  lasted  longer;  and  the  duration  of  the  low  pressure  was  a  better 
index  of  the  cardiac  weakness  than  was  the  intensity  of  the  fall  of  pressure. 

Too  much  emphasis  cannot  be  laid  upon  this  element  of  duration  of  the  effect  of  ex- 
ertion; whether  it  be  measured  by  change  of  blood-pressure,  change  of  pulse-rate,  short- 
ness of  breath,  rapidity  of  breathing,  duration  of  weakness,  nervousness,  insomnia  or  any 
other  symptoms  or  sign.  However,  J.  Parkinson  (Heart,  1917,  vi,  317)  has  found  that  in 
patients  suffering  from  "soldier's  heart"  the  quickening  of  the  pulse-rate  after  mild  exercise 
subsides  as  rapidly  as  it  does  in  normal  individuals,  but  in  spite  of  this  the  breathlessness 
persists  much  longer  in  the  patients  with  soldier's  heart  than  in  the  normal  individuals. 

For  practical  purposes,  the  panting  and  feeling  of  weakness  following  any  ordinary 
exercise  rarely  outlasts  the  exertion  by  more  than  fifteen  minutes'  rest;  and  when  these 
symptoms  outlast  it  more  than  half  an  hour  it  is  safe  to  state  that  either  the  heart  is  too 
weak  or  the  exertion  too  violent  for  that  individual,  which  is  only  another  way  to  para- 
phrase the  same  thing. 

Equally  important  with  the  making  of  the  functional  test  is  the  caution  to  make  it 
only  when  the  patient's  mind  is  distracted  from  the  exercise,  for  otherwise  the  psychic  ele- 
ment is  too  strong. 


FUNCTIONAL  TESTS  OF  CARDIAC  EFFICIENCY.  211 

Thus,  the  writer  recalls  a  woman  with  supposed  influenzal  myocarditis  who  was  pros- 
trated by  a  simple  arm  exercise  which  she  afterwards  performed  with  ease,  only  a  few  min- 
utes later,  when  her  mind  was  distracted.  Efforts  should  always  be  made  to  distract  the 
patient's  mind  while  performing  any  of  these  very  vital  tests  of  heart  function. 

That  a  close  relationship  exists  between  the  increase  in  blood-pressure 
and  the  increase  in  tonicity  (stimulation  of  augmentor  fibres),  which  results 
from  strain  put  upon  the  heart,  may  be  seen  from  the  curves  of  Hirsch- 
felder  and  Cameron  in  the  dog's  heart  (quoted  on  page  203,  and  shown  in 
Figs.  118  and  119).  It  is  probable  that,  in  most  cases,  rise  of  pressure  cor- 
responds to  increased  systolic  output  and  concomitant  increase  in  tonicity. 
It  must  be  realized,  however,  that  in  some  cases  the  rise  may  be  secondary 
to  stimulation  of  the  vasoconstrictor  centre  from  medullary  stasis  or  asphyxia, 
and  then  may  represent  an  unfavorable  condition. 

Several  objections  may  be  made  to  the  value  of  this  test: 

1.  G.  A.  Gordon  in  G.  A.  Gibson's  clinic  and  also  Professor  Dawson,  in  collaboration 
with  Professor  Eyster  and  also  with  Mr.  Hetfield,  have  shown  that  the  blood-pressure 
in  trained  athletes  falls  during  mild  exercise  exactly  as  it  does  in  broken 
compensation  ;  also  that  it  falls  when  the  "second  wind"  is  acquired  and  while  the 
person's  functional  power  is  increasing  rather  than  decreasing. 

2.  As  already  shown  by  Masing,  the  greatest  risesofblood-pressure  occur  in 
old  and  feeble  persons,  whom  the  exercise  brings  near  to  the  border-line  of  cardiac  overstrain. 

3.  In  persons  in  whom  the  fall  in  blood-pressure  occurs  as  a  result  of  the  test  exercise, 
the  general  symptoms,  respiratory  distress,  cyanosis,  etc.,  to  say  nothing  of  the  decrease 
in  the  size  of  the  pulse,  tachycardia  and  arrhythmia  resulting,  are  more  than  sufficient 
evidence  that  the  patient's  strength  has  been  overtaxed. 

4.  These  simpler  clinical  manifestations  are  more  delicate  indices  and  are  less  ambig- 
uous signs  than  are  the  changes  in  blood-pressure. 

The  recent  studies  of  Schott,  de  la  Camp,  v.  Criegern,  Hornung,  Moritz  and  his  pupils, 
taken  in  conjunction  with  the  physiological  experiments  of 
Frank,  Hirschfelder,  and  Cameron,  indicate  that  theonly  true 
numerical  criterion  of  cardiac  efficiency  is  whether  a  given 
strain  causes  it  to  diminish  in  size  (increase  in  tonicity=stimu- 
lation)  or  to  dilate   (decrease  in  tonicity=overstrain). 

Functional  studies  upon  the  border-land  between  functional  sufficiency 
and  cardiac  failure  are  of  the  most  fundamental  importance,  and  all  the  facts 
added  to  our  knowledge  of  the  subject  are  of  the  greatest  value  in  adding  to 
our  understanding  of  the  subject. 

Observation  versus  Estimation. — However,  it  must  be  admitted  that, 
in  order  to  be  decisive,  all  these  tests  usually  have  to  be  pushed  to  a  point  at 
which  the  appearance,  sensations,  and  signs  of  the  patient  are  in  themselves 
perfectly  characteristic  of  cardiac  insufficiency,  and  at  which,  for  diagnostic 
purposes,  a  little  common-sense  observation  is  at  least  as  unambiguous  as 
observation  with  elaborate  apparatus.  This  does  not  mean  that  exercise  tests 
are  unimportant.  On  the  contrary,  they  are  of  the  greatest  value;  and  no 
change  in  the  patient's  mode  of  living  during  convalescence  or  during  after-life 
should  be  undertaken  without  them.  But  their  importance  depends  more 
upon  the  care  with  which  the  physician  watches  the  general  appearance  and 
condition  of  the  patient,  the  rapidity  with  which  he  recovers  from  the  exer- 
cise,1 his  general  condition,  and  whether  nervousness,  irritability,  cough,  or 

1  Lowsley's  criterion  (the  return  of  the  systolic  pressure  to  normal)  should  be  taken 
into  account. 


212  DISEASES  OF  THE  HEART  AND  AORTA. 

insomnia  has  set  in  during  the  twenty-four  hours  following  it,  than  in  the 
numerical  changes  which  occur  at  the  moment  of  exercise.  The  symptoms 
to  be  looked  for  as  evidence  of  overwork  are  discussed  in  more  detail  in  the 
instructions  for  giving  Schott  exercises  (page  280).  These  are  subtler  mani- 
festations resulting  from  smaller  changes  than  may  be  detected  by  even  the 
most  refined  observations  by  mechanical  methods,  and  which  are  less  easily 
masked  by  ambiguities.  Moreover,  it  must  be  realized  that  any  one  form  of 
exercise  furnishes  data  which  may  depend  as  much  upon  the  condition 
of  the  skeletal  muscles  as  upon  the  heart.  The  blacksmith  with  a 
diseased  heart  may  be  able  to  do  more  work  than  the  book-keeper 
with  neurasthenia,  and  yet  under  the  conditions  in  which  he  lives,  even 
if  not  under  the  strength  test  arranged  for  the  average  man,  the  black- 
smith's heart  may  be  failing. 

Relation  of  Functional  Test  to  Mode  of  Life. — In  diagnosis,  prognosis,  and 
therapy,  the  testing  of  functional  insufficiency  is  a  matter  of  sociology  as  well 
as  physiology.  The  important  question  is  not  what  the  patient 
can  do  in  a  gymnasium,  but  what  he  can  do  and  what  he 
can  not  do  in  every-daylife.  Each  man  must  be  fit  for  his  own 
mode  of  life  or  must  be  made  to  change  it.  His  cardiac  power  must  be 
studied  with  reference  to  that  mode  of  life  rather  than  with  reference  to  a 
rigid  scheme. 

Probably  the  most  thorough  system  of  routine  functional  testing  ever 
instituted  was  that  resorted  to  by  J.  M.  da  Costa  during  the  Civil  War  before 
he  permitted  his  convalescents  from  cardiac  overstrain  to  return  to  active 
duty  with  their  regiments.  He  subjected  them  first  to  light  camp  duties, 
then  to  guard  duty,  then  to  provost  duty,  and  later  made  them  run  frequent 
races  comparable  to  changes  upon  a  battlefield — each  test  commensurate 
with  the  mode  of  life  which  the  patient  was  about  to  live.  Step  by  step  he 
ascertained  the  endurance  of  his  patients  without  overstraining  them,  and 
thus  obtained  a  series  of  permanent  cures  which  stands  as  a  worthy  monu- 
ment to  one  of  the  most  careful  and  brilliant  of  American  clinicians. 

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Physiol.,  Bonn,  1900,  Ixxxii,  1. 

Minkowski,  O.:  Zur  Deutung  der  Herzarhythmien  mittelst  des  cesophagealen  Kardio- 
gramme,  Ztsche.  f.  klin.  Med.,  Berl.,  1906,  lxii. 

Prince,  M.:  Physiological  Dilatation  and  the  Mitral  Sphincter  as  Factors  in  Functional 
and  Organic  Disturbances  of  the  Heart,  Am.  J.  M.  Sc,  Phila.,  1901,  cxxi,  188. 

Broadbent:    Quoted  from  Prince. 

Waller:  Die  Spannung  in  den  Vorhofen  des  Herzens  wahrend  der  Reizung  des  Halsmarkes, 
Arch.  f.  Physiol.,  Leipz.,  1878,  525. 

V.  Frey,  M.,  and  Krehl,  L. :  Untersuchungen  ueber  den  Puis,  ibid.,  1890,  p.  31. 

Biedermann,  W. :  Electrophysiology,  transl.  by  F.  A.  Welby,  Lond.,  1896. 

Kraus,  Fr.:  Die  Ermudung  als  Mass  der  Constitution,  Bibliothec.  Med.  Cassel.  Abth.  D., 
1897,  Heft  3. 

Stephens :  Blood-pressure  and  Pulse-rate  as  Influenced  by  Different  Positions  of  the  Body, 
J.  Am.  M.  Assoc,  Chicago,  1904,  xliii,  955. 

Herz,  H. :  Eine  Funktionspriifung  des  Kranken  Herzens,  Deutsch  med.  Wchnschr.,  Leipz., 
1905,  xxxi,  215. 

Cabot,  R.  C,  and  Bruce,  R.  B.:  The  Estimation  of  the  Functional  Power  of  the  Cardio- 
vascular Apparatus,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1907,  cxxxiv,  491. 

Marey,  E.  J. :  La  circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Paris,  1881. 

Katzenstein:  Ueber  eine  Funktionspriifung  des  Herzens,  Deutsche  med.  Wchnschr., 
Leipz.  and  Berl.,  1905,  xxxi,  695. 

Hoke,  E.,  and  Mende,  J.:  Ueber  die  Katzensteinsche  Methode  zur  Priifung  der  Herzkraft, 
Berl.  klin.  Wchnschr.,  1907,  xliv,  304. 

Levy:  Ueber  Kraftmessung  des  Herzens,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lx,  74. 

Fellner,  B.,  and  Riidinger,  C:  Beitrage  zur  Funktionspriifung  des  Herzens,  Berl.  klin. 
Wchnschr.,  1907,  xliv,  417,  475. 

Graupner:  Die  Messung  der  Herzkraft,  Miinchen,  1905. 

Baur,  Fr.:  Zur  Bestimmung  der  Leistungsfahigkeit  des  gesunden  und  kranken  Herzens 
durch  Muskelarbeit,  Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1904,  xxi,  620. 


III. 

SYMPTOMS  OF  CARDIAC  DISEASE. 

The  symptoms  for  which  a  patient  suffering  from  cardiac  disturbance 
presents  himself  to  the  physician  are  variable,  and  frequently  seem  so  far 
removed  from  the  site  of  disease  as  to  mask  their  real  origin  and  even  to  lead 
to  mistakes  in  diagnosis.  Accordingly,  it  is  important  to  consider  the 
symptoms  early  and  the  conditions  giving  rise  to  them,  remembering  that 
in  general  they  are  due  to  (1)  slowing  of  the  circulation  and  local  anaemia 
or  accumulation  of  CO2;  (2)  overfilling  of  the  veins  with  blood;  (3)  disturb- 
ances in  the  nervous  system,  of  circulatory  origin. 

The  following  are  the  main  symptoms  associated  with  cardiac  diseases: 
(1)  shortness  of  breath;  (2)  cough;  (3)  swelling  of  the  feet  and  legs; 
(4)  urinary  disturbances;  (5)  palpitation  of  the  heart,  precordial  pain, 
pain  down  the  arms;  (6)  digestive  disturbances,  indigestion,  vomiting, 
abdominal  pain,  jaundice;  (7)  general  nervousness,  occasionally  transitory 
delusions  and  hallucinations,  sometimes  fainting  spells.  i 

All  these  symptoms  are  liable  to  be  increased  after  exercise, 
excitement  or  worry,  on  account  of  the  increased  heart-rate  and 
often  increased  blood-pressure  that  accompany  them,  and  the  conse- 
quent increase  in  the  work  of  the  heart.  They  are  also  much  increased 
by  damp  and  sultry  weather  when  there  is  little  air  stirring.  The  patient's 
color  is  then  usually  pale,  showing  a  vasoconstriction  to  which  some  of  the 
embarrassment  is  probably  ascribable.  The  symptoms  usually  improve 
when  the  weather  becomes  clear.  To  avoid  hurry  and  worry 
is  the  cardinal  principle  in  the  treatment  of  the  patient  with 
a  weakened  heart,  and  no  sacrifice  is  too  great  in  rearranging  his  life  in  such 
a  way  that  this  end  may  be  attained. 

Much  that  cannot  be  done  by  the  cardiac  patient  at  the  usual  speed 
without  precipitating  an  attack  of  heart  failure  can  be  carried  out  by  him, 
without  any  ill  effect,  at  a  slower  rate.  It  is  often  not  the  amount  of  effort 
but  the  amount  of  effort  per  minute  that  counts.  A  patient  can  often  be  im- 
pressed by  this  fact  so  that  by  devoting  a  fraction  of  a  minute  more  to  cross- 
ing a  room  or  ascending  a  flight  of  stairs,  he  may  save  his  circulation  from 
a  flood  of  carbonic  acid  and  he  may  save  himself  many  hours  of  fatigue,  dys- 
pnoea and  palpitation. 

Even  the  amount  of  nervous  energy  spent  in  a  rapid  jerky  manner  of 
speech  is  by  no  means  inconsiderable. 

Patients  with  cardiac  failure,  and  especially  those  with  angina  pectoris, 
can  save  themselves  much  of  that  waste  of  energy  which  excitement  brings 
in  the  form  of  high  blood-pressure  and  heart  failure,  by  merely  adopting  a 
slower  enunciation.  For  slow  enunciation  is  the  expression  of  deliberation 
and  calmness  and  unconsciously  brings  these  in  its  wake,  while  rapid  speech 
is  one  of  the  attributes  of  those  who  waste  energy  in  every  motion  and  emo- 
tion; and  since  such  persons  often  fall  prey  to  cardiac  weakness,  arterio- 
sclerosis and  angina  pectoris,  conservation  of  energy  becomes  a  matter  of  im- 
portance.    Loud  and  rapid  speech  nourishes  excitement;  slow,  deliberate 

215 


216  DISEASES  OF  THE  HEART  AND  AORTA. 

enunciation  is  the  expression  of  deliberation  and  calmness,  and  often  uncon- 
sciously brings  these  in  its  wake.  Few  people  can  carry  on  sustained  passion 
or  vituperation  in  a  slow  drawl ;  and  merely  cultivating  a  slow  speech  may 
assist  greatly  in  lessening  the  waste  of  energy.  These  are  savings  which  ex- 
press themselves  in  lower  pulse-rate,  lower  blood-pressure,  and  lessened  heart 
strain,  and  are  well  worth  the  effort. 

RESPIRATORY  DISTURBANCES. 
DYSPNOEA. 

Shortness  of  breath  is  usually  the  earliest  and  most  common  sign  of 
cardiac  failure  and  especially  of  failure  of  the  left  ventricle  (broken  com- 
pensation). The  foundation  for  this  doctrine  was  laid  by  the  classical 
experiments  of  Welch  under  Cohnheim's  direction.  Welch  demonstrated 
that  in  conditions  in  which  the  force  of  the  left  ventricle  was  inpaired 
without  impairment  of  the  right,  oedema  and  congestion  of  the  lungs  set  in. 

V.  Basch  and  his  pupils,  Grossman,  Bettelheim,  and  Kauders,  have 
shown — in  a  very  careful  series  of  investigations  upon  animals — that 
dyspnoea  and  the  other  respiratory  disturbances  of  heart 
failure  are  due  chiefly  to  stasis  in  the  pulmonary  capil- 
laries and  veins,  and  are  associated  with  rise  of  pressure  in  the  left 
auricle.  Under  these  circumstances  the  elasticity  of  the  lungs  is  probably 
diminished  and  the  volume  of  lung  tissue  increases.  The  respiratory 
excursion  decreases.  These  conditions  disappear  when  the  output  of  the 
left  ventricle  (and  hence  the  suction-pump  action  of  that  chamber)  in- 
creases sufficiently  to  ^pump  out  the  excess  of  blood  from  the  lungs  and 
remove  the  stasis.  Accordingly,  as  is  the  common  clinical  experience, 
severe  dyspnoea  is  an  early  sign  of  mitral  lesions,  which  readily  comes 
and  goes  with  slight  overstrains;  while  in  aortic  disease  it  is  a  sign  of  a  severe 
break  in  compensation,  and  often,  indeed,  of  a  secondary  mitral  insufficiency. 

This  group  of  symptom  s — c  ough,  dyspnoea,  car- 
diac asthma,  pulmonary  hemorrhag  e — c  onstitute 
a  group  of  symptoms  characteristic  of. stasis  in  the 
pulmonary  veins  (broken  pulmonary  compensation), 
just  as  cyanosis,  enlargement  of  the  liver,  and  as- 
cending oedema  are  characteristic  of  failure  of  the 
right  heart.  In  Wilkinson  King's  "safety-valve  action  of  the  right 
ventricle,"  failure  of  the  latter  substitutes  a  state  of  broken  systemic  com- 
pensation for  one  of  broken  pulmonary  compensation. 

Rubow  has  shown  by  spirometric  investigations  that  in  cardiac  dys- 
pnoea there  is  a  tendency  for  the  lungs  to  assume  the  greatest  possible  vol- 
ume (diaphragm  descends  lower  and  lower)  just  as  is  the  case  in  emphysema. 

According  to  Kraus  the  amount  of  02  taken  up  by  the  blood  and  of  CO  2  given  off  per 
minute  is  practically  unchanged  in  cardiac  failure.  The  conditions  are  therefore  practically 
analogous  to  Zuntz  and  Schumburg's  experiment,  in  which  increasing  the  CO2  in  the  inspired 
air  caused  polypncea  and  caused  the  total  amount  of  air  taken  into  the  lungs  per  minute 
to  rise  tremendously  without  altering  the  amount  of  oxygen  taken  up  by  the  blood.  It 
is  probable  that  stasis  in  the  pulmonary  capillaries  stimulates  the  vagus  endings  in  the 
same  way  as  does  C02. 

Orthopnoea. — One  of  the  most  striking  features  of  cardiac  dyspnoea  is 
the  fact  that  it  is  increased  in  the  reclining  posture  and  relieved  by  sitting 


SYMPTOMS   OF   CARDIAC   DISEASE.  217 

up  (o  r  t  h  o  p  n  o  e  a),  although  this  position  favors  the  accumulation  of 
oedema  in  the  legs,  and,  as  Erlanger  and  Hooker  have  shown,  impedes  the 
total  velocity  of  the  circulation.  For  this  fact  there  may  be  several  expla- 
nations, or,  more  accurately,  there  may  be  several  factors  involved: 

1.  As  Rubow  has  shown,  when  the  patient  is  propped  up,  Ins  liver  and  diaphragm 
descend,  and  there  is  thus  more  air  space  available  in  the  thoracic  cavity. 

2.  Since  the  head  up  and  feet  down  position  tends  to  impede  the  return  of  venous 
blood  from  the  lower  extremities,  trunk,  and  abdomen,  it  thus  tends  to  equalize  the  activi- 
ties of  the  right  and  left  ventricles.  By  slowing  the  inflow  of  blood  into  the  lungs  it  enables 
the  weakened  left  ventricle  to  deplete  the  pulmonary  capillaries  more  effectually  than 
would  occur  if  more  blood  were  thrown  into  them  by  the  relatively  stronger  right  ventricle. 

3.  In  the  head  up  position  the  veins  of  the  medulla  drain  more  readily,  thus  diminish- 
ing venous  stasis  in  the  medulla  and  consequently  also  diminishing  the  effect  of  direct  CO  2 
stimulation  of  the  vagus  and  respiratory  centres.  This  effect  of  the  erect  position  in  dimin- 
ishing the  volume  of  ( i.e.,  the  blood  in)  the  brain  is  well  known  to  brain  surgeons,  who  some- 
times make  use  of  it  for  penetrating  to  otherwise  inaccessible  places. 

Cardiac  dyspnoea  is  particularly  marked  during  sleep,  partly  because 
the  diminished  sensitiveness  of  the  respiratory  centres  allows  CO2  to  accu- 
mulate (if  only  momentarily)  with  greater  ease  than  during  periods  of  wake- 
fulness, and  partly  because  the  muscles  of  the  larynx  relax,  the  laryngeal 
slit  is  narrowed,  and  air  enters  the  lungs  with  more  difficulty,  thus  allow- 
ing a  slight  asphyxia  to  set  in. 

Cardiac  Asthma. — Occasionally  the  respiratory  distress  takes  the  form 
of  a  definite  paroxysmal  dyspnoea  or  cardiac  asthma.  These  paroxysms 
are  particularly  common  in  aortic  insufficiency  or  coronary  sclerosis.  They 
frequently  occur  at  the  moment  of  awakening.  Porges,  Leimdorfer  and  Marco- 
vici,  as  well  as  Grey  and  Hirschf elder,  have  shown  that  there  are  two  types  of 
cardiac  dyspnoea:  One  due  to  stasis  in  the  pulmonary  air  circulation  or  to 
increased  venosity  of  the  blood,  accompanied  by  alveolar  air  of  normal  com- 
position (5-5.5  to  C02  partial  pressure  38  to  42  mm.  Hg) ;  the  other  due  to 
general  acidosis  or  to  local  acidosis  of  medulla  from  diminished  flow  of  ar- 
terial blood,  leading  to  over-stimulation  of  the  respiratory  centre.  These 
observations  have  been  extended  and  confirmed  by  Lewis,  Ryffel,  Wolf, 
Cotton  and  Barcroft  (Heart,  1913-1914,  v,  45)  as  well  as  by  Peabody  (Arch. 
Int.  Med.,  1914,  jriv,  236). 

While  the  patient  is  awake,  such  attacks  are  sometimes  brought  on 
by  the  act  of  defecation.  This  is  not  surprising,  since  defecation  presents 
a  typical  Valsalva's .  experiment,  in  which,  as  previously  shown,  a  great 
strain  is  thrown  upon  the  left  ventricle,  sometimes  severe  enough  to  pro- 
duce a  functional  mitral  insufficiency. 

Morphine  and  Strychnine  in  Cardiac  Dyspnoea. — Such  attacks  of  car- 
diac asthma  may  be  relieved  by  morphine,  but  the  continued  use  of  mor- 
phine for  this  purpose  often  has  a  bad  effect.  Though  it  momentarily  relieves 
the  distress,  it  also  diminishes  the  irritability'  of  the  respiratory  centre  and 
thus  allows  still  more  C02  to  collect  in  the  blood.  The  patient  then  requires 
still  more  morphine  to  quiet  him,  and  a  vicious  circle  is  introduced: 

Accumulation  of  CO2         t,  e 

in  the  lungs         "*   Paroxysm  of  acapnia 

t  1 

Dnninished  irritability  _  Mor  hine 
of  respiratory  centre 


218  DISEASES  OF  THE  HEART  AND  AORTA. 

On  the  other  hand,  morphine  itself  induces  Cheyne-Stokes  breathing  in 
animals  (Barbour,  J.  Pharmacol,  and  Exper.  Therap.),  and  may  lead  to  the 
very  condition  that  it  attempts  to  cure.  In  animals  this  effect  on  the  respir- 
atory centre  can  be  checked  by  the  administration  of  atropine,  and  the  same 
applies  to  man,  except  in  cases  of  auricular  fibrillation  in  which  the  effect  of 
the  latter  in  preventing  the  curative  action  of  digitalis  may  render  its  use 
inadvisable.  In  such  cases  strychnine  (2-5  mg.),  as  Eyster  has  shown,  may 
afford  a  certain  amount  of  relief.  After  the  first  few  doses  of  morphine  it  is 
frequently  possible  to  get  the  quieting  effect  by  injection  of  distilled  water 
or  by  atropine  or  strychnine  alone. 

In  the  choice  between  strychnine  and  atropine  it  must  be  borne  in  mind 
that  Edsall  and  Means  have  shown  that  the  latter  drug  is  the  more  powerful 
stimulant  of  the  respiratory  centre,  and  that  the  effectiveness  of  strychnine 
has  been  much  overrated  by  the  general  practitioner.  If  these  drugs  do  not 
suffice,  morphine  may  have  to  be  given,  but  it  is  best  to  give  some  atropine 
or  a  little  hyoscine  hydrobromide  (gr.  2T$— tm)  along  with  it,  as  hyoscine 
has,  besides  the  sedative  action  on  the  brain,  an  atropine-like  action  on  the 
respiratory  centre.  Hyoscine  may  also  be  substituted  for  morphine,  especially 
in  subsequent  injections,  but  care  must  be  taken  not  to  give  too  much. 

Cardiac  Asthma  from  Nasal  Disease. — Another  form  of  asthma  with  cardiac  symptoms 
has  its  origin  not  within  the  heart  but  in  the  nose.  Francois-Franck  in  1889  was  able  to 
demonstrate  that  cough,  laryngeal  spasm  (false  croup),  asthmai  and  a  reflex  bronchitis 
arise  reflexly  from  stimulation  of  the  nasal  mucosa.  He  was  able  to  reproduce  these  phe- 
nomena in  animals  by  stimulating  the  mucosa  of  the  septum.  They  were  accompanied 
by  acceleration  of  the  heart  and  vasoconstriction.  They  did  not  appear  when  the  latter 
had  been  cocainized;  or,  if  they  had  once  set  in,  they  disappeared  on  cocainization.  He 
found  that  these  effects  were  much  more  pronounced  in  animals  with  experimental  aortic 
insufficiency  than  in  normal  animals,  and  he  believes  that  such  exaggerated  responses  to 
nasal  reflexes  are  responsible  for  many  of  the  paroxysmal  respiratory  disturbances  in  car- 
diac patients  suffering  from  cardiac  disease,  and  especially  from  aortic  insufficiency.  It 
is  possible  that  they  may  give  rise  to  some  of  the  vasomotor  crises. 

It  is  important  to  differentiate  cardiac  asthma  from  the  bronchial  form. 
Both  may  be  accompanied  by  bronchitis  and  by  the  presence  of  rales.  In 
the  cardiac  form  there  is  no  impediment  to  either  expiration  or  inspira- 
tion, and  hence  only  a  simple  polypncea  is  observed,  while  in  bronchial  asthma 
there  is  stenosis  of  the  smaller  bronchi  with  hinderance  to  both  expiration 
and  inspiration,  and  hence  a  peculiar  labored  and  wheezing  breathing  with 
prolongation  of  expiration  which  is  quite  characteristic. 

C.  M.  Cooper  (The  Respiratory  Ratio:  A  Preliminary  Note,  J.  Am.  M.  Asso.,  Chicago, 
1909,  lii,  1182)  suggests  that  the  differential  diagnosis  in  doubtful  cases  may  sometimes 
be  made  by  noting  the  ratio  between  the  periods  during  which  the  breath  can  be  held 
in  full  inspiration  and  those  in  which  it  may  be  held  in  full  expiration.  In  normal  indi- 
viduals the  breath  may  be  held  in  inspiration  from  40  to  70  seconds;  in  expiration  from 

20  to  35  seconds    (i.e.,  ratio  „  „),    In    patients    with     cardiac    insufficiency  this    ratio 

(25\ 
—  V     In    bronchial    asthma,    on    the 

other  hand,  the  breath  can  be  held  longer  in  expiration  than  in  inspiration  and  the  ratio 

is  reversed   Qg^). 

It  seems  probable  that  this  ratio  will  prove  of  great  value  in  differentiating  between 
asthmatic  attacks  due  to  acute  failure  of  the  left  ventricle  and  those  which  arise  in  cases 
of  cardiac  diseases,  from  intercurrent  bronchial  asthma. 


SYMPTOMS  OF  CARDIAC  DISEASE.  219 

PULMONARY   (EDEMA. 

Occasionally  the  attack  of  cardiac  failure  is  very  severe  and  is  accom- 
panied by  cedema  of  the  lungs.  The  above-mentioned  experiments  of  Welch 
and  Cohnheim,  and  later  of  V.  Basch  and  his  pupils,  have  shown  that  this  is 
due  to  pulmonary  stasis  from  acute  failure  of  the  left  ventricle.  It  is  most 
frequent  in  cases  of  mitral  stenosis  in  which  pulmonary  stasis  readily  sets  in, 
and  is  the  complication  particularly  to  be  feared  during  pregnancy  and  labor. 

Experimentally,  pulmonary  oedema  is  readily  produced  by  overstraining  the  left  ven- 
tricle through  an  overdose  of  adrenalin  (L.  Loeb1).  Besides  conditions  of  cardiac  disease 
it  is  occasionally  encountered  after  operations  in  which  adrenalin  has  been  used,  especially 
when  in  large  amounts  or  upon  surfaces  from  which  it  is  readily  absorbed.  Occasionally,  as 
in  a  case  recently  known  to  the  writer,  sudden  death  results  from  this  cause  from  an  opera- 
tion otherwise  trivial. 

J.  L.  Miller  and  S.  A.  Matthews  have  recently  investigated  the  action  of  numerous 
poisons  in  producing  pulmonary  cedema,  and  have  found  that  mechanical  factors  in  the 
circulation  (failure  of  the  left  ventricle)  are  the  immediate  cause  of  the  pulmonary  cedema 
after  adrenalin,  iodides,  and  iodine,  but  that  acetic  ether,  nitric  oxide,  and  ammonia  cause 
it  to  appear  without  any  evidence  of  disproportion  between  the  action  of  the  two  ventricles. 
These  substances  apparently  act  entirely  by  injuring  the  walls  of  the  pulmonary  vessels 
and  by  increasing  the  secretion  of  the  alveolar  walls,  cells,  and  pulmonary  lymph. 

Signs  of  Pulmonary  (Edema. — The  onset  of  pulmonary  cedema  is  marked 
by  pallor,  cyanosis,  cough,  coarse  moist  rales  throughout  the  chest,  and  often 
by  a  frothy  serous  expectoration  which  may  be  very  profuse.  Friedrich 
Muller  has  shown2  that  this  expectoration  contains  considerable  albumen,  a 
fact  of  great  diagnostic  importance  in  doubtful  cases.  These  symptoms 
constitute  a  signal  for  immediate  action. 

Treatment. — The  strain  upon  the  left  ventricle  may  be  relieved  by 
inhalations  of  amyl  nitrite,  and  its  strength  may  be  increased  within  a  few 
minutes  by  intravenous  injection  of  strophanthus.  The  most  certain  pro- 
cedure, however,  is  venesection,  since  it  diminishes  the  work  of  the 
right  heart  at  once  and  thus  enables  the  left  ventricle  to  equalize  conditions. 
Accordingly,  pulmonary  cedema  is  the  signal  for  venesection  in  any  except 
the  most  anaemic  persons. 

For  the  cedema  itself,  atropine  (0.5-1.0  mg.,  rhr  to  to-  gr.,  hypodermati- 
cally)  should  be  given,  inasmuch  as  it  diminishes  the  bronchial  secretions  and 
does  away  with  the  cedema.    In  desperate  cases  larger  doses  should  be  used. 

HEMORRHAGE  FROM  THE  LUNGS. 

As  a  result  of  engorgement  of  the  pulmonary  capillaries  or  of  permanent 
injury  to  their  walls,  hemorrhages  from  the  lungs  may  occur  in  any  acute 
cardiac  overstrain,  but  they  are  most  frequently  seen  in  cases  of  mitral  disease. 
In  itself  such  a  pulmonary  hemorrhage  is  of  no  importance,  although  by  reliev- 
ing the  congestion  it  may  bring  a  great  deal  of  subjective  relief  to  the  patient.3 

1  Haven  Emerson  has  shown  that  this  occurs  only  when  the  chest  is  closed,  not  when 
the  chest  is  opened  and  artificial  respiration  substituted,  and  that  it  can  often  be  cured  by 
artificial  respiration  with  bellows  inflation.  Barringer  reports  good  results  from  artificial 
respiration  in  one  patient. 

2  To  demonstrate  the  presence  of  albumen  add  dilute  acetic  acid  to  the  sputum  to 
precipitate  all  the  mucin,  filter,  and  then  precipitate  the  albumen  from  the  filtrate  by  the 
addition  of  potassium  ferrocyanide. 

3  Wiggers  (Arch.  Int.  Med.,  1911,  viii,  17)  has  shown  that  pituitary  extract  diminishes 
pulmonary  hemorrhage  better  than  other  drugs. 


220 


DISEASES  OF  THE  HEART  AND  AORTA. 


On  the  other  hand,  the  conditions  which  bring  them  on  acutely  are  frequently 
those  of  severe  overstrain.  They  are  particularly  common  in  mitral  disease, 
in  pulmonary  insufficiency  and  sclerosis,  and  congenital  heart  diseases. 

It  is  always  of  the  greatest  importance  to  differentiate  between  such  an  haemoptysis 
and  that  of  an  early  pulmonary  tuberculosis,  and  only  the  most  careful  repeated  examina- 
tions, coupled  with  the  presence  of  the  cardiac  lesion  and  the  absence  of  signs  of  pulmonary 
disease,  give  sufficient  grounds  to  exclude  the  latter.  It  is  particularly  important  to  examine 
for  tubercle  bacilli  in  the  blood  spit  up,  since  after  a  hemorrhage  they  may  not  be  present 
again  in  the  sputum  for  several  months. 

Rest  and  the  general  measures  which  diminish  pulmonary  engorgement 
constitute  the  treatment. 

PULMONARY   EMBOLISM   AMD    HEMORRHAGES 

Pulmonary  embolism  with  infarction  is  a  not  uncommon  complication 
when  a  clot  forming  in  the  right  auricle  or  ventricle  is  loosened  into  the  circu- 
lation and  lodges  in  some  branch  of  the  pulmonary  artery.  These  infarcts 
may  be  large  or  small,  dependent  upon  the  artery  occluded,  and  upon  their 
size  depends  the  severity  of  the  symptoms  and  the  onset  of  dyspnoea. 

In  all  these  cases  there  is  an  area  of  dulness,  tubular  breathing, 
and  increased  vocal  fremitus  over  some  parts  of  the  lung,  and  the  expectoration  of  a  slimy, 
bloody  or  prune-juice  sputum,  which  differs  from  that  occurring  in  brown 
induration  in  being  much  richer,  deeper  in  color,  and  in  containing  a  great  deal  of  more  or 
less  changed  blood  intimately  mixed  with  the  mucus  instead  of  somewhat  separate  from  it. 
Pulmonary  embolism  is  sometimes  fatal  when  a  large  vessel  is  occluded,  but  usually  not  so 
in  the  first  instance.  Exactly  when  a  single  embolus  will  be  followed  by  a  shower  of  emboli 
and  a  fatal  result  cannot  be  foretold,  and  the  patient  lives  continually  under  a  sword  of 
Damocles,  although  in  some  cases  he  may  five  for  several  years  without  further  disturbance. 

CHEYNE-STOKES   BREATHING. 

Cheyne,  of  Dublin,  described  a  peculiar  form  of  respiration  in  which  there 
are  occasional  pauses  of  variable  duration,  from  several  seconds  to  half  a 


minute,  followed  by  inspirations  at  first  slow,  then  more  rapid,  then  again 


Fig.  122. —  The  two  types  of  Cheyne-Stokes  respiration  in  their  relations  to  the  blood-pressure 
curves.  (After  Eyster.)  A.  Intracranial  pressure  type — apnoea  accompanies  slowing  of  the  pulse  and 
fall  of  blood -pressure.  B.  The  cardiac  type— apncea  associated  with  rise  of  blood-pressure  and  quick- 
ening of  the  pulse-rate. 

lapsing  into  a  pause.  It  was  again  described  by  Stokes  in  1846  and  is  very 
common  in  bad  cases.  This  phenomenon  is  particularly  frequent  in  heart 
cases,  especially  in  aortic  disease,  and  is  usually  seen  when  the  patient  is  asleep. 
It  is  also  common  in  cases  of  brain  tumor,  apoplexy,  or  any  condition  where 
there  is  an  increased  intracranial  tension.  Not  infrequently,  in  cardiac  disease, 
the  patient  is  in  a  state  of  coma  or  semicoma  during  the  periods  of  apnoea  but 
fully  conscious  during  the  periods  of  dyspnoea.  During  the  former  the  pupils 
are  contracted  and  do  not  react;  during  the  latter  they  widen  and  react  again. 


SYMPTOMS  OF  CARDIAC  DISEASE.  221 

Eyster  has  found  that  the  occurrence  of  Cheyne-Stokes  respiration  is  always  associated 
with  the  slow  periodic  changes  of  blood-pressure  known  as  Traube-Hering  waves.  He  distin- 
guishes two  types :  In  the  first,  which  is  always  associated  with  increased  intracranial  tension, 
as  in  brain  tumor,  meningitis,  uraemia,  the  period  of  respiratory  activity  is 
associated  with  a  rise  of  blood-pressure  and  quickening  of  the  pulse,  the  period  of 
a  p  n  o  e  a  with  afallofblood-pressure  and  slowing  of  the  pulse  (Fig.  122,  A) . 

In  the  second  type,  the  common  form  in  cardiac  and  arterial  disease,  the  respi- 
ratory activity  is  associated  with  a  fall  in  blood-pressure  and  slowing  of 
the  pulse,  and  the  a  p  n  o  e  a  is  associated  with  rise  in  blood-pressure  and  quick- 
ening of  pulse-rate  (Fig.  122,  B).  Eyster  was  able  to  reproduce  the  first  group  in  animals 
by  raising  the  intracranial  tension,  and  found  that  whenever  the  intracranial  pressure  was 
above  the  mean  blood-pressure  apncea  occurred.  Then  the  blood-pressure  rose  through 
asphyxial  stimulation  of  the  vasomotor  centre,  and  when  it  overtopped  the  intracranial 
pressure,  respirations  again  set  in. 

Biot  has  described  another  type  of  respiration,  in  which  a  series  of  inspirations  equal 
in  rate  and  in  size  are  punctuated  by  long  apnoeic  pauses. 

Mosso  has  also  depicted  another  group  of  periodic  respirations  occurring  at  high 
altitudes,  apparently  from  low  CO2  content  of  the  blood  reaching  the  vasomotor  centre 
(acapnia),  in  which  there  is  with  each  respiratory  group  rise  of  blood-pressure 
and  s  1  o  w  i  n  g  of  the  pulse. 

Haldane,  Douglas,  and  Beddard,  as  well  as  Yandell  Henderson,  have  produced  Cheyne- 
Stokes  breathing  from  acapnia  by  very  rapid  breathing,  and  this  seems  to  bear  a  closer 
relation  to  the  cardiac  type  than  do  the  results  of  intracranial  pressure.  The  hyperpncea 
washes  out  the  CO  2  from  the  blood,  the  apncea  sets  in  until  the  C02  reaccumulates  in  the 
blood,  during  which  period  the  irritability  of  the  respiratory  centre  is  slightly  depressed, 
so  that  the  C02  gradually  accumulates  in  slight  excess.  Dyspnoea  and  hyperpncea  then 
set  in  and  the  performance  is  repeated. 

Barbour  (Jour.  Pharmacol.  andExper.  Therap.,  1913-14,  v,  393)  has  produced  Cheyne- 
Stokes  breathing  in  morphine  poisoning  (see  page  218).  The  morphine  lowers  the  irrita- 
bility of  the  respiratory  centre.  The  depressed  centre  then  responds  to  the  stimulus  of  a 
normal  amount  of  CO2  in  exactly  the  same  way  as  a  normal  centre  responds  to  a  diminished 
amount  of  CO2 — i.e.,  by  Cheyne-Stokes  breathing. 

The  irritability  of  the  respiratory  centre  can  be  increased  by  atropine 
sulphate  (1  mg.,  ^\  gr.)  hypo  or,  as  Eyster  has  shown,  sometimes  (1)  by  injec- 
tions of  strychnine  (1.5  mg.,  -^  gr.)  and  (2)  by  inhalations  of  C02.  The 
latter  observation  has  been  confirmed  by  Pembrey  and  Beddard,  who  were 
working  from  the  standpoint  of  Haldane.  Pembrey  was  able  to  cause  the 
periodic  breathing  to  return  to  normal  by  causing  the  patient  to  breathe 
either  pure  02  or  02  containing  an  excess  of  C02,  demonstrating  that  in  this 
case  the  action  of  the  respiratory  centre  could  be  restored  by  either  improving 
its  condition  and  increasing  its  irritability  through  increased  aeration,  or  by 
increasing  the  strength  of  the  respiratory  stimulus  by  increasing  the  concen- 
tration of  C02  in  the  lung  alveoli. 

The  occurrence  of  Cheyne-Stokes  respiration  is  a  grave  symptom.  It 
is  often  a  harbinger  of  death,  as  claimed  by  some  authors,  but  the  writer 
has  seen  many  patients  recover  from  it  and  even  live  for  several  years. 

COUGH. 

Patients  with  chronic  cardiac  trouble  are  very  apt  to  suffer  from  a  mild 
cough,  even  during  their  periods  of  remission,  and  especially  every  winter. 
Sometimes  this  may  even  be  mistaken  for  a  primary  bronchitis.  Primarily 
the  condition  is  due  to  engorgement  of  the  pulmonary  vascular  system,  with 
increased  secretion  of  the  bronchial  mucous  glands  as  a  result.1  It  represents 
a  state  of  mild  loss  of  pulmonary  compensation . 

JThe  pressure  of  a  dilated  left  auricle  upon  the  recurrent  laryngeal  nerve  often  causes 
cough. 


222 


DISEASES  OF  THE  HEART  AND  AORTA. 


In  somewhat  worse  form,  and  particularly  in  bad  cases  of  chronic  mitral  disease,  the 
alveolar  capillary  walls  become  so  much  injured  that  there  is  diapedesis  of  red  blood-cells 
into  the  alveoli.  These  die  and  are  taken  up  by  phagocytes  which  find  their  way  into 
the  sputum  in  the  form  of  "  Herzfehlerzellen " — large  endothelial  cells  containing  vacuoles 
and  numerous  brown  granules  of  haemosiderin.  The  expectoration  of  "Herzfehlerzellen" 
is  usually  associated  with  a  condition  of  brown  induration  of  the  lungs,  a  chronic  interstitial 
pneumonia  with  dilatation  of  the  pulmonary  capillaries,  tortuous  .condition  of  the  vessels, 
and  deposition  of  hsemosiderin  in  the  tissues. 

ACCUMULATIONS  OF  FLUID  IN  CARDIAC  DISEASE. 
(Edema. — When  a  case  of  heart  disease  reaches  the  stage  of  broken 
(systemic)  compensation  and  the  right  heart  fails  to  perform  its  function 
properly,  oedema  of  the  feet  and  legs  sets  in.  This  occurs  at  some  stage  of 
almost  every  case  of  heart  disease,  but  not  always  at  stages  of  equal  se  v  erity, 
sometimes  setting  in  quite  early,  sometimes  only  as  a  terminal  event.  Keith, 
Rowntree  and  Geraghty  have  shown  that  the  total  volume  of  blood  plasma 
is  sometimes  but  not  always  increased  in  cedema,  so  that  a  true  plethora  may 
or  may  not  be  present  (see  page  45). 

The  distribution  of  oedema  of  cardiac  origin  differs  characteristically 
.from  the  nephritic  type.  This  is  readily  comprehensible  when  it  is  recalled 
that,  as  Cohnheim  has  shown,  oedema  occurs  only  when  there  has  been  some 
injury  to  the  walls  of  the  vessels  and  capillaries.  In  nephritis  Heinecke 
and  Meyerstein  have  proved  the  existence  of  a  substance  in  the  blood  which 
injures  the  capillaries,  and  Kast  has  demonstrated  that  the  blood  of  nephritics 
contains  a  substance  with  lymphagogue  action.  As  might  be  expected  from  a 
poison  circulating  in  the  blood,  the  injury  occurs  simultaneously  throughout  the 
body.  Hence  in  nephritis  the  cedema  begins  quite  irrespectively  of  the  action 
of  gravity  and  is  especially  marked  in  the  face  and  eyelids.  In  cardiac  cedema 
there  is  no  such  lymphagogue  poison  at  work,  and  the  injury  to  the  capillary 

walls  is  the  result  of  local  stasis,  lack 
of  oxygen  in  the  cells  of  the  capillary 
walls  under  the  influence  of  the  slowed 
circulation.  Accordingly  it  begins 
where  circulation  is  slowest,  i.e.,  in  the 
dependent  portions — the  feet  and  legs 
— and  either  remains  localized  there, 
or,  if  the  condition  becomes  worse, 
progresses  upward  to  the  genitalia,  to 
the  abdominal  cavity  (portal  stasis), 
giving  rise  to  intense  ascites,  to  the 
subcutaneous  tissue  of  the  body  wall, 
and  finally  to  the  production  of  fluid 
ip  the  chest  (hydrothorax). 

.  •  .Occasionally  when  the  cedema  has  been 
long  continued  the  limbs  reach  tremendous 
proportions.  Some  four  years  ago  the  writer 
had  under  his  care  at  the  Johns  Hopkins 
Hospital  a  patient  who  reached  the  ward  in 
a  condition  of  very  marked  dyspnoea,  with 
legs  swollen  to  a  diameter  of  lOf  inches  and 
absolutely  elephantoid  in  appearance  (Fig. 
123).  The  skin  over  the  entire  legs  was  cov- 
ered with  papillomatous  outgrowths  so  suspicious  that  the  diagnosis  of  elephantiasis  vera 
was  seriously  entertained  by  some  members  of  the  hospital  staff.    The  patient  had  been  suf- 


Fig.  123. — Legs  of  a  patient  with  extreme 
cedema  (simulating  elephantiasis)  and  tremen- 
dous ulcers.  Diameter  of  the  left  leg  1(H  inches 
(25.5  cm.).  (Drawn  from  photographs  lent  by 
Dr.  W.  Preston  Miller,  of  Hagerstown,  Md.) 


SYMPTOMS  OF  CARDIAC  DISEASE. 


223 


fering  from  a  severe  aortic  insufficiency  for  about  a  year,  and  for  six  months  had  been  so 
orthopnceic  that  he  had  not  been  able  to  go  to  bed,  but  had  rested  sitting  bolt  upright  in  a 
chair  and  usually  with  feet  down.  There  were  tremendous  crypt-like  ulcers  about  10  cm. 
(4  inches)  in  diameter  on  both  legs,  each  covered  with  a  deep  layer  of  necrotic  tissue.  The 
patient  was  placed  in  bed  with  feet  raised  to  the  horizontal,  and  the  wound  dressed  with 
a  1-10000  potassium  permanganate  solution  and  tr.  digitalis  m.  xv  administered  every 
four  hours.  He  was  purged  freely  with  Epsom  salts.  He  improved  so  rapidly  that  within 
twelve  hours  the  circumference  of  the  legs  had  appreciably  diminished  and  within  a  few 
weeks  they  were  almost  normal.  The  patient  has  remained  quite  well  ever  since  and  is 
at  present  managing  a  farm  in  western  Maryland. 

Unfortunately,  oedema  does  not  always  disappear  so  satisfactorily.  It 
has  been  shown  that  the  oedema  fluid  is  richer  in  salts  than  is  the  blood,  and 
that  resorption  of  the  oedema  is  somewhat  favored  by  a  practically  salt-free 
diet,  such  as  one  consisting  of  milk,  sugar,  eggs,  meats,  bread,  sweet  butter, 
and  cereals  prepared  without  the  addition  of  salt.  The  diuretics,  especially 
those  of  the  caffein  group,  also  favor  resorption1;  free  purgation  aids  in  remov- 
ing fluid  from  the  body,  sometimes  as  much  as  3000  c.c.  per  day,  and  digitalis 
does  the  same  by  increasing  heart  action.  Besides  this,  the  oedema  can  be 
combated  by  raising  the  legs  to  the  horizontal,  by  massage,  by  passive  motion, 
or  even  by  occasional  active  motions  of  the  legs  made  in  the  horizontal  position. 

Drainage  of  Legs. — Sometimes  also  a  light  spiral  elastic  bandage  of  rubber  dam  may 
be  applied  to  the  legs,  beginning  at  the  feet  and  ascending  to  the  groin,  thereby  assisting 
the  drainage  and  replacing  the  lost  elasticity  of  the  skin.  When  these  means  are  insufficient, 
several  incisions  may  be  made  aseptically  in  the  skin  of  the  legs  and  drainage  aided  by 
applying  Bier's  suction  cups,  or  a  large  trocar  with  sides  perforated  (Curschmann's  modi- 
fication of  Southey's  tubes)  may  be  inserted  to  bring  about  free  mechanical  drainage. 

The  best  results  are  obtained  by  the  following  method,  described  by  Romberg:  Boil 
a  long  rubber  tube  fitted  with  a  pinch-cock  in  physiological  salt  solution.  After  removing 
the  point  from  the  trocar,  attach  the  rubber  tube  to  the  metal  tube  of  the  latter  and  place 
the  lower  end  of  the  rubber  tube  in  a  basin  of  boiled 
water  upon  the  floor  next  to  the  bed.  In  this  way  a 
siphon  is  established,  helping  the  drainage  of  the  fluid. 
The  tube  of  the  trocar  should  be  kept  in  place  in  the 
leg  by  tying  with  a  silk  ligature,  the  ends  of  which  are 
then  inserted  in  a  strip  of  adhesive  placed  loosely 
about  the  leg  above  the  trocar..  Romberg  states  that 
from  2  to  15  litres  of  fluid  may  be  removed  in  24  hours! 

The  oedema  often  involves  the  scrotum 
and  penis  until  they  are  enlarged  to  two  or 
three  times  the  ordinary  size,  and  phimosis 
or  paraphimosis  may  cause  considerable 
difficulty  in  micturition. 

Ascites. — Ascites  is  common  and  may 
cause  distress  by  pushing  up  the  diaphragm 
as  well  as  by  impeding  the  abdominal  circu- 
lation. It  is  often  advisable  to  remove  it 
mechanically  by  introducing  a  trocar  in  the   ..    Flh£24a^rsch+rTm?5  ™odifica" 

J        J  °  tion  of  the  bouthey  tubes  for  draining 

midline  midway  between  the  umbilicus  and  oedema  of  the  legs.   (After  Romberg.) 
the  symphysis,  under  aseptic  precautions  (after  first  emptying  the  patient's 
bladder),  and  allowing  the  fluid  to  drain  out.     In  so  doing  care  must  be 

1  Fleisher,  Hoyt,  and  Loeb  have  shown  that  the  presence  of  calcium  salts  in  infusion 
fluid  diminishes  the  formation  of  cedema,  but  this  observation  had  not  yet  received  an 
application  in  therapeutics  and  these  observers  have  found  that  this  does  not  apply  to 
cardiac  cedema. 


224  DISEASES  OF  THE  HEART  AND  AORTA. 

taken  to  keep  a  many-tailed  (Scultetus)  bandage  tight  across  the  abdomen, 
readjusting  it  several  times  during  the  tapping  for  fear  too  much  blood 
may  enter  the  relaxed  abdominal  vessels  when  the  pressure  about  them  is 
diminished  and  shock  result  therefrom  (see  page  48). 

Hydrothorax. — In  cases  with  severely  impaired  compensation  hydrothorax 
(usually  right-sided)  is  common.  Starling  and  Leathes,  Stengel,  and  Dutton 
Steele  have  demonstrated  that  its  frequency  upon  the  right  side  is  due  to 
the  position  of  the  great  azygos  vein,  which  drains  the  intercostal  spaces  and 
the  pleurse.  One  of  the  factors  producing  stasis  in  this  vein  is  the  fact  that 
the  latter  enters  obliquely  into  the  superior  vena  cava  (Fig.  4)  and  thus  its 
mouth  is  readily  closed  off.  Another  is  probably  the  fact,  which  the  writer 
has  noted,  that  the  mouth  of  the  vein  is  not  as  distensible  as  the  walls  of  the 
vein  above  it,  and  hence  imposes  some  obstruction  to  the  blood  flow.  In  all 
cases  of  heart  failure  in  animals  the  azygos  vein  may  be  seen  to  be  dilated 
above  its  entrance  into  the  vena  cava.  The  heart  in  hydrothorax  is  usually 
displaced  to  the  left.  The  respiration  shows  much  embarrassment:  (1)  from 
removal  of  a  considerable  part  of  the  right  lung,  (2)  from  compression  of  the 
left  lung  by  the  displacement  of  the  heart,  (3)  from  embarrassment  of  the 
heart  itself  from  the  displacement,  (4)  from  compression  of  the  venae  cavae, 
especially  during  defecation  and  exertion.  This  may  prevent  inflow  into  the 
heart  and  cause  sudden  death  (Calvert). 

The  fluid  should  always  be  removed  promptly  by  paracentesis  thoracis. 
This  process  is  unfortunately  not  without  danger,  sudden  death  occasionally 
resulting  in  spite  of  the  greatest  care. 

The  writer  has  seen  two  deaths  of  this  kind,  and  they  occur  with  about  the  same 
frequency  in  the  experience  of  most  clinicians.  A  very  valuable  contribution  to  this  field 
has  been  made  by  the  studies  of  Capps  and  Lewis,  showing  that  the  visceral  layer  of  the 
inflamed  pleura  is  especially  sensitive,  and  upon  handling  or  touching  it  two  reflex 
phenomena  result,  a  vagal  inhibition,  sometimes  so  intense  as  to  stop  the 
heart,  and  a  paralysis  of  the  vasomotor  centre  which  gives  rise  to  a  marked  fall  of  blood- 
pressure.  According  to  these  observations  it  is  advisable  to  diminish  vagal  tone  with  a  pre- 
liminary hypodermic  injection  of  0.5  to  1  mg.  atropine  (gr.  ^o  to  gV)  about  15  minutes 
before  beginning  the  tapping,  and  to  have  at  hand  a  hypodermic  syringe  loaded  with  1-1000 
adrenalin  chloride  solution  to  restore  promptly  the  vasomotor  tone  in  case  of  collapse. 

RENAL  COMPLICATIONS  OF  CARDIAC  DISEASES. 
RENAL    CHANGES. 

Albuminuria  and  diminished  secretion  of  urine  are  invariable  results 
of  broken  compensation.  They  may  also  occur  after  severe  exertion,  prob- 
ably as  the  result  of  excessive  pressure  in  the  veins.  The  stasis  in  the  vena 
cava  and  renal  vein  has  been  shown  to  give  rise  to  albuminuria,  and  the  slow- 
ing of  the  circulation  through  the  kidney  is  sufficient  to  account  for  the  dim- 
inution of  the  urine  secreted. 

The  kidneys  of  such  cases  (Osier's  arteriosclerotic  kidneys)  are  usually  of  the  large 
red  or  "beefy"  type,  with  both  cortex  and  medulla  increased  in  size,  the  capsule  adherent, 
and  diffuse  interstitial  changes  as  well  as  some  parenchymatous  degeneration.  The  red 
color  is  probably  due  to  the  venous  congestion. 

It  is  of  great  importance  to  differentiate  between  a  primary  cardiac 
disease  with  secondary  renal  involvement  and  primary  chronic  nephritis 
with  secondary  arteriosclerosis,  cardiac  hypertrophy,  and  cardiac  insuffi- 
ciency. At  an  early  stage  of  the  disease  a  careful  study  of  the  chloride  metabo- 
lism and  its  relation  to  urine  concentration  may  be  of  great  help. 


SYMPTOMS  OF  CARDIAC  DISEASE. 


225 


Urine  in  Chronic  Heart  Failure. — I  n  cardiac  cases  the  power  of  ex- 
creting NaCl  is,  as  a  rule,  not  as  much  impaired  as  in  renal 
cases.  If  5  Gm.  NaCl  be  added  to  the  diet  on  one  occasion  there  should  be  an  abrupt 
rise  in  the  NaCl  content  of  the  urine.  If  the  kidney  cells  are  damaged  it  will  be  gradually 
excreted  during  2-4  days.  The  phenolsulphonphthalein  excretion  is  undiminished  unless 
compensation  is  badly  broken,  is  never  much  below  fifteen  per  cent.,  and  rises  to  nearly 
normalsoon  after  improvement  begins  (Rowntree  and  Geraghty,  J.  Am.  M.  Assoc,  1911,  lvii, 
811).  At  certain  stages  renal  function  may  be  impaired  to  an  equal  degree  by  venous 
engorgement  and  by  primary  renal  disease,  but  in  cardiac  cases  renal  function  returns 
as  stasis  passes  off. 

These  renal  changes  are  in  severe  cases  associated  with  local  acid  intoxication  of  the 
kidneys  (M.  H.  Fischer,  Nephritis  and  (Edema). 

Newburgh,  Henderson  and  Palmer  (Arch.  Int.  Med.,  1913,  xii,  146),  who  have 
investigated  the  hydrogen  ions  of  the  kidneys,  state  that  they  have  never  encountered  recov- 
ery in  a  patient  whose  urine  was  acid  to  methyl  red  (or  paranitrophenol;  concentration  of 
hydrogen  ions  1 :  100,000  normal  or  H+log-5) .  This  simple  test  seems  to  be  an  important  factor 
in  prognosis. 

SENSORY  SYMPTOMS  ABOUT  THE  HEART. 

Palpitation. — Under  normal  conditions  one  is  not  conscious  of  sensory 
impressions  from  the  region  of  the  heart.  Einthoven,  Flohil,  and  Battaerd 
have  shown,  however,  that  an  afferent  impulse  is  transmitted  up  the  vagi 
by  each  heart-beat,  and  there  are  probably  similar  impulses  transmitted 
through  the  intercostal  nerves  from  the  parietal  pleura,  mediastinum,  and 
chest  wall,  against  which  the  heart  is  beating.  Under  normal  conditions 
these  sensations  do  not  reach  consciousness,  but  they  occasionally  do  so 
when  the  general  nervous  sensibility  is  increased,  as  by  coffee,  tobacco,  or 
hyperthyroidism,  in  neurasthenic  and  hysterical  states,  or  when  the  beat  of 
the  heart  is  more  forcible  than  usual.  The  distinct  sensation  caused  by  each 
beat  of  the  heart  is  known  as  palpitation.  It  is  frequently  associated  with 
cardiac  weakness  and  irregularities,  and  has  been  thought  by  some  writers 
to  be  clearly  associated  with  extrasystoles.  b 

But  while  it  is  true  that  extrasystoles 


VAG. 


RESP. 


CAROT. 


-H--i    1    i    MR    k \\m \\n    ;-- 

f^I-M]|PMmUj;: 

Fig.  125. — Electrical  record  of  afferent  impulses  travelling  up  the  vagi.  (After  Einthoven,  Flohil, 
and  Battaerd.)  VAG.,  record  of  centripetal  electrical  wave  in  the  vagus  ;  RESP.,  respiration;  CAROT., 
carotid  tracing.  A.  In  quiet  breathing.  B.  In  apncea.  The  large  electrical  waves  are  due  to  respiration  ; 
the  small  ones  to  the  cardiac  contraction. 

frequently  give  rise  to  palpitation  and  also  that  the  patient  can  often  dis- 
tinguish between  strong  beats  and  weak  beats,  nevertheless  there  are  many 
cases  of  extrasystoles  without  palpitation  and  of  palpitation  without  extra- 
systoles. Hirschf elder  has  shown  that  palpitation  may  occur  without  any 
motor  disturbance  in  the  heart's  action  and  without  any  change  in  the  reflex 
response  of  the  heart  to  various  stimuli.  Hewlett  has  found  the  c  wave 
unusually  large  and  sudden  in  a  case  of  palpitation,  and  believes  that  the 
"earlier  movements  of  the  ventricle  were  exerted  with  unusual  speed." 
15 


226  DISEASES  OF  THE  HEART  AND  AORTA. 

However,  this  finding  is  not  uniform  in  cases  of  palpitation,  and,  moreover, 
would  not  explain  the  occurrence  of  palpitation  from  weak  extrasystoles  in 
which  these  movements  are  executed  slowly.  Such  changes  in  the  venous 
pulse  are  often  found  in  vigorously  beating  hearts  without  any  palpitation 
whatever.  Palpitation  is  therefore  to  be  regarded  as  a  purely  sensory  phe- 
nomenon, which,  though  it  is  frequently  associated  with  cardiac  disturbances, 
may  occur  quite  independently. 

The  category  of  sensations  in  which  palpitation  should  be  placed  and  the  path  which 
the  sensation  traverses  are  not  perfectly  clear.  It  is  evidently  a  pressure  or  touch  sensation, 
perfectly  distinct  and  limited  to  the  period  of  systole.1  It  is  always  sharply  localized, 
usually  referred  to  either  the  apex  or  the  bifurcation  of  the  trachea — the  two  sites  at  which 
the  heart  exerts  direct  pressure  or  traction  upon  the  surrounding  structures.  In  this  dis- 
tinctness it  differs  entirely  from  other  visceral  sensations,  which  are  less  definite  in  time 
and  in  site,  and  also,  as  a  rule,  more  nearly  allied  to  pain  sensation.  It  thus  differs  greatly 
from  the  pain  sensations  arising  in  and  about  the  heart,  and  hence  suggests  that  it  should 
be  placed  in  a  different  category.  Whether  the  path  of  the  sensation  is  up  the  vagi  or 
through  the  thoracic  nerves  cannot  at  present  be  stated.2 

Another  point  in  favor  of  the  view  that  palpitation  is  an  extracardiac  sensation  is  the 
fact  that  quite  similar  sensations  may  be  felt  in  the  abdominal  aorta  and  radial  arteries 
when  there  is  visible  pulsation  (to-and-fro  motion)  of  the  latter  with  pressure  and  traction 
upon  the  skin  and  surrounding  structures. 

The  continuance  of  the  sensation  is  very  wearing  upon  the  patient, 
especially  when  the  heart  is  irregular.  Often  he  is  able  to  distinguish  be- 
tween large  and  small  beats,  and  is  constantly  reminded  of  the  pathological 
condition  and  usually  much  worried  about  it.  The  sensation  is  not  entirely 
dependent  upon  psychic  phenomena;  for  in  one  case  under  the  writer's  obser- 
vation (I.e.)  it  disappeared  for  five  minutes,  while  the  blood-pressure  and  pulse- 
rate  rose  after  exercise  when  the  patient  was  under  examination,  although 
he  had  his  mind  fixed  upon  the  disturbance  throughout  the  entire  procedure. 

Palpitation  is  frequently  the  result  of  tea  or  coffee  drinking,  smoking, 
digestive  disturbances;  it  often  occurs  with  various  forms  of  cardiac  diseases, 
but  seems  to  have  no  relation  to  the  latter.  Relief  is  very  difficult  to  obtain. 
Except  for  removing  the  causal  factor,  application  of  an  ice-bag  or  a  cold- 
water  coil  over  the  heart  is  about  the  best  remedy.  The  bromides  of  potas- 
sium, ammonium,  and  strontium  are  of  some  value,  as  are  also  vibratory 
massage  and  the  application  of  sinusoidal  currents. 

Precordial  Pain. — Precordial  pain  is  a  less  definite  sensation  than  palpi- 
tation. It  is  continuous  throughout  the  cardiac  cycle,  is  less  definitely  local- 
ized, and  more  commonly  associated  with  referred  sensory  disturbances 
resembling  other  types  of  visceral  sensation.  It  seems  to  bear  a  somewhat 
closer  relation  to  dilatation  of  the  heart,  and,  as  a  rule,  accompanies  more 
severe  organic  diseases,  being  especially  common  in  aortic  and  mitral  lesions. 
There  is  sometimes  precordial  tenderness  (see  page  385). 

Sir  William  Ewart  (Brit.  M.  J.,  1899,  ii,  1178;  1911,  ii,  805)  claims  that 
precordial  pain  may  be  relieved  by  inhalations  of  carbonic  acid  gas  well  diluted 
with  air  (see  page  241).  The  writer's  experience  with  this  mode  of  treatment 
is  limited,  but  he  has  seen  some  unexpected  benefit  from  its  use.  Except 
for  causing  increased  depth  of  respiration,  its  mode  of  action  is  unexplained. 

1  Sir  Lauder  Brunton  has  independently  advocated  the  same  view. 

2  Sir  Lauder  Brunton  (On  Digitalis,  Collected  Papers  on  Circulation  and  Respiration, 
Lond.  and  N.  Y.,  1907,  p.  52,  and  Therapeutics  of  the  Circulation,  Lond.,  1908,  p.  110) 
has  given  the  same  explanation,  ascribing  it  to  the  beating  of  the  apex  against  the  chest  wall. 


SYMPTOMS  OF  CARDIAC  DISEASE.  227 

Frequently  in  heart  diseases,  and  especially  in  cases  of  aneurism  and  angina,  there  is 
marked  pain  radiating  down  either  or  both  arms.  In  fact  these  may  be  the  first  symp- 
toms given  by  an  aneurism.  It  is  easily  seen  from  the  distribution  of  the  cardiac  nerves 
(page  18,  Fig.  18)  that  a  lesion  in  the  vicinity  of  the  sympathetic  fibres  might  give  sensations 
which,  reaching  one  of  the  cervical  spinal  ganglia,  would  be  referred  to  its  peripheral  dis- 
tribution in  the  cutaneous  region  innervated  by  that  segment,  usually  down  the  arm.  Hence 
the  frequency  of  these  pains.  Not  only  cardiac  condition,  but  high  blood- pressure  in  the 
aorta  may  cause  this  distress.  It  is  difficult  to  relieve  this  symptom.  If  lowering  of  the 
blood-pressure  with  nitroglycerin  fails  to  bring  it  about,  codeine,  15  to  20  mg.  (|-  to  §  gr.) 
should  be  tried,  and,  if  that  does  not  suffice,  morphine  may  have  to  be  resorted  to,  but 
should  always  be  avoided  as  long  as  possible. 

DIGESTIVE  DISTURBANCES. 

One  of  the  first  effects  of  weakening  of  the  heart  is  engorgement  of  the 
■veins  of  the  portal  system,  and  this  in  turn  brings  about  a  catarrhal  condi- 
tion in  the  mucosa,  and  especially  the  gastric  mucosa,  with  consequent 
symptoms  of  indigestion.1  Fermentation  frequently  takes  place,  and  the 
inflation  of  the  stomach  with  gas,  displacing  the  diaphragm  upwards  and 
shifting  the  heart  more  towards  the  horizontal,  tends  to  increase  its  embar- 
rassment. Overloading  the  stomach,  the  transdiaphragmatic  neighbor  of  the 
heart,  should  therefore  always  be  avoided;  and  the  patient  will  be  saved  much 
suffering  if  he  is  kept  on  a  light,  easily  digestible  diet,  consisting  largely  of 
eggs,  milk,  and  carbohydrates,  just  enough  in  quantity  to  keep  him  from 
losing  weight.  Friedrich  Muller  has  shown  a  diminished  power  of  absorption 
of  fats  in  heart  disease.  Perhaps  this  may  be  due  to  the  fact  that  the  high 
venous  pressure  prevents  the  thoracic  duct  from  emptying  itself  properly, 
or  perhaps  because,  as  H.  M.  Evans  has  shown,  a  high  portal  pressure  causes 
the  lymphatics  of  the  intestines  to  collapse. 

On  the  other  hand,  meats  and  other  foods  containing  purin  bodies  in 
large  quantities  (sweetbreads,  lungs,  liver,  etc.,  also  coffee  and  tea,  and  alcohol 
in  all  forms)  do  distinct  harm  by  raising  the  blood-pressure  and  by  increasing 
the  viscosity  of  the  blood  (page  60). 

The  engorgement  of  the  gastric  and  oesophageal  veins  sometimes  leads 
to  exudation  of  blood  into  the  stomach  and  to  vomiting  of  blood. 

Abdominal  Pain  from  Distended  Liver. — One  of  the  commonest  symp- 
toms of  failing  compensation  is  very  intense  abdominal  pain  felt  over  the 
region  of  the  liver.  This  organ  may  become  much  distended,  and,  as  shown 
by  Salaman,  may  be  expanded  until  its  blood  content  is  several  degrees  above 
the  normal.  Under  this  expansion  there  is  marked  tension  upon  the  capsule 
of  the  liver  (Glisson's  capsule)  which,  in  turn,  gives  rise  to  pain.  This  symp- 
tom is  really  so  clearly  bound  up  with  the  failure  of  compensation  itself  that  it 
subsides  with  resumption  of  the  latter,  or  after  some  time  the  capsule  of  the 
liver  will  have  become  sufficiently  stretched  and  it  will  then  cease  to  be  painful. 

Abdominal  pain  also  results  from  arteriosclerosis  of  the  gastric  and 
mesenteric  arteries,  from  vascular  crises  as  well  as  from  abnormally  great 
pulsation  of  the  abdominal  aorta. 

Catarrhal  Jaundice. — Like  the  gastric  mucosa,  the  bile  passages  undergo 
catarrhal  inflammation  from  the  venous  engorgement,  and  a  definite  catarrhal 
jaundice  may  accompany  the  failure  of  compensation.    Usually,  the  jaundice 

1  Einhorn  (Berl.  klin.  Wchnschr.,  1889,  xxvi,  1042)  has  found  that  absence  of  HC1  is 
common  in  these  cases,  and  Hoffmann  obtains  considerable  benefit  by  administering  HC1 
to  them. 


228  DISEASES  OF  THE  HEART  AND  AORTA. 

is  mild  and  barely  perceptible,  the  color  being  sallow  and  icteroid  rather  than 
icteric.  The  presence  of  this  slight  icteric  hue  in  a  patient  with  heart  disease 
should  always  lead  to  the  suspicion  of  broken  compensation  or  tricuspid 
insufficiency,  and  is  always  a  sign  of  danger. 

PSYCHIC  DISTURBANCES. 
An  anxious  expression  is  so  commonly  manifested  by  patients  suffering 
from  heart  disease  that  a  certain  type  is  spoken  of  as  "the  cardiac  fades." 
This  facies  is  difficult  to  describe,  but  may  be  said  to  be  characterized  by 
bright,  watery,  somewhat  staring  eyes,  wide  palpebral  slits  (without  definite 
exophthalmus  or  other  signs  of  Basedow's  disease),  rather  tensely  held  mouth, 
and  the  rest  of  the  face  a  little  sunken,  though  not  to  the  degree  present  in 
the  "abdominal  facies."  Many  cardiac  cases,  perhaps  from  the  difficulty 
which  they  are  constantly  experiencing  in  getting  their  breath,  feel  irritable 
and  peevish  to  a  considerable  degree,  and  not  infrequently  the  onset  or  increase 
of  peevishness  is  an  early  sign  that  the  cardiac  condition  has  become  worse. 

DELUSIONS. 

Occasionally,  especially  in  patients  with  irregular  heart  action,  definite 
psychoses  set  in.  These  are  especially  common  during  the  night  and  early 
morning,  disappearing  again  during  the  waking  hours. 

The  patient  usually  awakens  from  his  sleep  unable  to  recognize  the  place  where  he  is, 
which  he  usually  locates  somewhere  else,  and  then  regards  the  doctors,  nurses,  and  attend- 
ants as  inhabitants  of  the  more  familiar  scenes,  often  mistakenly  recognizing  them  as  people 
of  his  acquaintance  in  those  places.  He  usually  regards  his  confinement  in  bed  as  a  sign 
of  some  attempt  upon  his  life,  and  the  administration  of  medicine  as  a  certain  attempt  to 
poison  him.  Of  this  fact  he  is  always  certain,  although  he  may  admit  that  there  is  some 
doubt  in  his  own  mind  as  to  the  correctness  of  some  of  his  other  ideas.  For  example,  one 
delirious  patient  under  the  writer's  care  as  house  physician  mistook  him  for  an  old  friend 

from  home,  and  said  that  he  liked ,  and  had  great  confidence  in  him,  but  he  could  not  see 

why did  want  to  poison  him.    But  he  would  recognize  no  other  possible  motive. 

Occasionally,  when  daylight  comes  or  some  one  familiar  object  appears,  the  patient 
suddenly  recognizes  his  surroundings,  wakes  up  as  from  a  dream,  and  may  even  explain 
exactly  the  nature  of  and  reasons  for  his  delusions.  Under  the  influences  of  these  delusions, 
patients  are  often  very  hard  to  manage,  but  their  attitude  is  more  commonly  a  defensive 
than  an  offensive  one,  resisting  confinement  and  treatment,  and  attempting  to  leave  the 
ward  or  room  peaceably,  rather  than  showing  maniacal  pugnaciousness  primarily.  They 
can  usually  be  persuaded  by  gentle  means  to  remain  where  they  are  for  a  time,  especially 
as  their  minds  are  almost  always  confused;  they  realize  that  they  are  not  perfectly  well, 
and  the  nurse  or  physician  can  lead  the  argument  along  its  logical  conclusions  to  a  reason 
why  they  should  return  to  bed  and  to  rest  for  the  time  being.  After  some  minutes'  argu- 
ment of  this  kind  the  patient  can  usually  be  given  a  hypodermic  of  morphine  and  gotten 
back  to  bed  with  much  less  injury  to  himself  than  if  forcible  means  were  attempted.  He 
can  then  usually  be  kept  in  bed  by  an  attendant  constantly  present. 

The  reason  for  these  delusions  is  not  very  certain,  but  in  some  cases 
they  may  be  regarded  as  "waking  dreams"  not  very  different  from  those 
of  somnambulists,  and  perhaps  like  the  night  terrors  of  children  with  adenoids. 
They  may  be  asphyxial  in  origin,  associated  more  or  less  with  cerebral  arterio- 
sclerosis and  cerebral  anaemia,  of  which  perhaps  the  frequent  high  blood- 
pressure  may  be  another  expression.  This  delusional  insanity  is  a  bad  omen, 
and  its  onset  often  precedes  the  fatal  outcome  by  only  a  few  days  or  weeks. 
Duroziez  and  H.O.Hall  have  called  attention  to  the 


SYMPTOMS  OF  CARDIAC  DISEASE.  229 

fact  that  in  some  cases  these  delusions  may  be  due 
solely  to  the  digitalis  and  may  disappear  entirely  when  the  drug 
is  discontinued. 

Eisner  has  encountered  a  case  of  temporary  insanity  due  to  digitalis  in  which  the  pa- 
tient committed  murder  while  insane  from  the  use  of  the  drug.  When  the  cause  became 
known  he  was  acquitted  by  the  jury.1 

HALLUCINATIONS. 

Definite  hallucinations  of  sight  and  hearing  are  also  not  uncommon. 

Henry  Head  has  observed  that  these  are  especially  common  in  aortic  disease  about 
the  time  of  twilight,  and  are  usually  quite  simple  in  character,  the  auditory  hallucinations 
consisting  in  simple  rhythmic  sounds  (associated  with  the  heart-beats?),  such  as  of  knocking 
or  of  bells  tolling,  the  visual  hallucinations  usually  taking  the  form  of  the  faceofaman 
or  woman  seen  stationary  at  the  foot  of  the  bed  or  slowly  stalking  across  the  room. 
The  face  is  ashy  white,  the  eyes  black  and  staring,  and  the  contour  invariably  indefinite 
and  surrounded  by  a  mass  of  wavy  black  hair.  If  the  body  is  seen  at  all,  it  is  poorly  outlined 
as  though  draped  in  a  black  gown.  Head  found  this  hallucination  quite  constant  and  seen 
by  many  patients,  though  they,  as  a  rule,  recognized  the  hallucinatory  character  and  spoke 
of  it  only  after  the  physician  had  gained  their  confidence.  The  writer  has  also  elicited  the 
same  answers  from  a  number  of  patients,  after  prefacing  the  question  by  a  statement  that 
visual  hallucinations  were  not  uncommon  in  their  disease  and  were  to  be  regarded  merely 
as  troublesome  but  not  significant  features  of  the  disease  itself.  All  who  gave  positive 
answers  accurately  described  the  hallucinatory  vision  as  above. 

Head  states  that  highly  colored  and  rapidly  moving  visions  do  not 
occur  frequently  in  heart  cases,  but  the  writer  has  seen  one  very  marked 
exception  to  this  rule. 

This  was  in  the  case  quoted  on  page  618 — a  young  railroad  engineer,  23  years  old, 
of  temperate  habits  and  excellent  family  history,  who  had  a  very  adherent  pericardium. 
For  several  years,  especially  when  his  cardiac  condition  became  worse,  he  suffered  from 
seeing  a  few  feet  before  him  swarms  of  large  animals,  lions,  tigers,  etc.,  all  highly  colored, 
leaping  rapidly  about.  He  recognized  these  as  hallucinations  at  the  time,  but  stated  that 
the  sight  irritated  him  so  that  he  lost  his  self-control,  and  he  begged  to  be  placed  in  solitary 
confinement  for  a  few  days  until  the  hallucinations  passed  off.  He  was  then  once  more  a 
perfectly  rational  being. 

Like  the  delusions,  these  cardiac  hallucinations  are  probably  due  either 
to  anaemia  or  venous  stasis  in  brain,  but  especially  in  the  special  centres,  or 
in  the  retina,  middle  ear,  visual  or  auditory  centres,  giving  rise  to  rudimentary 
sensations  which  the  mind  translates  or  distorts  into  the  above-mentioned 
pictures. 

Syncopal  attacks  also  occur  in  some  forms  of  heart  disease  as  a  result 
of  cerebral  anaemia  and  will  be  discussed  in  detail  in  Part  III,  Chapter  XI, 
under  the  head  of  Adams-Stokes  disease.  The  feeling  of  faintness  and  weari- 
ness unaccompanied  by  syncope  will  be  discussed  under  "cardiac  neuroses," 
etc.  (Part  IV,  Chapter  II). 

BIBLIOGRAPHY. 
Symptoms  of  Cardiac  Disease. 

Grossmann,  Bettelheim   and  Kauders.     Quoted  on  page  214. 

Eyster,  J.  A.  E. :  Clinical  and  Experimental  Observations  upon  Cheyne-Stokes  Respiration, 
J.  Exper.  Med.,  N.  York  and  Lancaster,  1906,  viii,  265. 

Welch,  1.  c,  page  213. 

Emerson,  H. :  Artificial  Respiration  in  the  Treatment  of  (Edema  of  the  Lungs.  A  Sugges- 
tion based  on  Animal  Experimentation,  Arch.  Inter.  Med.,  Chicago,  1909,  hi,  368. 

1  H.  O.  Hall,  personal  communication. 


230  DISEASES  OF  THE  HEART  AND  AORTA. 

Barringer,  T.  B.:  Pulmonary  (Edema  Treated  by  Artificial  Respiration,  Report  of  a  Case, 

ibid.,  1909,  in,  372. 
Miller,  J.  L.:  Trans.  Assoc.  Am.  Phys.,  Phila.,  1909.    Also,  Miller,  J.  L.,  and  Matthews 

S.  A. :  A  Study  of  the  Mechanical  Factors  in  Experimental  Acute  Pulmonary  (Edema, 

Arch.  Int.  Med.,  Chicago,  1909,  iv,  356. 
Miiller,  Fr. :  Die  Erkrankungen  der  Bronchien,  Die  deutsche  Klinik.,  Berl.  and  Vienna, 

iv,  279;  quoted  from  Romberg. 
Mosso,  A.:  Fisiologia  dell  uomo  sulla  Alpi,  Arch.  Ital.  de  Biol.,  1905,  xliii;  and  other  articles 

quoted  on  page  35. 
Pembrey,  M.  S.,  Beddard,  A.  P.,  and  French,  H.:  Observations  on  Two  Cases  of  Cheyne- 

Stokes  Respiration,  Proc.  Physiol.  Soc,  Lond.,  1906,  p.  vi. 
Kast,  A.:  Ueber  lymphagoge  Stoffe  im  Blutserum  Nierenkranker,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1902,  lxxiii,  562. 
Heineke  and  Myerstein:  Experimentelle  Untersuchungen  ueber  den  Hydrops  bei  Nieren- 

krankheiten,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1908,  xcii,  101. 
Francois-Franck,    Ch.    A.:  Contribution    a    l'etude    experimentale    des.  nevroses    reflexes 

d'origine  nasale,  Arch,  de  physiol.  des  hommes  et  des  anim.,  Par.,  1889,  5e  ser.,  i,  538. 
Starling,  E.  H.:  Physiologic  Factors  Involved  in  the  Causation  of  Dropsy,  Lancet,  Lond., 

1896,  cl,  1407. 
Meltzer,  S.  J.:  (Edema,  Am.  Med.,  Phila.,  1904,  hi,  19,  59,  151,  161. 
Pearce,  R.  M.:  The  Production  of  (Edema.  Arch.  Int.  Med.,  Chicago,  1909,  hi,  423. 
Pearce,  R.  M.:  An  Experimental  Study  of  the  Influence  of  Kidney  Extracts  and  of  the 

Serum  of  Animals  with  Renal  Lesions  upon  Blood-pressure,  J.  Exper.  M.,  1909,  xi,  430. 
Fleisher,  M.  S.,  Hoyt,  D.  M.,  and  Loeb,  L.:  Studies  in  (Edema.    I.  Comparative  Investi- 
gation into  the  Action  of  Calcium  Chloride  and  Sodium  Chloride  on  the  Production 

of  Urine,  Intestinal  Fluid,  and  Ascites,  J.  Exper.  Med.,  N.  York  and  Lancaster,  1909, 

xi,  291. 
Fleisher,  M.  S.,  and  Loeb,  L.:  The  Influence  of  Myocarditic  Lesions  on  the  Production  of 

Ascites,  Intestinal  Fluid,  and  Urine  in  Animals  Infused  with  Solutions  of  Sodium 

Chloride  and  of  Sodium  Chloride  and  Calcium  Chloride,  J.  Exper.  Med.,  N.  York  and 

Lancaster,  1909,  xi,  480. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart,  1906. 
Capps,  J.  A.:  Some  Observations  on  the  Effect  on  the  Blood-pressure  of  Withdrawal  of 

Fluid  from  the  Thorax  and  Abdomen,  J.  Am.  M.  Assoc,  Chicago,  1907,  xlviii,  22. 
Starling,  E.  H.,  and  Leathes,  J.  B.:  The  Arris  and  Gale  Lectures  on  Some  Points  in  the 

Pathology  of  Heart  Disease,   Lancet,  Lond.,  1897,  i,  569. 
Stengel,  A.:  Right-sided  Cardiac  Hydrothorax,  Univ.  Penn.  M.  Bull.,  Phila.,  1901,  xiv,  103. 
Steele,  J.D.:  Pleural  Effusion  in  Heart  Disease,  J.  Am.  M.  Assoc,  Chicago,  1904,  xliii,  927. 
Calvert,  W.  J.:  Sudden  Death  in  Pleurisy  with  Effusion  due  to  Change  of  Position,  Johns 

Hopkins  Hosp.  Bull.,  Bait.,  1908,  xix,  44. 
Capps,  J.  A.,  and  Lewis,  D.  D.:  Observations  upon  Certain  Blood-pressure-lowering  Re- 
flexes that  Arise  from  Irritation  of  the  Inflamed  Pleura,  Am.  J.  M.  Sc,  Phila.  and 

N.  Y.,  1907,  cxxxiv,  868. 
Einthoven,  W.,  Flohil,  A.,  and  Battaerd,  P.  J.  T.  A.:  On  Vagus  Currents  Examined  with 

the  String  Galvanometer,  Quart.  J.  Exper.  Physiol.,  Lond.,  1908,  i,  243.    Ueber  Vagus- 

strome,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxiv,  246. 
Hirschf elder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1906,  xvii,  299. 
Hewlett,  A.  W.:  The  Venous  Pulse,  Science,  Lancaster,  1909,  xxix,  515. 
Miiller,  F.    Quoted  from  Romberg. 
Evans,  H.  M.:  Personal  communication. 

Salaman,  R.  N.:  The  Pathology  of  the  Liver  in  Cardiac  Disease,  Lancet,  Lond.,  1907,  i,  4. 
Duroziez,  P.:  Du  delire  et  du  coma  digitaliques,  Gaz.  hebdom.,  Par.,  1874,  xi,  780. 
Hall,  H.  O.:  The  Hallucinations  of  Digitalis:    Does  Digitalis  Cause  Hallucinations,  Delir- 
ium, or  Insanity  under  Certain  Conditions?     Am.  Med.,  Phila.,  1901,  i,  598.     The 

Delirium  and  Hallucinations  of  Digitalis,  ibid.,  1905,  ix,  489. 
Head,  H:  Certain  Mental  Changes  that  Accompany  Visceral  Disease;  Brain,  Lond.,  1901, 

xxiv,  345. 


IV, 

GENERAL  PRINCIPLES  OF  TREATMENT  OF  FAILURE 
OF  THE  HEART. 

The  best  index  of  the  treatment  of  the  patient  is  his  own  condition, 
sensations,  and  general  appearance.  Physical  examinations,  determination 
of  blood-pressure  and  pulse-rate,  as  well  as  of  increase  in  the  product  of 
pulse-pressure  by  pulse-rate  (velocity  coefficient),  venous  tracings,  and 
gas  analysis  aid  in  the  interpretations  of  the  condition,  and  particularly 
in  discovering  where  the  fault  in  the  mechanism  of  the  circulation  lies;  but 
the  changes  of  conditions  themselves  are  often  very  subtle  and  manifest 
themselves  in  the  general  condition  of  the  patient  before  they  can  be  detected 
on  examination. 

QUIET. 

The  most  important  element  in  the  treatment  of  cardiac  failure  is  rest 
as  complete  as  possible.  In  all  cases  of  heart  failure  or  disease  in  the  heart 
the  patient  should  be  confined  to  bed,  if  necessary  propped  up  with  pillows, 
and  should  be  kept  there  until  the  acute  symptoms  have  subsided  and  have 
remained  quiescent  for  several  days. 

As  Morton  Prince  has  shown,  mental  excitement  and  worry  are  impor- 
tant factors  in  bringing  about  acute  dilatation  of  the  heart ;  but  they  are  usually  contrib- 
uting factors  rather  than  sole  causes. 

The  effect  of  mental  activity  upon  the  circulation  is  to  bring  about  vasoconstriction, 
of  both  extremities  and  viscera,  a  slight  rise  of  blood-pressure,  and  increase  in  the  pulse- 
rate;  all  of  which  taken  together  considerably  increase  the  total  work  of  the  heart  (i.e., 
roughly  speaking,  the  product  of  maximal  pressure  by  pulse-rate).1 

A  good  night's  sleep  is  often  the  best  remedy  for  the  patient  with  a 
weak  heart,  and  almost  any  method  by  which  it  may  be  procured  may  prove 
a  good  therapeutic  procedure.  Small  doses  of  bromides,  if  necessary  aided 
by  a  little  trional,  veronal,  or  other  hypnotic,  often  suffice  for  this  purpose 
and  allow  the  heart  a  few  hours'  respite  in  which  the  other  therapeutic 
measures  may  have  opportunity  to  act. 

However,  it  must  be  borne  in  mind  that  in  persons  who  are  much  worried, 
mental  rest  and  absence  of  distractions  or  occu- 
pation are  not  necessarily  synonymous.  Indeed,  the 
removal  of  other  subjects  for  thought  may  serve  only  to  centre  the  patient's 
mind  upon  himself  and  his  ailments  and  may  increase  rather  than  diminish 
the  nervous  strain.  This  should  be  carefully  guarded  against.  The  daily 
routine  should  therefore  be  accommodated  to  both  the  general  condition  and 
the  temperament  of  the  patient.  If  possible  absolute  rest  and  isolation  should 
be  secured  for  the  worst  cases  of  heart  failure,  but  even  for  these  patients 
a  few  minutes'  conversation  with  a  cheerful  friend,  whose  demeanor  is  quiet 
and  soothing,  may  be  of  actual  benefit.     Reading  should  not  be  allowed  to 

1  Cannon  and  de  la  Paz  have  shown  that  excitement  causes  a  hypersecretion  of  the 
adrenals  (Am.  J.  Physiol.,  1911,  xxviii,  64). 

231 


232  DISEASES   OF   THE   HEART   AND    AORTA. 

patients  in  the  worst  stages,  but  a  little  reading  of  the  lightest  and  least 
exciting  sort  may  otherwise  be  allowed. 

Rest,  Distraction,  and  Spa  Treatment. — As  Mackenzie  states,  it  is  chiefly 
due  to  the  element  of  mental  distraction  combined  with  the  judicious 
supervision  of  a  physician  and  the  favorable  climatic  conditions,  which 
make  the  Spa  treatments  of  cardiac  disease  so  successful;  although,  as 
he  states,  each  Spa  physician  has  evolved  some  method  of  treatment  which 
he  regards  as  of  special  benefit,  when  the  actual  benefit  has  been  due  to  the 
air  and  restfulness  itself.  Nevertheless,  it  must  be  confessed  that  the  treat- 
ments at  Nauheim  by  the  late  August  Schott  (page  268)  have  been  of  great 
benefit,  and  being  founded  upon  sound  physiological  doctrines  have  been 
applicable  elsewhere  as  well.  The  physician  must  always  realize  that, 
however  little  there  may  be  in  the  Spa  treatments  per  se,  the  combination 
of  the  mental  rest  and  change  of  air  with  the  baths  and  dietetic  treatment 
is  one  which  the  patient  whose  condition  warrants  a  trip,  should  not  forego. 
Rest  in  Bed. — The  bed  should  not  be  so  high  above  the  floor  as  to  make 
it  hard  to  get  in  and  out;  it  should  if  possible  have  a  metal  frame  and  a  good 
rather  firm  mattress.  It  should  be  provided  with  a  good  back  rest  ready 
for  use  in  case  the  patient  finds  it  more  comfortable,  and  plenty  of  pillows 
should  be  available. 

In  dealing  with  cases  of  mild  cardiac  failure  it  may  be  impossible  in 
private  practice  to  compel  the  patients  to  remain  in  bed  all  the  time,  and 
then  it  may  suffice  to  insist  upon  their  lying  down  for  several  hours  a  day 
without  absolutely  remaining  in  bed.  Under  these  circumstances  the 
physician  must  insist  that  the  patient  remain  quiet  all  day  upon  a  sofa 
or  in  a  wheel  chair  with  legs  raised.  A  short  period  of  such  absolute  rest 
is  better  than  a  much  longer  period  of  relative  invalidism,  for  it  enables 
the  dilated  heart  to  bail  itself  out,  to  regain  its  former  dimensions  and 
tonicity,  and  permits  the  heart-rate  to  return  to  normal.  It  is  important 
that  the  patient  should  remain  horizontal  rather  than  in  sitting  or  in  stand- 
ing posture,  since  the  latter  tends  to  slow  the  circulation  (cf.  Erlanger  and 
Hooker,  quoted  on  page  37).  The  rest  should  continue  until  all  symptoms 
have  subsided,  until  cardiac  distress,  pain,  and  palpitation  have  disappeared, 
and  respiration  has  again  returned  to  normal.  If  possible  the  subsidence 
of  tachycardia  or  irregularity  of  the  pulse  should  be  awaited;  but  these  may 
persist  for  some  time  even  in  spite  of  the  improvement  in  the  patient's 
general  condition,  and  may  have  to  be  disregarded.  After  the  symptoms 
have  subsided  (in  severe  cases  after  the  symptoms  have  remained  quies- 
cent for  a  few  days) ,  the  patient  may  be  allowed  to  get  out  of  bed  and  sit 
up  in  an  arm  chair  or  wheel  chair  for  a  little  while.  At  first  this  period 
should  be  very  short,  to  avoid  exhaustion,  but  it  may  be  gradually  increased 
and  he  may  soon  be  allowed  to  walk.  (For  exercises  to  be  taken  by  patient 
with  cardiac  disease  see  page  284.) 

COLD    APPLICATIONS    OVER   THE    HEART. 

The  application  of  cold  to  the  precordium  is  of  value  both  for  the 
cardiac  symptoms  (palpitation  and  pain)  on  the  one  hand,  and  for  diminu- 
tion of  the  heart-rate  on  the  other.    This  may  be  carried  out  by  the  applica- 


TREATMENT   OF   FAILURE   OF   THE   HEART.  233 

fcion  of  a  simple  ice-bag  (especially  containing  a  mixture  of  ice  and  salt) 
which  may  be  kept  in  close  application  to  the  skin  by  tying  it  around  the 
chest  and  shoulders  with  a  strong  elastic  four-tailed  bandage.  The  ice-bag 
should  be  changed  every  hour  or  two  in  order  to  keep  up  an  intense  cooling.1 

In  hospital  use  or  in  well-supplied  houses  the  use  of  the  cardiac  tube  is  most  satisfac- 
tory. This  consists  of  a  coil  of  thin-walled  rubber  or  aluminum  tube  applied  over  a  wet 
compress  to  the  precordium.  A  stream  of  cold  water  from  a  cooler  is  kept  flowing  slowly- 
through  the  tube.  The  cooling  of  the  skin  thus  obtained  is  excellent  and  without  any 
discomfort  to  the  patient.  Its  effects  have  been  tested  both  clinically  and  experimentally 
by  Winternitz  and  da  Silva. 

These  observers  found  that  the  application  of  cold  to  the  precordium  brought  about 
in  dogs  a  cooling  of  both  the  anterior  and  posterior  surfaces  of  the  pericardium,  amount- 
ing to  l°-5°,  and  was  accompanied  by  a  slowing  of  the  pulse  and  rise  of  blood-pressure 
from  120  to  190  mm.  Hg.  In  man  the  pulse-rate  did  not  begin  to  fall  for  fifteen  minutes 
after  the  application,  and  reached  its  height  within  an  hour,  lasting  in  turn  about  an  hour 
after  removal  of  the  cold.  In  normal  individuals  they  found  the  pulse-rate  falling  from 
72  to  64,  68  to  52,  78  to  68;  in  other  cases,  chlorosis  84  to  72,  pericarditis  84  to  78,  mitral 
stenosis  60  to  40.  Simultaneously  the  blood-pressure  rises  and  the  pulse  increases  in  vol- 
ume. There  is  evidently  both  a  reflex  vasoconstriction  from  stimulation  of  the  vasomotor 
centre  and  a  reflex  stimulation  of  the  vagus.  Besides  this,  da  Silva  thinks  that  there  is  a 
direct  stimulation  of  the  heart  muscle.  It  will  be  noted  that  these  effects  are  exactly  those 
brought  about  by  digitalis,  and  hence  enthusiastic  hydrotherapists  are  in  the  habit  of 
speaking   of   the   ice-bag   as    ''physiological   digitalis.'' 

Its  use  is  attended  with  less  clanger,  but  in  cases  of  extreme 
fibrous  or  fatty  degeneration  of  the  heart,  cyanosis 
and  collapse  occasionally  occur.  Hence  it  should  be  ap- 
plied very  mildly  in  cases  where  these  conditions  are  suspected. 

There  can  be  no  doubt  that  the  ice  application  is  not  as  efficient  as  the  use  of  digitalis 
in  slowing  and  strengthening  the  heart,  but  when  the  two  are  vigorously  used  at  the  same 
time  they  may  greatly  reinforce  one  another,  and  the  vigorous  use  of  a  good  ice-bag  may 
enable  satisfactory  effects  to  be  obtained  with  smaller  doses  of  digitalis  than  would  other- 
wise suffice. 

VENESECTION. 

When  the  patient  is  in  very  bad  condition,  deeply  cyanotic,  and  rest- 
less or  nervous,  and  the  area  of  cardiac  dulness  is  increased  to  the  right, 
a  free  venesection  will  often  bring  the  greatest  relief.2 

Technic  of  Venesection.  —  Venesection  is  best  performed  in  the  following  manner: 
The  skin  over  the  flexor  surface  of  the  elbow-joint  is  scrubbed  with  green  soap  and  washed 
with  warm  water,  then  with  alcohol,  and  lastly  with  1-2000  bichloride  solution.  An  elastic 
or  gauze  bandage  is  tied  about  the  upper  arm  tightly  enough  to  cause  the  veins  to  stand  out 
but  not  to  obliterate  the  pulse  at  the  wrist.  The  largest  vein  visible  (usually  the  median 
cephalic)  is  selected  and  a  small  slit  in  the  skin  just  alongside  of  (not  over)  the  vein  is  made 
with  a  curved  bistoury,  which  is  then  pushed  in  through  the  slit  in  the  skin  and  under  the 
vein.  It  is  then  twisted  so  that  the  edge  is  turned  upward  towards  the  skin  against  the 
vein  and  the  vein  cut  through  without  again  piercing  the  skin.  A  very  free  flow  of  blood 
is  obtained,  especially  by  keeping  the  arm  dependent  and  if  the  patient  is  made  to  clench 
and  open  his  hands  rapidly.  From  300  to  1200  c.c.  (12  ounces  to  2+  pints)  can  thus  be 
removed  in  less  than  twenty  minutes,  usually  with  great  relief  to  the  patient.     Breathing 

1  When  a  mixture  of  ice  and  salt  is  used  it  is  possible  to  actually  freeze  the  skin,  an 
accident  which  must  be  carefully  avoided.   . 

2  The  haemoglobin  should  always  be  tested  before  performing  a  venesection;  and  it 
should  not,  as  a  rule,  be  performed  if  the  haemoglobin  is  below  70  per  cent. 


234 


DISEASES    OF   THE   HEART   AND    AORTA. 


becomes  easier,  the  head  clearer,  and  the  general  condition  better,  but  the  crucial  point  is 
reached  when  the  co'or  changes  and  the  cyanosis  gives  way  to  a  healthy  rosy  color  in  the 
lips  and  elsewhere.  This  indicates  that  the  overstrained  heart  has  been  unburdened,  and 
the  bleeding  need  not  be  pushed  much  further.  Indeed  it  should  not  be,  for  to  cause  an 
anaemia  is  dangerous.     All  that  is  desired  is  to  relieve  the  distention  of  the  right  heart. 


Fig.  126. — Insertion  of  the  knife  in  venesection.     A.   Lateral  view. 


Cross  section  of  arm. 


Effect  of  Venesection  on  the  Circulation. — The  value  of  venesection  can  often  be  seen 
in  experiments  upon  animals.  It  is  not  at  all  uncommon  to  find  a  heart  failing  and  an 
auricle  already  paralyzed  from  overdistention,  in  which  a  free  venesection  gives  immediate 
relief,  and  the  auricle  as  well  as  the  ventricle  resumes  forcible  contractions.  The  effect  of 
this  procedure  upon  the  blood-pressure  is  variable  and  depends  to  a  certain  extent  upon 
the  phenomena  present  before  the  venesection. 


Before  Venesection. 

After  Venesection. 

Blood-pressure. 

Condition. 

1.  Normal  or  elevated 

2.  High 

Heart  distended  but  circulation 
still  sufficient 

Circulation  slowed.  Vasocon- 
striction through  stimulation 
of  medulla  by  excess  of  C02 
in  the  blood 

Circulation  slowed;  heart  fail- 
ing. Unable  to  keep  up  cir- 
culation through  medulla  in 
spite  of  vasoconstriction 

Fall  of  blood-pressure  from  emp- 
tying of  vascular  system  and 
diminished  viscosity  of  blood.1 

Fall  of  blood-pressure;   occasion- 

3. Low  or  normal  .... 

ally  compensated  by  increased 
force  of  heart-beat  and  dimin- 
ished viscosity  of  blood. 
Blood-pressure  rises  on  account 
of  marked  increase  in  force  of 
heart-beat  in  spite  of  empty- 
ing of  vascular  system  and  of 
relaxation  of  peripheral  vessels. 

Quite  independently  of  these  changes  the  right  border  of  cardiac  dul- 
ness  recedes  one  or  more  centimetres  toward  the  sternum,  the  venous  pressure 
should  fall,  and  the  general  condition  should  improve  (cf.  Fig.  127  and  case  on  page  329). 

Contraindications  to  Venesection. — However,  it  must  be  borne  in  mind 
that  venesection  can  do  harm  as  well  as  good.  Cushing  has  shown  that  in 
conditions  with  increased  intracranial  tension,  among  them  apoplexy,  the 


1  Heubner  has  shown  that  two-thirds  of  the  viscosity  of  the  blood  is  due  to  the  cor- 
puscles, hence  venesection  cannot  fail  to  reduce  the  viscosity. 


TREATMENT   OF   FAILURE   OF   THE    HEART. 


235 


high  blood-pressure  is  a  phenomenon  of  physiological  compensation,  which 
is  necessary  in  order  to  maintain  the  circulation  through  the  medulla.  In 
conditions  with  long-continued  high  blood-pressure,  especially  chronic 
nephritis,  this  may  also  be  the  case.  In  these  conditions  venesection  with 
a  view  to  lowering  the  arterial 
pressure  is  contraindicated;  but 
in  these,  as  in  other  conditions, 
it  is  still  the  procedure  of  choice 
to  relieve  pulmonary  oedema  or 
acute  dilatation  of  the  right  heart. 
The  venesection  should  be  carried 
only  to  the  point  of  relieving  the 
venous  stasis,  not  to  that  of  low- 
ering the  arterial  pressure.1 


DIET. 

Rest  for  the  gastro-intestinal 
tract  is  quite  as  important  for 
the  heart  as  is  rest  for  the  mus- 
cles. Erlanger  and  Hooker  have 
shown  that  "  an  increase  in  pulse- 


Fig.  127. — Effect  of  venesection  on  the  cardiac  out- 
line, showing  diminution  in  size  of  right  heart.  (Case 
of  G.  G.)  Solid  line  indicates  cardiac  outline  before 
venesection,  broken  line  after  venesection. 


BEFORE  VENESECTION     AFTER  VENESECTION 


pressure  becomes  manifest  within 

a  few  minutes  after  the  beginning  of  the  meal,  reaches  its  maximum  within 
one  or  two  hours,  and,  as  a  rule,  declines  somewhat  more  slowly.  It  seems 
to  pass  off  within  one  or  two  hours  after  the  maximum  has  been  reached. 
The  pulse-rate  is  always  distinctly  increased  with  the  ingestion  of  meals. 

....  The  product  P.  P.  X 
P.  R.,  representing  the  velocity, 
follows  the  curve  of  the  pulse- 
pressure,"  hence  the  velocity 
of  flow  and  the  work  of  the 
heart  are  increased.  Accord- 
ingly, the  diet  should  be  light, 
just  enough  to  keep  the  patient 
nourished  without  ever  giving 
him  a  sense  of  fulness  or  to 
allow  gas  to  form  in  the  stom- 
ach and  intestines.  Distention 
of  the  stomach  pushes  up  the 
diaphragm  and  causes  the 
heart  to  lie  more  transversely 
in  the  thorax,  embarrassing 
its  action,  causing  a  diminution  in  the  systolic  output  and  an  increase 
in  the  pulse-rate.  Not  infrequently  this  is  also  associated  with  onset 
of  precordial  pain  and  constriction.  Accordingly  a  very  light  diet 
is  necessary  for  the   patient   suffering  from  heart  failure.     The  1  a  c  t  o  - 

1 V.  Tabora  ( Verhandl.  d.  Kong,  f .  innere  Med.,  1909,  xxvi,  382)  finds  that  venous  stasis 
can  be  relieved  by  placing  tourniquets  about  both  arms  and  both  legs  as  well  as  by  venesection. 


Fig.  128. — Typical  effect  of  venesection  upon  the  circu- 
lation.   Arrows  indicate  change  in  blood-pressure. 


236  DISEASES  OF  THE  HEART  AND  AORTA. 

cereal  diet  is  the  best,  consisting  mainly  of  milk,  eggs,  custards,  junket, 
toast,  zweiback,  and  crackers.  The  numerous  prepared  cereal  foods  contain 
large  amounts  of  bran  and  other  substances  which  leave  bulky  fecal  residues. 
If  given  in  large  quantities,  they  keep  the  bowels  full,  push  up  the  diaphragm, 
and  thus  embarrass  the  work  of  the  heart,  though  in  some  persons  this  is 
counterbalanced  by  their  purgative  action.  Meat  should  be  given  sparingly, 
partly  because  the  purin  bodies  (xanthin,  hypo-xanthin)  tend  to  raise  the 
blood-pressure  and  increase  the  work  of  the  heart,  and  more  particularly 
because  the  meat  fibres  are  relatively  slow  in  digestion.  For  this  reason  it 
is  better  to  take  the  proteid  food  in  the  forms  mentioned  above.  Finely 
hashed  Hamburg  steak,  lamb  chops,  or  chicken  are  the  best  forms  of  meat. 

Liquid  and  Salt. — Liquids  should  be  limited  to  1500  c.c.  (three 
pints)  a  day  in  cases  where  oedema  is  present,  since  an  excess  of  liquid 
ingested  causes  further  accumulation  of  oedema  as  well  as  bringing  on  a 
slight  overfilling  of  the  blood-vessels,  and  thereby  increasing  the  work  of 
the  heart. 

Salt  should  also  be  withheld  from  the  food  as  far  as  possible,  since 
Widal  and  Javal,  Strauss  and  Richter  have  shown  that  it  is  a  contributing 
factor  in  the  production  of  oedema,  and  Barie  reports  good  results  from  the 
diminution  of  NaCl  in  the  diet  in  diseases  of  the  circulation. 

Barie  recommends  the  following  articles  as  a  basis  for  a  diet  low  in 
sodium  chloride:  Type  I — Unsalted  bread  500  Gm.  (18  oz.),  raw  meat  400 
Gm.  (14  oz.),  butter  80  Gm.  (2£  oz.),  sugar  100  Gm.  (3J  oz.).  Type  II— Pota- 
toes 1000  Gm.  (32  oz.),  raw  meat  400  Gm.  (14  oz.),  butter  80  Gm.  (2|  oz.), 
sugar  150  Gm.  (5  oz.). 

Sample  Diet. — An  excellent  diet  for  severe  heart  cases,  which  may  at 
least  serve  as  a  basis  for  other  variations,  is  the  following,  slightly  modified 
from  that  used  for  cardiac  cases  in  the  wards  of  the  Johns  Hopkins  Hospital: 

8  a.m.  Cereal,  soft  egg,  toast,  milk  200  Gm.  (vi  oz.). 
10  a.m.  Milk  200  c.c.  (vi  oz.),  soft  egg,  crackers. 

Dinner  (noon).  Soup,  chicken,  potatoes. 

4  p.m.  Milk  200  c.c.  (vi  oz.). 

Supper,  6  p.m.  Milk  200  c.c.  (vi  oz.),  soft  egg,  crackers,  prunes.1 

9  p.m.  Milk  200  c.c.  (vi  oz.),  bread. 

Karell's  Milk  Diet. — In  cases  of  broken  compensation  with  extreme 
oedema  great  success  has  sometimes  been  attained  by  limiting  the  diet  to 
600  to  800  c.c.  of  milk  in  24  hours  (Karell,  Hoffmann,  Jacob  and  Hirsch- 
feld),  even  in  cases  in  which  all  other  therapeutic  measures  have  failed. 
Professor  Barker  has  occasionally  obtained  excellent  results  by  increasing 
the  proteid  intake  upon  this  diet  through  the  addition  of  nutrose  to  the 
milk.  However,  striking  results  with  this  method  are  by  no  means  the 
rule,  and  it  is  to  be  used  with  caution. 

Alcohol. — A  very  little  alcohol,  either  as  wine,  or  as  brandy  or  whiskey, 
may  be  allowed  to  persons  accustomed  to  its  use.     Beer  is  less  advisable, 

1  It  is  important  to  avoid  giving  stewed  fruits  which  contain  much  acid,  such  as  peaches 
and  apricots,  along  with  the  milk,  as  the  digestion  of  patients  with  broken  compensation 
is  very  easily  disturbed,  and  an  attack  of  vomiting  places  a  considerable  strain  on  the  heart. 


TREATMENT   OF   FAILURE   OF   THE   HEART.  237 

since  it  carries  with  it  large  quantities  of  liquid  and  often  disturbs  the 
digestion  as  well,  whereas,  wine,  whiskey,  or  brandy  in  small  quantities 
improves  it.  Against  this  is  balanced  the  deleterious  effect  of  alcohol  upon 
the  heart  muscle.  Large  quantities  tend  to  produce  fatty  degeneration  of 
the  latter.  Whether  small  quantities  have  any  such  effect  in  the  individual 
case  is  uncertain,  but  it  must  be  borne  in  mind  that  the  injured  organ  is 
much  more  susceptible  to  deleterious  influences  than  is  the  healthy  organ. 
It  is  a  safe  rule  that,  in  persons  not  already  addicted  to  its  use,  brandy  or 
whiskey  be  given  only  in  doses  which  serve  as  carminatives,  and  not  in 
doses  intended  for  stimulation.  Even  the  psychic  effect  may  often  be 
secured  as  well  by  small  doses  as  by  large  ones.  One  point  in  favor  of  alco- 
hol in  man  as  against  animal  experimentation  lies  in  the  fact  that  in  such 
persons  it  greatly  increases  the  sense  of  well  being  and  removes  psychic 
depression  and  worry.  The  latter  may  be  especially  straining  upon  the 
heart,  and  hence  every  effort  should  be  made  use  of  to  ward  it  off,  especially 
during  certain  crises;  but  it  should  be  borne  in  mind  that  the  patient  may 
easily  become  dependent  upon  the  drink  to  arouse  his  spirits  and  in  this 
state  more  harm  than  good  is  done.  The  greatest  judgment  should  be  used 
in  the  administration  of  alcohol  even  in  small  quantities,  and  it  should  even 
then  be  reserved  for  crises  when  the  stimulation  of  every  fibre  is  all-impor- 
tant. On  the  other  hand,  alcohol  should  never  be  withdrawn  suddenly  from 
persons  addicted  to  its  use,  since  this  procedure  often  precipitates  an  attack 
of  delirium  tremens,  but  moderate  doses  (whiskey  15  c.c.  or  \  oz.  every 
four  hours)  should  be  given. 

Tea  and  Coffee. — Whether  tea  and  coffee  should  be  given  depends 
largely  upon  the  patient.  In  some  persons  these  cause  marked  general 
nervousness,  sleeplessness,  tremor,  and  even  palpitation  and  irregularity;1 
others  have  established  a  tolerance  such  that  no  effect  at  all  is  produced. 
The  caffein  itself  is  an  excellent  cardiac  tonic  of  the  digitalis  order,  and 
where  its  effects  on  the  nervous  system  are  not  manifest  it  may  prove  an 
excellent  adjuvant  to  the  treatment.  (A  cup  of  coffee  or  of  strong  tea  contains 
about  0.1-0.2  Gm.,  V/2  to  3  gr.;  the  pharmacological  dose  of  pure  caffein 
being  0.05  to  0.25  Gm.)  As  a  rule  it  is  safer  to  remove  them  from  diet,  but 
in  this  as  in  all  other  rules  individual  exceptions  can  be  made. 

Tobacco  should  not  be  used  under  any  circumstances.  Besides  the  ner- 
vous symptoms,  it  produces  vasoconstriction,  and  often  irregularities,  palpita- 
tion, and  even  precordial  pain.  Hence  it  is  particularly  to  be  avoided  in 
cases  of  cardiac  disease. 

PURGATION. 

In  patients  with  cardiac  disease,  and  especially  in  those  with  broken 
compensation,  the  question  of  purgation  assumes  unusual  importance.  In 
these  patients  purgation  seems  to  have  a  threefold  beneficial  action:  first, 
by  eliminating  the  products  of  waste  and  putrefaction,  to  which  they  are 
particularly  sensitive;  secondly,  by  relieving  the  distention  of  the  bowels 
from  gas  which  tends  to  push  up  the  diaphragm  and  to  embarrass  the  heart 
by  placing  it  in  a  more  transverse  position;  and  thirdly,  by  removing  fluid 
from  the  body  through  the  bowels.     This  last  effect  is  probably  of  con- 

1  Coffee  from  which  the  caffein  has  been  removed  may  be  used  with  impunity. 


238  DISEASES   OF   THE   HEART   AND    AORTA. 

siderable  importance,  since  Askanasy,  Kast,  and  others  have  shown  that 
broken  compensation  is  accompanied  by  hydremic  plethora.  Hydrsemic 
plethora  causes  a  rise  in  venous  pressure  and  a  dilatation  of  the  heart  (Roy 
and  Adami,  Cameron),  thus  embarrassing  the  circulation.  Moreover,  in 
broken  systemic  compensation  the  venous  stasis  also  affects  the  kidneys 
and  diminishes  the  excretion  of  fluid,  so  that  the  bowel  becomes  an  impor- 
tant accessory  channel  of  elimination.  It  is  therefore  the  hydragogue 
purgatives  which  are  indicated  in  cardiac  failure  and  not  merely  the  pur- 
gatives which  increase  peristalsis. 

In  most  cases  the  best  method  of  procedure  is  to  start  movement  of  the 
bowels  with  calomel  in  either  large  single  doses  (0.3-0.6  Gm.,  grs.  v-x)  or  in 
small  divided  doses  (.006  Gm.,  gr.  TV  half-hourly).  The  dose  of  calomel 
should  always  be  accompanied  by  a  small  dose  of  bicarbonate  of  soda 
(0.3-0.6  Gm.,  gr.  v-x)  to  avoid  disturbing  the  digestion.  Still  more  certain 
purgation  is  obtained  by  giving  a  single  dose  of  calomel  and  rhubarb  in 
equal  quantities  (0.3  Gm.,  gr.  v),  given  at  night.  In  all  cases  the  calomel 
should  be  followed  by  a  saline  purgative  the  next  morning.  Epsom  salt 
or  some  aperient  water  is  preferable  to  Seidlitz  powders  or  effervescent 
citrate  of  magnesia,  partly  because  of  the  action  of  the  organic  acids  upon 
the  residium  of  calomel,  but  chiefly  because  the  carbonic  acid  in  the  drug 
distends  the  bowels  and  pushes  up  the  diaphragm,  thus  embarrassing  the 
action  of  the  heart.  However,  Epsom  salts  and  aperient  waters  sometimes 
cause  nausea,  and  in  such  cases  the  advantages  gained  from  the  mildness  of 
the  Seidlitz  powder  may  outweigh  its  deleterious  effects. 

After  constipation  has  been  overcome  purgation  with  salines  should  be 
continued  vigorously  until  the  oedema  has  completely  disappeared.  Just 
how  vigorously  this  purgation  should  be  maintained  is  a  matter  of  some 
dispute.  Some  clinicians,  who  regard  presence  of  fluid  as  the  most  dele- 
terious factor,  believe  that  the  best  results  are  obtained  with  ten  to  fifteen 
fluid  stools  in  twenty-four  hours,  with  the  elimination  of  two  or  three  litres 
by  the  bowel.  As  the  result  of  these  strains  upon  the  heart,  sudden  death  at 
stool  is  by  no  means  uncommon,  especially  in  cases  of  aortic  insufficiency  and 
coronary  sclerosis.  Extreme  purgation  and  other  strains  should  be  avoided 
when  possible.  The  amount  of  effort  at  stool  and  the  strain  upon  the  patient 
may  be  materially  lessened  by  the  use  of  a  commode  instead  of  a  bedpan. 
In  private  houses  an  extemporized  commode  may  be  made  by  removing  the 
seat  from  a  cane-bottomed  chair,  substituting  a  piece  of  wood  or  cardboard 
covered  with  oil  cloth,  with  a  suitable  hole,  and  placing  the  vessel  below. 

Mr.  W.  E.  Dandy  has  shown  that  the  rise  of  arterial  pressure  during 
the  act  of  defecation  is  from  30  to  50  mm.  Hg,  and  Mr.  C.  C.  Cody  has  found 
a  corresponding  rise  in  the  venous  pressure.  These  observations  are  sup- 
ported by  the  fact,  as  stated  above,  that  sudden  death  at  stool  is  by  no 
means  uncommon  in  cases  of  cardiac  disease,  especially  in  cases  of  aortic 
insufficiency,  and  occurs  even  when  the  movements  have  been  kept  soft 
by  daily  purgation  with   salts. 

In  this,  as  in  most  other  therapeutic  procedures,  extreme  measures 
are  to  be  avoided  and  treatment  should  be  directed  to  secure  a  few  easy 
bowel  movements  without  too  much  disturbance  to  the  patient.  In  many 
cases  one  or  two  compound  cathartic  pills  (colocynth,  jalap,  gamboge,  and 


TREATMENT  OF  FAILURE  OF  THE  HEART.  239 

calomel)  at  night  and  a  dose  of  Epsom  salts  or  aperient  water  in  the  morn- 
ing maintain  just  the  correct  number  and  quality  of  stools.  Compound 
jalap  or  compound  licorice  powders  are  also  useful  from  time  to  time.  In 
stubborn  cases  elatcrium  or  a  drop  of  croton  oil  may  be  resorted  to,  but 
should  be  used  with  extreme  caution. 

On  the  other  hand,  cascara,  aloes,  strychnine,  belladonna,  castor  oil, 
phenolphthalein,  and  the  other  purgatives  which  purge  by  increasing  peri- 
stalsis, are  of  less  value  in  the  stage  of  broken  compensation,  since  they  do 
not  deplete  the  portal  system  nor  relieve  the  hydrsemia,  though  they  are 
satisfactory  enough  when  compensation  has  been  reestablished. 

MASSAGE. 

Massage  of  the  muscles  brings  about  a  dilatation  of  their  capillaries  and 
thus  lowers  the  resistance  through  this  part  of  the  circulation. 

In  this  respect  the  effect  is  similar  to  that  of  exercise,  but,  as  very  much 
less  C02  is  given  off,  the  velocity  of  the  blood  strain  does  not  have  to  be  in- 
creased. The  blood-pressure  falls  and,  in  contrast  to  the  effect  of  exercise, 
the  strain  upon  the  heart  is  diminished.  ^- 

It  is,  therefore,  not  surprising  that  in  most  patients  suffering  from  poorly 
compensated  cardiac  disease,  massage  of  the  limbs  should  furnish  considerable 
relief.  When  the  heart  is  not  too  severely  weakened,  the  effect  upon  the 
circulation  of  lymph  also  facilitates  the  absorption  of  cedema. 

Massage  of  the  abdomen  alone  has  been  recommended  by  Cautru  and 
Studzinski,  and  the  latter  has  reported  excellent  results  in  twenty-two  cases. 
The  treatment  was  usually  accompanied  by  fall  of  blood-pressure,  owing  to  the 
dilatation  of  the  abdominal  vessels.  Besides  this  effect,  however,  abdominal 
massage  also  tends  to  prevent  constipation  and  to  dispel  accumulations  of 
gas,  both  of  which  effects  furnish  considerable  relief  for  the  cardiac  condition- 
Vibration  of  the  Precordium. — Besides  these  more  general  forms  of  mas- 
sage, Zabludowski,  Selig,  and  Rimbach  state  that  considerable  benefit  may 
be  obtained  for  precordial  pains,  mild  angina  pectoris,  and  other  sensory 
disturbances  about  the  heart,  by  gentle  vibratory  massage  or  mechanical 
vibration  over  the  precordium.  The  vibrations  should  be  carried  out  either 
with  the  balls  of  all  four  fingers  of  the  right  hand  or  with  the  soft  pad  of  the 
mechanical  vibrator,  and  should  be  begun  under  gentle  pressure  well  out  in 
the  lower  left  axilla,  gradually  passing  upward  and  inward  over  the  precordium 
until  the  entire  cardio-aortic  area  has  been  covered. 

Selig  and  Rimbach  have  made  use  of  this  method  in  cases  of  dilatation 
of  the  heart,  which  they  studied  by  means  of  the  orthodiagraph.  In  these 
cases  they  claim  to  have  obtained  not  only  relief  of  the  subjective  symptoms 
but  actual  diminution  of  the  dilatation  as  the  result  of  the  vibratory  massage. 

Rimbach  states  that  his  observations  were  controlled  by  Dr.  Bassenge 
and  Prof.  Steyrer,  but  the  results  of  a  greater  number  of  cases  must  be  awaited 
before  this  effect  upon  cardiac  dilatation  can  be  regarded  as  general. 

ELECTRICITY. 

Faradization  of  the  precordium  and  left  arm,  and  particularly  the  use 
of  sinusoidal  currents  over  these  areas,  may  be  considered  as  a  form  of 
counterirritation  which  may  prove  very  efficient  in  relieving  precordial  pain 


240  DISEASES  OF  THE  HEART  AND  AORTA. 

and  discomfort;  but  care  should  be  taken  not  to  use  currents  of  so  great 
a  severity  as  to  produce  real  pain. 

A  somewhat  different  effect  is  that  secured  by  Prof.  J.  O.  Hirschfelder  in 
patients  of  angina  pectoris  (see  page  395)  by  applying  the  galvanic  current 
with  a  large  anodal  pad  (4  cm.  in  diameter)  over  the  vagus  in  the  neck  and 
a  large  cathode  (6-12  cm.  in  diameter)  over  the  precordium.  He  recommends 
gradually  increasing  the  current  to  20  milliamperes  for  five  minutes,  changing 
the  anode  to  the  other  side  of  the  neck  and  repeating.  The  relief  obtained 
under  this  treatment  warrants  its  further  trial. 

High=frequency  Currents  (d'Arsonvalisation). — Many  writers,  especially 
of  the  French  school,  incline  to  the  use  of  high-frequency  currents  (d'Arson- 
val),  especially  in  cases  of  arteriosclerosis,  Raynaud's  disease,  and  other  con- 
ditions involving  the  peripheral  circulation.  It  seems  to  bring  about  dilata- 
tion of  the  peripheral  vessels  and  fall  of  blood-pressure,  as  has  been  reported 
by  Zimmern  and  Riffaut. 

Marque  has  reported  excellent  results  in  a  very  stubborn  case  of  Ray- 
naud's disease  treated  by  high-frequency  currents  over  the  lower  cervical 
and  upper  thoracic  vertebrae,  and  Zimmern  and  Riffaut  claim  a  beneficial 
effect  upon  the  circulation  in  endarteritis  obliterans. 

Except  in  Raynaud's  disease,  in  which  the  effects  upon  the  spinal  centres 
and  ganglia  are  to  be  considered,  there  seems  to  be  no  reason  for  regarding 
it  as  very  different  from  other  means  of  securing  intense  dilatation  of  the 
cutaneous  vessels. 

SURGICAL   MEASURES   FOR   THE   RELIEF   OF   HEART  FAILURE. 

For  patients  whose  hearts  are  beating  so  heavily  against  the  chest  wall 
that  this  factor  alone  seemed  materially  to  increase  the  work  of  the  heart, 
Alexander  Morison,  in  1897,  advised  cutting  the  ribs  over  the  heart,  and  thus 
allowing  the  organ  free  movement.  This  operation  was  carried  out  at  his 
suggestion  in  1908  upon  a  patient  with  aortic  insufficiency,  who  obtained 
thereby  considerable  relief  from  palpitation  and  precordial  pain. 

The  same  operation  (cardiolysis)  was  devised  independently  by  Brauer, 
in  1904,  for  the  relief  of  pericardial  adhesions,  in  which  it  has  been  employed 
with  great  success  (see  page  620). 

G.  A.  Gibson  has  also  found  some  relief  following  thoracostomy  in  a 
patient  with  mitral  stenosis  and  adhesions  between  the  outer  layer  of  peri- 
cardium and  the  chest  wall  but  not  involving  the  pericardial  cavity  itself. 

The  second  operation  might  also  be  performed  in  cases  of  extreme  flat- 
ness or  narrowness  of  the  chest  (oppressio  cordis,  cf.  page  698),  provided  the 
heart  was  so  cramped  as  to  give  rise  to  symptoms  of  severe  cardiac  weakness 
that  could  not  be  relieved  by  other  means. 

The  results  thus  far  from  thoracostomy  are  sufficiently  good  to  justify 
its  use  for  the  relief  of  costapericardial  adhesions  (see  page  620),  but  in  other 
forms  of  cardiac  failure  it  should  be  resorted  to  only  after  unusual  considera- 
tion of  all  factors. 

INHALATION   OF   OXYGEN. 

Leonard  Hill  and  Flack  have  shown  that  inhalations  of  oxygen  greatly 
increase  the  endurance  of  men  and  animals  when  performing  muscular  work. 


TREATMENT  OF  FAILURE  OF  THE  HEART.  241 

This  applies,  however,  only  when  the  work  reaches  the  point  of  strain.  For 
example,  he  found  that  it  had  no  effect  in  increasing  the  speed  of  race-horses 
running  on  a  level  track,  whereas  ordinary  work-horses  pulled  a  load  uphill, 
when  fatigued  and  then  given  an  inhalation  of  oxygen,  more  rapidly  and  with 
less  exertion  than  they  had  done  when  fresh  to  the  task. 

Similarly,  little  effect  was  noticed  upon  the  ability  of  athletes  to  perform 
the  exercises  to  which  they  had  been  trained;  but,  on  the  other  hand,  the 
endurance  of  untrained  men  was  greatly  increased.  The  effect  of  oxygen 
inhalations,  even  on  a  trained  man  working  to  the  full  limit  of  his  endurance, 
was  tested  by  Flack  upon  Wolffe,  the  English  Channel  swimmer.  Flack 
accompanied  the  swimmer  in  a  small  boat.  When  he  became  fatigued  and 
about  to  give  up  the  effort,  Flack  allowed  him  to  inhale  oxygen  occasionally, 
with  the  result  that  from  a  condition  of  exhaustion  he  was  able  to  swim  for 
several  hours  further  without  dyspnoea  or  cardiac  distress. 

Mackenzie  has  made  use  of  this  method  in  the  treatment  of  cardiac 
disease,  and  has  found  that  in  some  cases  it  gives  a  certain  amount  of  relief, 
especially  for  restless  nights;  though  the  relief  was  neither  as  great  nor  as 
universal  as  he  had  anticipated.  Sir  Clifford  Allbutt  and  Herz  have  also  used 
it  with  good  results. 

Mackenzie  makes  use  of  Hill  and  Flack's  method  of  inhaling  the  con- 
centrated oxygen  from  under  a  mask,  which  can  be  made  extemporaneously 
by  inserting  the  patient's  head  into  a  lady's  hat-box,  cutting  out  one  side  so 
as  to  fit  around  the  neck.  A  more  convenient  mask  may  be  made  from  a 
piece  of  light  mackintosh,  near  one  margin  of  which  a  piece  six  inches  square 
is  cut  out  and  replaced  by  gluing  on  a  piece  of  transparent  celluloid  to  cover 
the  face.  This  margin  of  the  mackintosh  is  held  tightly  around  the  head 
with  an  elastic  band,  while  the  lower  border  is  slightly  packed  around  the  neck. 
The  oxygen  is  led  into  it  through  a  rubber  tube.  The  writer,  however,  pre- 
fers to  use  a  simple  fountain  syringe  as  an  inhaler,  allowing  the  patient  to 
place  the  funnel  end  of  the  syringe  over  his  mouth  and  nose  while  the  rubber 
tube  of  the  syringe  is  connected  with  the  glass  tube  of  the  wash-bottle  through 
which  the  gas  is  led  (Fig.  129) . 

Hill  finds  that  for  this  purpose  the  most  convenient  manner  of  securing 
oxygen  is  by  generating  it  from  a  gasogen  containing  oxylithe  (Na203),  from 
which  the  gas  is  generated  by  contact  with  water,  and  is  stored  in  a  15-litre 
gas-bag.    Sodium  perborate  may  be  substituted  for  the  oxylithe. 

INHALATION    OF    CARBON   DIOXIDE. 

As  early  as  1899,  Sir  William  Ewart,  believing  that  the  beneficial  effect 
of  the  Nauheim  baths  was  due  largely  to  the  inhalation  of  the  carbonic  acid 
which  floated  in  the  air  above  the  water,  recommended  the  inhalation  of  this 
gas  by  patients  as  a  preliminary  to  the  Nauheim  treatment,  and  reported 
considerable  benefit  from  its  use.  He  found  it  particularly  serviceable  in  the 
attacks  of  cardiac  dyspnoea  of  aortic  insufficiency  and  of  mitral  disease,  in 
cases  of  precordial  pain,  and  in  angina  pectoris. 

In  cases  of  Cheyne-Stokes  breathing,  as  well  as  in  cardiac  asthma,  Eyster, 
Pembrey,  and  Allbutt  recommend  the  inhalation  of  oxygen  containing  two 
or  more  per  cent,  of  carbon  dioxide  to  regulate  breathing  and  prevent  the 
onset  of  acapnia. 
16 


242 


DISEASES  OF  THE  HEART  AND  AORTA. 


For  convenience  of  administration  Ewart  recommends  obtaining  the 
carbonic  acid  by  allowing  it  to  bubble  off  from  the  ordinary  carbonated  water 
obtained  from  a  soda  siphon.  The  latter  is  squirted  into  a  pressure  bottle, 
where  it  may  be  kept  and  gradually  given  to  the  patient.  The  writer 
finds  it  still  more  convenient  simply  to  allow  the  patient  to  squirt  the  soda 
water  gradually  into  a  Mason  jar  or  into  a  fountain  syringe  in  the  manner 
described  above,  and  to  allow  him  to  breathe  with  his  mouth  immediately 
above  the  mouth  of  the  jar  or  the  funnel  of  the  syringe.  The  number  of 
cases  in  which  the  use  of  C02  is  desirable,  and  the  use  of  C02  baths  as  well, 
is  questionable.    Certainly  all  cases  with  any  degree  of  acidosis  or  dyspnoea 


Fig.  129. — Effect  of  inhalation  of  carbon  dioxide  on  the  ventilation  of  the  lungs  (.after  Peabody, 
a     v    t   x    m  j     ir>in         •    o,^      t,     *-i   4.-  a-   ■     ^     Ventilation  of  lungs  after  inhaling  CO2     _, 

Arch.  Int.  Med.,  1915,  xvi,  846).     Ventilation  coefficient— = r-, r. — : .   The 

.Normal  lung  ventilation 
shaded  curve  shows  response  of  normal  individuals  to  increasing  percentage  of  CO2.     Black  lines  show 
response  of  patients  with  acidosis. 

when  at  rest  should  be  excluded,  for  Peabody  (Arch.  Int.  Med.,  1915,  xvi, 
846)  has  shown  that  in  such  cases  the  respiratory  rate  is  doubled  by  inhala- 
tion of  2  to  3  per  cent.  C02,  while  normal  individuals  require  4  to  5  per  cent, 
to  produce  the  same  effect. 

INHALATION    OF   RAREFIED   AIR. 

In  cases  of  failure  of  the  right  heart  in  stenosis  and  mitral  insufficiency, 
and  also  in  some  cases  of  failure  of  the  left  heart,  Kuhn  has  advocated  dimin- 
ishing the  resistance  in  the  pulmonary  circulation  by  the  use  of  his  suction 
mask.  This  device  is  a  small  tightly  fitting  mask  about  the  size  of  a  chloro- 
form mask  which  is  held  over  the  face  by  a  strap  around  the  head,  so  that 
it  fits  air-tight  about  the  mouth  and  nose.  It  is  provided  with  two  valves, 
one  allowing  the  air  to  enter  the  mask,  the  other  allowing  it  to  leave. 

By  regulating  the  pressure  at  which  the  inspiratory  valve  opens,  it  is 
easy  to  bring  about  any  desired  rarefaction  of  the  air  within  the  mask,  which 


TREATMENT  OF  FAILURE  OF  THE  HEART  243 

the  patient  should  use  for  several  hours  a  day.  When  the  mask  is  applied 
it  gives  rise  to  a  certain  amount  of  dyspnoea,  which  may  be  somewhat  annoy- 
ing and  in  the  more  severe  cases  may  entirely  preclude  its  use.  After  the 
patient  has  learned  to  accommodate  his  breathing  to  suit  the  new  conditions, 
however,  this  element  disappears.  The  patient  should  begin  by  using  the 
mask  for  a  few  minutes  at  a  time  and  then  gradually  increase  the  period 
and  the  frequency  of  application  until  he  is  using  it  for  many  hours  a  day. 

Albrecht;  recommends  that  the  rarefaction  of  the  air  in  the  mask  should 
not  be  greater  than  3  mm.  Hg,  but,  as  this  is  almost  one-third  of  the  negative 
pressure  in  the  thoracic  cavity,  and  in  view  of  the  low  mean  blood-pressure 
in  the  pulmonary  arteries,  its  effect  would  naturally  be  considerable.  Indeed, 
Gerhardt  has  shown  experimentally  that  such  a  diminished  pressure  greatly 
increases  the  rate  of  blood  flow  through  the  lungs,  and  has  shown  that  it 
causes  the  lungs  of  a  dog  to  become  engorged  with  blood. 

Kuhn,  Morelli,  Bruhl,  Zabel,  Albrecht,  and  Gerhardt  claim  excellent 
results'  from  the  use  of  this  suction  mask  in  patients  with  heart  disease,  espe- 
cially in  mitral  stenosis  (Morelli) ;  and  it  is  worthy  of  a  more  extended  trial. 

Not  satisfied  with  the  result  of  simple  suction  of  the  lungs  in  inspiration, 
Albrecht  adds  a  spring  upon  the  expiration  valve  of  the  mask,  so  that  expira- 
tion must  be  forced  at  a  slightly  positive  pressure,  thus  massaging  the  lungs 
by  the  change  of  pressure  between  the  inspiration  and  expiration.  Kuhn, 
however,  apparently  with  good  reason,  objects  that  this  imposes  too  great 
a  strain  upon  the  patient,  and  prefers  the  simple  inspiration  of  rarefied  air 
with  expiration  at  the  atmospheric  pressure. 

The  use  of  the  suction  mask  is  also  of  value  in  the  treatment  of  the 
anaemia  which  is  a  frequent  concomitant  of  cardiac  disease,  since,  as  Kuhn 
and  others  have  shown,  it  acts  like  high  altitudes  in  stimulating  the  forma- 
tion of  red  blood-corpuscles.  Kuhn  has  also  shown  that  the  continued  use 
of  the  suction  mask  leads  to  a  gradual  increase  in  the  chest  capacity,  particu- 
larly in  the  type  of  long  flat-chested  individuals  whose  thorax  is  normally 
held  in  the  position  of  exaggerated  expiration  (see  page  697). 


BIBLIOGRAPHY.. 

General  Principles  in  the  Treatment  of  Cardiac  Diseases. 

Erlanger  and  Hooker.     Quoted  on  page  54. 

Winternitz  and  da  Silva.    Quoted  from  Buxbaum,  Lehrbuch  der  Hydrotherapie,  Leipz., 

1903. 
Widal,  F.,  and  Javal,  A.:  La  cure  de  dechloruration;  son  action  sur  l'cedeme,  sur  l'hydra- 

tation  et  sur  ralbuminurie  a  certaines  periodes  de  la  nephrite  epitheliale,  Bull,  et 

mem.  Soc.  Med.  d.  hop.  de  Par.,  1903,  3  s.,  xx,  733. 
Widal,  F.,  and  Lemierre:  Pathogenie  de  certaines  cedemes  brightiques;  action  du  chlorure 

de  sodium  ingere,  ibid.,  1903,  3  ser.,  xx,  678. 
Widal,  F.:  Die  Kochsalzentziehungskur  in  der  Brightschen  Krankheit,  Verhand.  d.  Kong. 

f.  innere  Med.,  Wiesbaden,  1909,  xxvi,  43. 
Strauss,  H. :    Zur  Frage  der  Kochsalz  und  Fliissigkeitszufuhr  bei  Herz  und  Nierenkranken, 

Therap.  d.  Gegenwart,  Berl.-Wien,  1903,  N.  F.  v,  433;  Symposium  on  Therapeutics, 

Med.  News,  N.  Y.,  1903,  Ixxxiii,  673;  also  Die  Chlorentziehung  bei  Nierenund   Herz- 

wassersucht,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1909,  xxvi,  91. 
Die  Chlorentziehung  bei  Nieren-  und  Herzwassersucht,  Verhandl.  d.  Kong.  f.  innere  Med., 

Wiesbaden,  1909,  xxvi,  91. 


244  DISEASES  OF  THE  HEART  AND  AORTA. 

Richter,  P.  F.:     Experimentelles    ueber  Nierenwassersucht,  Berl.  klin.  Wchnschr.,  1905, 

xlii,  384. 
Barie,  E.:  The  Dechloridation  Treatment  in  Diseases  of  the  Heart,  Internat.  Clin.,  Phila., 

1906,  16th  ser.,  i,  26.    Cf.  also  Symposium  in  Verhandl.  d.  Kong.  f.  innere  Med., 

Wiesb.,  1909,  xxvi. 
Karell,  quoted  from  Romberg. 

Hoffmann,  F.  A.:  v.  Leyden's  Handbuch  der  Ernahrungstherapie,  1898,  i,  579. 
Jacoby,  L.:  Ueber  die  Bedeutung  der  Karellkur  bei  der  Beseitigung  schwerer  Kreislauf- 

storungen  und  der  Behandlung    der    Fettsucht,  Munchen.  med.  Wchnschr.,  1908, 

lv,  839. 
Hirschfeld,   F.:  Die  Karell'sche  Milchkur  und  die  Unterernahrung  bei  Kompensations- 

storungen,  ibid.,  1908,  lv,  1587. 

Massage  and  Electricity. 

Cautru,  F. :  Action  du  massage  cardioabdominal  sur  le  travail  relatif  du  cceur,  Rev.  de 

therap.  med.-chir.,  Par.,  1909,  lxxvi,  73;  and  Bull.  gen.  de  therap.,  Par.,  1909,  clvii,  127. 
Studzinski:  Zur  Frage  der  Bauchmassage  bei  Herzkrankheiten,  Zentralbl.  f.  innere  Med., 

Leipz.,  1909,  xxx,  641. 
Zabludowski,  J.:  Technik  der  Massage,  2d  ed.,  Leipz.,  1903. 
Selig,  A.:  Klinische  Beobachtungen  ueber  Herzvibration,  Therap.  Monatsh.,  Berl.,  1907, 

xxi,  204;  and  Berl.  klin.  Wchnschr.,  1907,  xliv,  804. 
Rimbach :  Orthodiagraphischer  Nachweis  der  Einwirkung  der  Herzmassage  auf  die  Grosse 

des  Herzens  und  die  Weite  der  Aorta,  Verhandl.  d.  Kong,  f .  innere  Med.,  Wiesbaden, 

1908,  xxv,  329;  and  Discussion  by  Selig. 
Hirschf elder,  J.  O.:  Personal  communication. 
Zimmern,  A.,  and  Riffaut:  Note  sur  un  malade  ayant  presente  sous  l'influence  du  courant 

de  haute  frequence  (lit  condensateur)  un  abaissement  notable  de  la  pression  aterielle, 

Arch,  d'electric.  med.,  Bordeaux,  1909,  xvii,  803. 

Surgical. 

Gibson,  G.  A.:  The  Relief  of  Cardiac  Enlargement  by  Surgical  Methods,  Edinb.  M.  J., 

1910,  N.  S.,  v,  293. 
Morison,  A.:  On  Thoracostomy  in  Heart  Disease,  Lancet,  Lond.,  1908,  ii,  7. 
Hill,  L.,  and  Flack,  M.:  Oxygen  in  Muscular  Exercise  and  as  a  Form  of  Treatment,  Brit. 

M.  J.,  Lond.,  1908,  ii,  967. 
Mackenzie:  Diseases  of  the  Heart,  N.  Y.,  1910,  2d  ed.,  p.  278. 
Allbutt,  Sir  T.  C:  Article  on  Diseases  of  the  Circulation  in  Musser  and  Kelly's  Modern 

Treatment,  Phila.,  1911. 
Herz,  M.:  Sauerstoffbehandlung  bei  Herzkrankheiten,  Prager  med.  Wchnschr.,  1909. 
Ewart,  W. :  On  the  Prebalnear  Treatment  of  Heart  Disease  by  Inhalations  of  CO2,  and  on 

the  Uses  of  the  Inhalations  in  Cardiac  Dyspnoea  and  Anginoid  Pain,  Brit.  M.  J., 

Lond.,  1899,  ii,  1178;  A  Simple  Method  for  the  Therapeutic  Inhalation  of  Carbonic 

Acid  Gas,  ibid.,  1911,  ii,  805. 
Kuhn,   E.:  Die  Anwendung   der   Lungensaugmaske  bei   Lungen  Kranken,   Blutarmut, 

Asthma,  Herzschwache,  und  Schlaflosigkeit,  Zusammenfassende  Ergebnisse  aus  der 

Literatur  und  Praxis,  Therap.  Monatsh.,  Berl.,  1910,  xxiv,  487;  also  Die  Behandlung 

der  Herzschwachezustanden  und  Stauung  im  Venengebiete  durch  negativen  Druck 

in  der  Brusthohle,  Verhandl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1911,  xxviii,  206. 
Albrecht,  E.:  Ueber  einseitige  Druckanderung  der  Lungenleft  als  Hilfsmittel  fur  Diagnose 

und  Therapie  von  Herzerkrankungen,  ibid.,  1911,  xxviii,  201. 
Gerhardt,  D.:  Discussion  of  foregoing  papers,  ibid.,  1911,  xxviii,  208. 
Morelli,  Ueber  die  wirkung  der  Kuhnsche  Lungensaugmaske  bei  Herzkrankheiten,  Ztschr. 

f.  klin.  Med.,  Berl.,  1909,  lxvii. 
Bruhl,  W.:   Ueber  die  Einatmung  verdunnter  Luft  in  ihrer  Wirkung  auf  den  Kreislauf 

und  das  Herz,  Thesis,  Marburg,  1911. 
Zabel,  quoted  from  Kuhn. 


V. 
THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE. 

It  does  not  lie  within  the  scope  of  this  work  to  enter  into  a  detailed 
discussion  of  the  pharmacology  of  the  drugs  used.  The  reader  is  referred 
to  the  text-books  upon  this  subject,  especially — 

Cushny,  A.  R.:  A  Text-book  of  Pharmacology  and  Therapeutics,  Philadelphia  and 
New  York. 

Sollmann,  Torald  :  Text-book  of  Pharmacology. 

Hatcher,  R.  A.,  and  Wilbert,  M.:  The  Pharmacopoeia  and  the  Physician,  Chicago, 
1907  (published  by  the  American  Medical  Association). 

Meyer,  H.  H.,  and  Gottlieb,  R.:  Die  experimentelle  Pharmakologie  also  Grundlage 
der  Arzneibehandlung,  Berl.,  1910. 

Brunton,  Sir  T.  Lauder:  Collected  Papers  on  Circulation  and  Respiration,  Lond.  and 
N.  Y.,  1907;  and  Therapeutics  of  the  Circulation,  Lond.,  1908. 

The  drugs  used  in  the  treatment  of  cardiac  disease  may  be  of  value 
through  their  action  on  the  following  systems: 

I.  Upon  the  Heart  Muscle — digitalis,  strophanthus,  strychnine,  squills,  caffeine. 
II.  Upon  the  Peripheral  Vessels — constrictors:   camphor,  strychnine,  adrenalin, 
ergot,  digitalis,  nicotine  (tobacco),  caffeine;  dilators:  amyl  nitrite,  nitroglycerin,  sodium 
nitrite,  erythrol  tetranitrate. 

1.  Acting  upon  the  Cardiac  Nerves. 

A.  Slowing  the  heart  through  stimulation  of  the  vagus:  aconite,  digitalis,  strophanthus, 
sometimes  strychnine  and  caffeine,  nicotine,  veratrum  viride,  muscarin,  very  large  doses  of 
potassium  salts,  bile  salts,  blood  in  jaundice. 

B.  Increasing  the  heart-rate  through  paralyzing  the  vagi:  atropine,  cocaine,  amyl  nitrite 
and  other  nitrites. 

C.  Increasing  rate  through  stimulation  of  accelerators:  adrenalin,  amyl  nitrite,  and 
other  nitrites. 

D.  Paralyzing  accelerators:    apocodein. 

2.  Diminishing  Venous  Pressure  and  Stasis  by  Depleting  Portal  System: 
purgative  series,  especially  calomel,  the  saline  and  the  vegetable  purgatives. 

3.  Drugs  which  Increase  the  Tonicity  of  the  Cardiac  Muscle  in  pharmaco- 
logical doses:  digitalis,  strophanthus,  strychnine,  amyl  nitrite,  nitroglycerin,  calcium 
chloride  (transitory  effect). 

4.  Drugs  which  Decrease  Tonicity:  potassium  salts,  chloroform,  formic  acid,  salt 
infusion,  ether,  adrenalin. 

Tonicity  is  practically  unaffected  by  small  doses  of  aconite,  though  slightly  diminished 
by  larger  ones. 

DIGITALIS. 

Foremost  among  the  drugs  used  in  treatment  of  circulatory  diseases 
are  the  preparations  of  digitalis,  introduced  into  medical  practice  by  Wither- 
ing in  1785.  He  says  of  it:  "In  the  year  1775  my  opinion  was  asked 
concerning  a  family  receipt  for  the  cure  of  the  dropsy.  I  was  told  that  it 
had  long  been  kept  a  secret  by  an  old  woman  in  Shropshire,  who  had  some- 
times made  cures  where  the  more  regular  practitioners  had  failed.  .  .  . 
The  medicine  was  composed  of  twenty  or  more  different  herbs,  but  it  was 
not  very  difficult  for  one  conversant  in  these  subjects  to  perceive  that 

245 


246  DISEASES  OF  THE  HEART  AND  AORTA. 

the  active  herb  could  be  no  other  than  the  foxglove.  ...  I  soon  found 
the  foxglove  to  be  a  very  powerful  diuretic.  .  .  I  use  it  in  ascites,  ana- 
sarca, and  hydrops  pectoris."  He  then  cites  the  results  obtained  in  the 
treatment  of  over  100  cases,  many  of  which  would  be  worthy  of  modern 
therapeutics. 

Drugs  of  Digitalis  Series.1 — Digitalis,  strophanthus,  apocynum,  convallaria  majalis, 
squill  (scilla),  erythropholceine,  helleborein,  antiarin  (antiaris  toxicara). 

Digitalis  consists  of  the  dried  leaves  of  Digitalis  'purpurea  collected  from  the  plant 
at  the  commencement  of  the  second  year's  growth.  It  should  not  be  kept  more  than  one 
year.    Average  dose  pulv.  digitalis  =0.05  Gm.  (1  grain). 

Preparations.  Dose. 

Gram.  English. 

Fluidextractum  digitalis 0.05  T»l  1 

Extractum  digitalis 0.01  gr.  1/5 

Infusum  digitalis 

(1.5%  digitalis+10%  alcohol+15%  cinnamon  water) 8.00  Z  u 

Tinctura  digitalis 1-00  "Ixv 

(10%  of  crude  digitalis  in  dil.  alcohol) 

A  very  satisfactory  form  for  administering  digitalis  and  a  purgative  at  once  is  Addi- 
son's (or  Niemayer's)  pill,  made  up  according  to  the  following  prescription: 

Pulvis  digitalis  1  -- 0.6  gr.  x 

Pulvis  scute.  .  J 

Hydrarg.  chloridi  mit 0.08  gr.  1  1/4 

M.  fiat  in  pil.  x  seu  capsulas  x. 
Sig.     One  pill  every  three  hours. 

The  calomel  may  be  increased  to  gr.  x,  or  may  be  replaced  by  blue-mass  (massa 
hydrarg.)  or  gray  powder  (hydrargyrum  cum  creta)  in  capsules. 

The  efficacy  of  Addison's  pill  depends  upon  the  care  taken  to  secure  an  active  prepa- 
ration of  digitalis  in  making  it.  Moreover,  its  action  may  be  uncertain,  owing  to  the  fact 
that  a  certain  amount  of  digitalis  is  eliminated  with  the  stool  without  having  been  absorbed. 

Derivatives  of  Digitalis. — Digitoxin — the  most  active  substance  derived  from 
digitalis,  producing  all  the  digitalis  effects;  soluble  in  alcohol;  insoluble  in  water,  except 
in  the  presence  of  digitonin.  Prepared  in  soluble  form  with  digitonin  under  the  trade  name 
"Digalen"  (Cloetta).     "Digalen,"  dose  1  c.c. 

Digitalin  (digitalinum  verum  Kiliani) — a  white  amorphous  glucoside,  less  toxic  than 
digitoxin  but  otherwise  resembling  it  in  physical  properties  and  pharmacological  action. 
Dose  2-6  mg.  (gr.  aWo)- 

Roughly,  digitoxin  is  six  times  more  potent  than  an  equal  weight  of  digitalinum  verum 
(Fraenkel). 

Digitalin  "German" — amorphous  powder,  soluble  in  water  and  alcohol;  a  mixture 
of  pure  digitalin,  digitalein,  and  digitonin.    Dose  2-6  mg.  (gr.  %0-Ko). 

Digitalein  and  digitonin  are  other  somewhat  similar  substances,  the  latter  of  which  is 
a  saponin-like  body  which  has  little  pharmacological  action. 

Digipuratum  (Extractum  digitalis  depuratum),  prepared  free  from  digitonin  accord- 
ing to  Gottlieb's  formula,  contains  digitoxin  and  digitalin,  and  is  soluble  in  alkalies  but 
insoluble  in  water  and  in  acids.  It  is  said  to  be  less  prone  to  produce  nausea  than  the 
other  digitalis  preparations  and  is  of  very  constant  strength. 

Strophanthus — the  ripe  seeds  of  Strophanthus  Kombe.  Tinctura  strophanthi,  10 
per  cent,  of  the  drug  in  65  per  cent,  alcohol.    Dose  0.5  c.c.  (n\,viii). 

standardization  of  digitalis  preparations. 

The  chief  point  to  be  considered  in  the  choice  of  digi- 
talis preparations  is  to  obtain  a  preparation  of  uniform 
strength.     Digitalis  leaves  even  of  the  second  year's  growth  vary  greatly  in  the  amount 

1  A  very  full  discussion  of  these  drugs  is  given  in  Cushny's  article. 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.         247 

of  the  active  principles  which  they  contain,  as  well  as  in  the  stability  of  the  latter,  for  the 
leaves  contain  enzymes  which  break  up  the  digitalis  glucosides.  In  order  to  obviate  this 
the  leaves  must  be  dried  at  a  moderate  heat,  and  kept  in  a  dry,  dark  place. 

In  order  to  keep  the  leaves  permanently  Max  Winckel  has  devised  a  process  whereby 
these  enzymes  are  said  to  be  completely  destroyed.  Age  in  itself  is  not  always  an  objec- 
tion, for  Hale  has  found  leaves  over  eight  years  old,  kept  in  a  paper  bag,  which  were  of 
about  the  same  strength  as  recently  purchased  leaves. 

The  strength  of  digitalis  preparations  may  be  estimated 
either  chemically  or  by  their  action  on  animals.  The  chemical 
assay  is  based  on  rather  uncertain  quantitative  determinations  of  the  digitoxin,  and  does 
not  always  show  a  parallelism  to  the  activity  of  the  drug,  since  the  latter  may  also  be  due 
to  the  digitalin  and  digitalein  contained. 

The  action  of  the  drug  on  animals  may  be  tested  in  several  ways,  and  among  different 
observers  there  is  still  some  uncertainty  as  to  which  method  should  be  pursued.  The 
activity  may  be  tested  on  frogs,  in  which  the  action  is  mainly  on  the  heart  muscle,  or  on 
mammals,  in  which,  as  in  man,  the  central  nervous  system  is  also  brought  into  play.  In 
frogs  the  activity  has  been  tested  upon  the  excised  heart,  the  exposed  heart  (Focke),  and 
upon  the  intact  animal.  The  latter  seems  not  only  easiest  but  most  satisfactory.  Hough- 
ton (of  Parke,  Davis  &  Co.)  recommends  using  as  a  standard  the  dose  per  gramme  of  frog 
which  kills  the  animal  in  twelve  hours  after  injection  into  the  dorsal  lymph-sac.  Worth 
Hale,  in  a  very  exhaustive  study,  decides  in  favor  of  the  method  of  Famulener  and  Lyons, 
in  which  the  standard  dose  (per  gramme  of  frog)  is  that  which, 
when  injected  through  the  mouth  into  the  anterior  lymph- 
sac,  brings  the  ventricle  to  a  condition  of  permanent  sys- 
tole at  the  end  of  exactly  one  hour.  This  method  is  the  easiest  to  carry 
out,  and  requires  only  a  small  number  of  ordinary  and  healthy  medium-sized  frogs  about 
30  G.  (one  ounce)  in  weight.    Each  assay  should  cost  about  fifty  cents. 

Dose  of  digitalis  when  diluted  to  tincture  strength,  per  gramme  of  frog,  0.024-0.030  mg. 

Hatcher  prefers  cats,  for  strophanthus  at  least,  using  as  his  criterion  the  dose  of 
strophanthin  (diluted  vshxsu  with  0.6  per  cent.  NaCl)  which  will  kill  a  cat  within  an  hour 
after  intravenous  injection.  Rowntree  and  Macht  (Jour  Am.  Med.  Assoc,  1916,  lxvi,  870) 
inject  10  c.c.  infusion  of  digitalis  per  Kg.,  then,  5  min.  later,  1  c.c.  every  two  minutes  until 
death  ensues.  This  is  the  easiest  method  to  carry  out  and  gives  quite  constant  results,  6  to 
8  c.c.  per  Kg.  cat  representing  the  lethal  dose  the  best  foreign  digitalis  and  for  the  leaves  of 
digitalis  grown  at  the  medicinal  plant  gardens  of  Wisconsin. 

Morris  finds  the  same  values  for  digitalis  grown  at  Minnesota  but  finds  that  digitalis 
lutea  causes  less  irritation  than  digitalis  purpurea  though  possessed  of  the  same  activity 
and  toxicity.1 

For  the  history  of  digitalis  and  its  uses  see: 
Brunton,  T.  Lauder:  On  Digitalis,  with  some  Observations  on  the  Urine  (Thesis  presented 

to  Edinburgh  University,  1866),  Lond.,  1868;   also  Collected  Papers  on  Circulation 

and  Respiration,  1st  ser.,  Lond.  and  N.  Y.,  1907,  p.  30. 
Winckel,   Max:    Ueber  den  Wert  der  frischen  Folia  Digitalis  und  ihre  Konservierung, 

Muenchen.  med.  Wchnschr.,  1911,  lviii,  575. 
Hale,  Worth :  Digitalis  Standardization  and  the  Variability  of  Crude  and  of  Medicinal  Prep- 
arations, Bull.  No.  47,  Hyg.  Lab.  U.  S.  Pub.  Health  and  Mar.  Hosp.  Serv.,  Wash.,  1911. 
Pratt,  J.  H.:  The  Potency  of  Digitalis  Preparations,  Boston  M.  and  S.  J.,  1910,  clxiii,  279. 
Famulener  and  Lyons:  Proc.  Assoc.  Am.  Pharm.  Assoc,  1902,  i,  415,  quoted  from  Hale. 
Hatcher,  R.  A.,  and  Bailey,  H.  C:   Tincture  of  Strophanthus  and  Strophanthin,  J.  Am. 

M.  Assoc,  Chicago,  1909,  lii,  5;  and  Hatcher,  R.  A.:    Note  on  Strophanthin,  ibid., 

1910,  liv,  1954. 

Strophanthus. — According  to  the  United  States  Pharmacopoeia,  strophanthus  is 
prepared  from  the  ripe  seeds  of  strophanthus  kombe;  but  Wilbert  states  that  the  latter 
is  practically  out  of  the  market  and  is  largely  replaced  by  strophanthus  hispidus  and  stro- 
phanthus gratus.  The  active  principle  of  strophanthus  kombe  and  strophanthus  hispidus  is 
strophanthin  (methylouabain),  while  that  of  strophanthus  gratus,  the  probable  source  of 
"crystalline  strophanthin,"  is  ouabain,  a  substance  twice  as  toxic  as  strophanthin.  A 
closely  related  substance,  acocantherin,  derived  from  the  wood  of  the  acocanthaceae,  is 
dimethylouabain  and  is  about  one-fourth  as  toxic  as  ouabain. 

lR.  E.  Morris:    Personal  communication. 


248  DISEASES  OF  THE  HEART  AND  AORTA. 

Squill. — The  sea-onion  (scilla  maritima)  deprived  of  its  dry  membranaceous  outer 
scales  and  cut  into  thin  slices.    Dose,  0.05-0.2  G.  (gr.  i  to  hi)  in  pills. 

Acetum  scillse  (U.S.P.,  B.P.).    Dose  1-2  c.c.  (n\.  xv  to  xxx). 

Apocynum  Cannabinum  (the  dried  rhizome  of  Canadian  hemp). 

Fluidextractum  apocyni,  U.S. P.  (extract  made  in  10  per  cent,  glycerin,  60  per  cent, 
alcohol,  and  30  per  cent,  water).    Dose  1  c.c.  (n\  xv). 

Convallaria.  The  dried  rhizome  and  roots  of  Convalleria  majalis  (lily  of  the  valley) . 
Dose  0.5  G.  (gr.  viii). 

Fluidextractum  convallarise.     Dose  0.3  c.c.     (rt\viii). 

Euonymus  (U.S. P.),  Euontmi  Cortex  (B.P.). — The  bark  of  the  roots  of  the  Wahoo. 

Euonymus  atropurpureus,  U.S. P.,  Extractum  Euonymi  0.05  to  0.2  G.  (gr.  i  to  hi) 
B.P.  Extractum  enonymi  siccum  0.05  to  0.15  G.  (gr.  i  to  hi). 

Other  drugs  having  a  similar  action  but  not  in  the  Pharmacopoeia  are: 

Erythrophlceum,  the  bark  of  the  casca  or  sassy  bark  (erythrophlceum  guiniense). 

Helleborus  niger  (the  Christmas  rose) — not  the  white  hellebore;  the  pheasant's  eye 
(adonis  vernalis);  the  upas  (Antiaris  toxicaria),  the  Acocantheria,  Thevetia  grandiflora, 
and  coronilla;  also  substances  isolated  from  the  skin  of  frogs  (phrynin  Faust)  and  bufagin 
(Abel  and  Macht). 

Derivative  and  Active  Principle. — Strophanthin  (methyl  ouabain) — a  white  crystalline 
glucoside  of  constant  composition  and  action,  soluble  but  undergoing  decomposition  in 
water.    Hence  best  prescribed  in  dilute  alcohol. 

EFFECT   OF   DIGITALIS   ON    THE   NORMAL   HEART. 

Fraenkel  and  Schwartz  and  also  Cloetta  have  shown  that  in  therapeutic 
doses  digitalis  has  no  effect  upon  the  normal  heart,  either  in  affecting  the 
strength  of  the  beat  or  in  bringing  about  hypertrophy.  Neither  has  it  any 
effect  upon  the  perfectly  compensated,  undilated  heart  with  a  valvular 
lesion.  Its  chief  effects  are  seen  in  dilated  hearts  whose  myocardium  still 
retains  some  reserve  power  and  in  cases  of  auricular  fibrillation.  In  the 
severest  stages  of  cardiosclerosis  and  fatty  degeneration  it  may  stimulate 
the  fibres  beyond  the  limit  of  their  power,  and  thus  do  actual  harm,  and 
even  hasten  the  end. 

GENERAL   ACTION   OF   DIGITALIS. 

Drugs  of  the  digitalis  series  affect  the  heart  through  their  action  on  three 
separate  structures, — the  vagi,  the  cardiac  muscle,  and  the  vasoconstrictors. 

There  is  some  evidence  that  the  action  of  digitalis1  upon  the  heart  muscle 
is  due  to  a  definite  chemical  combination  with  the  latter,  uniting,  as  Schlio- 
mensun  has  claimed,  with  the  phosphatid  fraction  (cuorin).  Karaulow  has 
shown  that  the  digitonin  is  detoxified  by  cholesterin,  but  that  digitoxin, 
digitalin,  and  strophanthin  are  not. 

Action  of  Therapeutic  Doses. — In  ordinary  therapeutic  doses  by  mouth 
the  effect  of  digitalis  does  not  assert  itself  for  24  to  72  hours,  though  it  may  set 
in  immediately  after  intravenous  or  very  soon  after  intramuscular  injections. 

In  bringing  about  the  usual  therapeutic  effects  the  pulse-rate  becomes 
slower  (Withering),  the  contractions  larger  and  more  forcible  (Traube  and 
Lauder  Brunton),  and  the  tonicity  of  the  heart  muscle  is  increased  (Cushny, 
Cameron),  so  that  the  quantity  of  residual  blood  in  the  ventricles  is  dimin- 
ished and  dilatation  of  the  heart  is  lessened. 

1  For  convenience  the  action  of  digitalis  as  prototype  of  the  digitalis  series  is  discussed 
in  detail,  and  the  differences  in  the  actions  of  the  various  members  of  the  series  will  be 
discussed  later. 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.  249 

Very  often,  as  H.  Turnbull  in  Mackenzie's  clinic  has  pointed  out,  a 
sinus  or  neurogenic  arrhythmia  (instability  of  rhythm)  sets  in  from  inter- 
mittent action  of  the  over-stimulated  vagi,  so  that  the  originally  rapid  rate 
of  the  heart  may  change  to  a  slow  one  with  irregularity  in  which  short  series 
of  rapid  beats  alternate  with  short  series  of  slow  ones,  showing  a  normal 
("  double  ")  venous  pulse. 

The  beneficial  action  of  the  digitalis  is  brought  about  through  increasing 
the  force  of  the  heart-beat  and  the  tonus  of  the  muscle, — the  one  leading  it 
to  drive  out  more  blood  with  each  beat,  the  latter  preventing  it  from  over- 
filling in  diastole,  both  effects  tending  to  diminish  dilatation. 

The  effect  of  digitalis  upon  the  coronary  circulation  is  somewhat  uncer- 
tain, for  Oswald  Loeb  found  that  it  diminished  the  blood-flow  through  the 
coronary  vessels  in  the  excised  heart;  but  G.  S.  Bond,  in  the  writer's  labora- 
tory, demonstrated  that  with  the  heart  in  situ  the  flow  is  increased  after 
digitalis  and  strophanthin  throughout  the  period  during  which  the  general 
blood-pressure  is  elevated. 

These  effects  are  produced  chiefly  through  stimulation  of  the  vagus, 
and  may  be  prevented  in  animals  by  a  section  of  the  vagi  (Traube  and  Lauder 
Brunton)  and  by  the  administration  of  atropine  (Cameron). 

In  animal  experiments,  and  usually,  but  not  always,  in  human  beings, 
there  is  a  moderate  rise  in  blood-pressure,  due  (Blake,  1839,  Traube,  1861, 
and  Lauder  Brunton,  1866)  in  part  to  constriction  of  the  peripheral  arteries. 

In  man  this  rise  in  blood-pressure  may  or  may  not  be  present,  and,  as 
Mackenzie  states,  excellent  results  may  be  obtained  in  many  cases  without 
any  change  in  the  blood-pressure  whatever. 

Toxic  Effects. — While  these  effects  represent  the  favorable  action  of 
digitalis,  larger  doses  give  rise  to  real  disturbances  in  the  heart's  action. 
These  effects  fall  into  four  categories: 

(1)  Weakening  in  the  contractile  power  of  the  heart,  as  shown  by  the 
onset  of  a  pulsus  alternans. 

(2)  A  partial  or  complete  blocking  of  the  impulses  passing  from  auricle 
to  ventricle  (digitalis  heart-block) ;  and 

(3)  The  onset  of  paired  beats  due  to  the  genesis  of  ventricular  extra- 
systoles. 

(4)  Of  a  rapid  heart-rate  arising  independently  in  the  ventricle  (ventric- 
ular tachycardia).  Dependent  upon  a  variety  of  conditions,  either  of  these 
effects  may  predominate,  or  both  may  coexist,  especially  in  the  severer 
degrees  of  poisoning. 

The  mildest  of  all  these  effects,  the  onset  of  an  alternating  pulse  (pulsus 
alternans),  gives  no  clinical  manifestations  save  a  slight  feeling  of  general 
weakness  corresponding  to  a  diminution  in  the  strength  of  alternate  beats 
of  the  heart,  which  are  well  shown  upon  the  sphygmogram.  Cases  of  this 
sort  have  been  reported  by  Guillaume  and  Mackenzie,  in  the  former  of  which 
it  was  associated  with  occasional  blocking  of  impulses  at  the  auriculoven- 
tricular  bundle. 

Heart-block  resulting  from  large  doses  of  digitalis  have  been  reported 
by  Cushny,  v.  Tabora,  and  Erlanger  in  animals,  and  by  Mackenzie,  Hewlett, 
and  Rihl  in  man.  The  stage  most  frequently  encountered  clinically  is  a 
sudden  halving  of  the  ventricular  rate  and  pulse-rate  without  change  in  the 


250  DISEASES  OF  THE  HEART  AND  AORTA. 

rate  of  the  auricles  (2  :  1  rhythm)  as  shown  by  the  pulse  or  electrocardio- 
gram. This  represents  a  state  of  partial  block,  which  in  most  cases  may  be 
promptly  relieved  by  injection  of  atropine  0.5  to  1.0  mg.  (gr.  Tl  o  to  ex)  and 
passes  off  soon  after  the  digitalis  is  discontinued  (Cushny,  Morris  and  Sil- 
berberg,  Heart,  1912-1913,  iv,  33).  In  animal  experiments  with  larger  doses 
the  block  becomes  complete  and  can  no  longer  be  relieved  by  atropine,  for 
not  only  the  vagus  (especially  the  left  vagus)  but  also  the  fibres  of  the  His 
bundle  have  been  acted  on  by  the  poison.  Hirschfelder  (Jour.  Pharmacol, 
and  Exper.  Therap.,  1915,  vi,  597)  has  shown  that  if  the  auricular  stimulus  is 
increased  by  increased  electrical  stimulation  impulses  otherwise  blocked  by 
digitalis  will  pass  down  the  His  bundle.  The  degree  of  block  thus  depends 
upon  the  intensity  of  stimulation. 

Mackenzie  has  encountered  a  number  of  cases  in  which  the  administra- 
tion of  digitalis  gave  rise  to  absolute  arrhythmia  with  auricular  fibrillation. 

While  these  phenomena  are  going  on  at  the  supraventricular  levels  of 
the  heart,  changes  are  also  taking  place  in  the  properties  of  the  ventricular 
muscle  itself,  which  manifests  a  gradually  increasing  tendency  toward  initiat- 
ing an  independent  rhythm. 

The  onset  of  paired  beats  due  to  ventricular  extrasystoles  may  be  re- 
garded as  the  first  sign  of  overaction  of  digitalis.  Ritchie  and  Cowen  believe 
that  the  latter  arise  on  account  of  increased  pressure  within  the  ventricle 
during  diastole,  especially  in  slow  hearts,  just  as  they  may  arise  when  the 
aorta  or  pulmonary  artery  is  clamped;  and  that  the  undue  irritability  of  an 
enfeebled  heart  tends  to  increase  this  tendency.  Some  doubt  is  thrown  upon 
this  theory  by  the  experiments  of  Brandenburg,  Straub,  and  di  Cristina,  who 
have  shown  experimentally  that  digitalis  actually  tends  to  diminish  the  car- 
diac irritability  and  that  stimuli  which  give  rise  to  extrasystoles  before  the 
injection  of  digitalis  are  ineffectual  after  it.  Another  theory,  which  is  very 
suggestive  but  by  no  means  proved,  has  been  advanced  by  Cushny.  Cushny 
has  supposed  that  the  occasional  extrasystoles  represent  the  periodic  mani- 
festations of  an  independent  rhythm  arising  in  the  ventricles  themselves, 
just  as  is  seen  in  complete  block.  According  to  this  view,  the  condition  would 
correspond  to  a  pararrhythmia  in  the  sense  of  Wenckebach.  Both  the  im- 
pulses from  the  auricles  and  those  arising  in  the  ventricles  are  conceived  as 
effective,  but  the  one  which  becomes  active  first  at  the  end  of  the  refractory 
period  gives  rise  to  the  next  beat. 

This  stage  of  digitalis  action,  like  all  severe  forms  of  arrhythmia,  is  accom- 
panied by  a  corresponding  retardation  of  the  circulation,  so  that,  unless  com- 
pensated by  still  further  vasoconstriction,  a  fall  in  blood-pressure  ensues. 

The  onset  of  either  of  these  disturbances,  whether  heart-block  or  the 
extrasystoles,  shows  that  the  action  of  the  drug  has  been  too  severe,  the 
extrasystoles  being,  as  a  rule,  less  disconcerting  than  the  heart-block.  Both, 
as  a  rule,  pass  off  within  a  day  or  two  after  the  drug  has  been  discontinued; 
although  palpitation  may  persist  a  great  deal  longer. 

In  the  third  stage  of  digitalis  action,  termed  by  Cushny  the  stage  of  inco- 
ordination, a  complete  block  occurs  between  the  auricles  and  the  ventricles, 
probably  owing  to  a  toxic  action  upon  the  fibres  of  the  His  bundle.  The 
auricles  still  beat  very  slowly  under  the  influence  of  the  vagi,  but  the  ventricles 
beat  at  an  independent  rhythm.     As  the  action  of  the  drug  becomes  more 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.         251 

and  more  pronounced,  this  rhythm  tends  to  increase  in  rapidity,  so  that  the 
condition  of  the  heart  at  this  stage  may  be  summarized  as  auricular  inhi- 
bition, complete  heart-block,  and  ventricular  tachycardia.  While  this  repre- 
sents the  end  stage  of  digitalis  poisoning  as  seen  in  animals,  it  is  not  commonly 
observed  in  man,  but  a  case  has  been  reported  recently  by  Hewlett  and  Bar- 
ringer  in  which  this  form  of  irregularity  was  encountered  shortly  before  death 
in  a  man  who  had  received  rather  large  doses  of  digitalis,  apocynum,  and 
strophanthus. 

Effect  of  Digitalis  on  the  Electrocardiogram.— Cohn  and  Fraser  (Jour. 
Exper.  Med.,  1915,  xxi,  592)  have  shown  that  an  appreciable  lengthening  of 
the  P :  R  interval  (a-c  interval  on  the  venous  pulse)  can  be  noted  before  the 
overaction  of  digitalis  begins  to  assert  itself  and  that  the  inversion  of  the 
T  wave  is  a  common  effect  of  digitalis.  The  physical  mechanism  of  the 
phenomenon  is  not  explained. 

In  frogs  and  in  cold-blooded  animals  the  ventricle  never  relaxes  and  the 
heart  ceases  beating  tightly  contracted  in  systole;  but  in  mammals,  perhaps 
owing  to  asphyxia  of  the  muscle,  the  great  increase  in  tone  is  lost  shortly 
before  death,  and  the  heart  dies  in  diastole,  unless,  as  Gottlieb  has  shown, 
large  doses  of  calcium  are  given  along  with  the  digitalis. 

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Jl  b  g  d  e 

Fig.  130. — Tracings  showing  the  action  of  digitalis  upon  the  dog's  blood-pressure.  (After  Cushny.) 
A,  normal;  B,  therapeutic  stage,  with  increased  blood-pressure  and  moderate  slowing  of  the  pulse,  but 
quickened  blood-flow;  C,  excessive  inhibition,  causing  low  blood-pressure  and  slowed  circulation;  D,  still 
further  slowing,  with  slight  arrhythmia;  E,  third  stage,  irregularity  with  further  rise  of  blood  pressure 
from  excessive  vasoconstriction. 

Effect  on  the  BIood=Pressure. — T  he  rise  of  blood-pressure 
due  to  digitalis  is  in  part  due  to  the  increased  force 
and  output  of  the  heart,  in  part  to  the  constric- 
tion of  the  peripheral  and,  especially,  the  abdomi- 
nal blood-vessels.  The  velocity  of  blood  flow  (as  shown  by  product 
of  pulse-pressure  X  pulse-rate)  is  usually  increased  when  this  effect  is  brought 
about  (Fellner,  Fraenkel).  Strophanthus  causes  less  vasoconstriction  than 
digitalis,  and  hence  usually  affects  the  minimal  pressure  less  than  the  maxi- 
mal, but  increases  the  velocity  of  blood  flow  without  causing  so  great  a  strain 
upon  the  heart.  Unfortunately,  the  preparations  of  strophanthus  are  less 
reliable  for  continuous  action. 


252 


DISEASES  OF  THE  HEART  AND  AORTA. 


Occasionally  it  is  found  that  both  digitalis  and  strophanthus  actually 
lower  the  maximal  blood-pressure.  This  occurs  especially 
in  the  cases  where  the  circulation  through  the  medullary  centres  is  impaired 
by  venous  stasis  or  arteriosclerosis,  or  failure  of  the  heart,  and  the  high 
blood-pressure  is  merely  the  result  of  general  reflex  vasoconstriction  from 
the  ischsemia  of  the  centre  (high-pressure  stasis).     When  the  force  of  the 

heart  is  increased  and  the  blood  passing 
through  the  centre  is  better  aerated,  the 
vasoconstrictor  influence  is  no  longer  ex- 
erted and  the  general  blood-pressure  then 
falls. 

Effect  of  Digitalis  on  Tonicity. — C 1  i  n  - 
ically  the  most  important  action 
of  digitalis  is  its  effect  upon  the 
tonus  of  the  cardiac  muscle,  in 
preventing  and  in  overcoming  dilatation, 
and  it  is  in  dilated  hearts  that  the  bene- 
ficial action  of  digitalis  is  most  pronounced. 
Francois-Franck  (1882)  demonstrated  that 
the  administration  of  digitalis  did  away 
with  the  transitory  functional  tricuspid  in- 
sufficiency which  resulted  from  stimulation 
of  the  vagus.  Cushny  and  Cameron  have 
shown  marked  increase  in  tonicity,  as  shown 
by  diminution  in  cardiac  volume.  More- 
over, Cloetta  has  demonstrated  that  the 
prolonged  administration  of  digitalis  pre- 
vents the  heart  from  dilating  in  experi- 
mental aortic  insufficiency  (positive  intra- 
ventricular pressure  during  diastole).  The 
hearts  of  animals  which  have  been  treated 
with  digitalis  are  smaller  and  stronger  than 
those  which  have  not  been  so  treated  (see 
page  479).  Colbeck,  Gossage,  and  others 
have  also  emphasized  the  importance  of 
this  effect  on  cardiac  tonus. 


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Fig.  131. — Variations  in  blood-prea- 
Bure  in  a  patient  under  the  influence  of 
digitalis  and  nitroglycerin.  MAX,  maxi- 
mal blood-pressure;  MIN,  minimal  blood- 
pressure;  PP,  pulse-pressure;  PPXPR, 
pulse-pressure  X  pulse-rate ;  DISC.  DIG- 
ITALIS, discontinue  digitalis. 


Relation  of  Pulse-pressure  to  Symptoms  in  One  of  Fraenkel's  Cases. 


Time. 


Blood-pressure. 


Max.       Min. 


Pulse. 


Pulse-pressure 
X  Pulse-rate. 


Urine  in 
24  hours. 


Jan.  27,  10.30 
10.40 
10.45 
11.00 

Jan.  28 

Jan.  31 

Feb.    1  ..... 


268 
286 


260 


206 
206 


156 


92 

84 


1600 


5640 

7490 

1  mg.strophanthin  intravenously 
Diuresis  begins 

80       I        7904  6050 


Dyspnoea  increasing. 
Pulse  feels  larger. 


No  feeling  of  constric- 
tion.    Sleeps  well. 


(Edema  almost  disappeared. 

(Edema  completely  disappeared. 

Patient  makes  uninterrupted  recovery  with  no  further  medication. 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE. 


253 


SQUILLS  AND  STROPHANTHUS. 

The  other  members  of  the  digitalis  series  which  are  of  the  greatest  clinical 
importance  are  strophanthus  and  squills.  The  latter  is  of  some  value  in 
patients  whose  stomachs  do  not  tolerate  digitalis,  for  it  exerts  a  very  similar 
action  upon  the  heart,  but  has  less  tendency  to  produce  nausea  and  vomiting. 
It  is  also  given  along  with  digitalis  and  calomel  in  Addison's  (Niemeyer's) 
and  Mackenzie's  pills,  the  latter  of  which  is  preferable  on  account  of  the 
smaller  dosage. 

Strophanthus  possesses  all  the  actions  of  digitalis  except  that  it  causes 
considerably  less  vasoconstrictions  than  the  latter,  and  consequently  strength- 
ens the  heart  without  imposing  so  much  strain  upon  it. 


Vasoconstriction 


Vol.  Leg 


Fig.  132. — Effeet  of  digitalis  on  cardiac  tonicity  in  the  dog.  (Experiment  by  Dr.  Cameron.)  Upper 
curve,  volume  of  the  hind  leg,  taken  with  a  plethysmograph,  showing  vasoconstriction;  second  curve, 
volume  of  the  ventricles;  lower  curve,  blood-pressure  taken  with  the  Huerthle  membrane  manometer. 
Time  in  seconds.  A  small  dose  of  tincture  of  digitalis  injected  into  the  jugular  vein  at  the  arrow.  The 
effect  upon  tonicity,  T+,  outlasts  both  the  rise  in  blood-pressure  and  the  vasoconstriction. 


There  has  been  a  great  deal  of  discussion  regarding  the  activity  and 
toxicity  of  strophanthus  preparations,  and  a  number  of  cases  of  strophanthus 
poisoning  have  been  reported  on  the  one  hand  and  of  comparative  inactivity 
on  the  other. 

This  uncertainty  of  action,  as  Hatcher  and  Bailey  have  shown,  is  due 
to  the  fact  that  strophanthin,  the  active  principle,  is  absorbed  very  irregularly 
from  the  digestive  tract;  so  that  under  certain  circumstances  several  doses 
may  be  entirely  unabsorbed  in  the  intestine,  and  under  others  may  be  ab- 
sorbed with  fulminant  rapidity  and  four  or  five  times  the  usual  dose  may 
suddenly  become  active.  When  injected  intravenously  or  intramuscularly, 
however,  strophanthus  acts  with  great  regularity,  and  in  a  very  large  series 
of  experiments  by  Hatcher  and  Bailey  to  determine  the  toxicity  of  strophan- 
thin the  limit  of  variation  was  three  per  cent. 

Albert  Fraenkel  has  shown  that  very  striking  effects  may  be  obtained 
clinically  within  a  few  minutes  after  the  intravenous  injection  of  0.5  to  1  mg. 


254  DISEASES  OF  THE  HEART  AND  AORTA. 

(gr-  ih  to  ¥V)  of  amorphous  strophanthin  (of   Boehringer   or  Merck),  or 
about  one  half  that  dose  of  the  crystalline  strophanthin  (Thorns)  (ouabain?). 1 

An  example  of  Fraenkel's  remarkable  therapeutic  effects  may  be  quoted  here: 

Patient,  aged  57,  male,  admitted  to  Strassburg  Hospital  November  17,  1905.  Had 
rheumatic  fever  in  1869  and  again  in  1886.  Palpitation  when  at  work,  and  occasional 
swelling  of  legs  since  1900.    Drinks  considerably. 

Present  Condition. — Considerable  oedema  of  legs,  thighs,  and  scrotum.  Moderate 
ascites.  Dulness  and  diminished  breath  sounds  over  right  base.  X-ray  shows  heart  shadow 
enlarged  to  left  and  right:  dynamic  dilatation  of  aorta.  Pulse  irregular,  104  per  minute, 
maximum  pressure  180.  Pulv.  folia  digitalis  0.1  Gm.  (1J  gr.)  three  times  a  day  brought 
pulse  down  to  86  in  4  days,  to  76  in  6  days,  increasing  diuresis  from  2000  to  4500  and  5800 
respectively. 

Another  attack  of  pain  in  joints  on  December  1 ;  left  clinic  "improved"  on  December 
11.  Returned  January  25,  1906.  (Edema  as  before;  ascites  marked — abdomen  108  cm. 
in  circumference.  Liver  palpable  four  fingers'  breadth  below  costal  margin.  Spleen  pal- 
pable. Dulness  and  diminished  fremitus  over  base  of  right  lung.  Heart  dilated  more  than 
before;  impulse  not  palpable;  first  sound  at  apex  reduplicated;  second  accentuated,  espe- 
cially over  pulmonic  area.  Slight  gallop  rhythm.  Heart  action  rapid  and  regular.  Marked 
orthopncea  and  very  distressing  cough.    Patient  has  had  no  sleep  for  several  nights. 

The  following  table  shows  the  effects  of  the  intravenous  administration  of  strophan- 
thin upon  his  blood-pressure,  urine  output,  and  symptoms.  The  product  of  pulse-pressure 
and  pulse-rate  furnishes  a  very  rough  index  of  the  velocity  of  blood-flow. 

Fraenkel's  observations  have  been  confirmed  by  Otfried  Muller,  Fleisch- 
mann,  Bailey,  and  a  host  of  others;  and  strophanthin  may  be  said  to  have 
passed  the  experimental  stage  and  to  have  reached  general  clinical  use.  It 
may  be  given  either  as  one  or  two  single  doses  intravenously,  or,  when  pro- 
longed action  is  desired,  particularly  when  digitalis  is  not  well  borne,  it  may 
be  given  in  small  daily  doses  {\  to  |  mg.  crystalline  strophanthin,  Thorns) 
injected  very  deep  into  the  muscle.  The  site  of  injection  must  also  be  massaged 
for  a  few  minutes  after  the  injection. 

As  a  rule,  the  intravenous  injection  of  strophanthin  does  not  cause  any 
discomfort  to  the  patient;  but  if  the  injection  is  not  made  directly  into  the 
lumen  of  the  vein  and  any  of  the  fluid  enters  the  wall  or  the  perivascular 
tissues,  it  may  give  rise  to  considerable  pain.  Occasionally  the  injection 
may  be  followed  by  a  severe  chill  and  transitory  fever. 


CLINICAL   APPLICATION   OF   DRUGS   OF   THE    DIGITALIS   SERIES. 

Although  it  is  probably  true,  as  Wenckebach  has  put  it,  that  "  every 
man  has  his  own  way  "  of  using  digitalis,  it  may  be  said  in  general  that  digitalis 
should  be  given  for  dilatation  of  the  ventricles  and  fibril- 
lation of  the  auricles. 

As  was  already  shown  by  Withering,  it  is  the  drug  par  excellence  for  ascites, 
anasarca,  and  broken  compensation;  and,  when  these  conditions  are  met 

1  Difficulty  is  often  encountered  in  making  an  intravenous  injection,  either  because 
the  vein  is  small  or  because  it  slips  under  the  needle.  In  order  to  obviate  this,  J.  J.  Watson 
suggests  anchoring  the  vein  by  transfixing  it  with  an  ordinary  sewing  needle  thrust  through 
the  skin  and  the  wall  of  the  vein  and  partly  out  through  the  skin.  The  hypodermic  needle 
may  then  be  inserted  readily  into  the  vein,  the  injection  made  without  difficulty,  and  par- 
ticularly without  escape  of  strophanthin  into  the  perivascular  tissues. 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.         255 

with,  its  prompt  use  may  lead  to  almost  unhoped-for  improvement.  In 
these  cases  it  acts  in  part  by  its  direct  action  on  the  heart,  increasing  the 
strength  of  the  beat  and  tonicity  of  the  heart  muscle,  and  in  part  by  improv- 
ing the  circulation  through  limbs  and  kidneys  and  by  its  diuretic  action,  all 
of  which  become  important  factors  in  removing  oedema. 

Owing  to  the  marked  effect  in  increasing  cardiac  tonicity,  digitalis  and 
its  congeners  also  find  their  usefulness  in  all  cases  of  permanent  or  transitory 
dilatation  of  the  heart  before  the  trouble  has  gone  on  to  an  actual  break, 
whether  of  long  standing  or  acute.  There  is  no  reason  to  wait  for  loss  of 
compensation.  Dilatation,  in  itself,  accompanied  as  it  is  by  a  tendency  to 
easy  overstraining,  represents  a  condition  of  lowered  tonicity  and  is  best 
treated  by  digitalis.  No  better  examples  of  this  can  be  cited  than  the  excel- 
lent results  obtained  by  Da  Costa  in  the  overworked  soldiers  of  the  Civil 
War,  whom  digitalis  and  rest  promptly  returned  to  their  normal  strength. 

In  valvular  disease  digitalis  is  not  required  when  the  lesion  is  fully  com- 
pensated and  the  patient  free  from  symptoms,  but  it  should  be  used  vigor- 
ously whenever  symptoms  present  themselves  even  in  transitory  attacks. 

In  chronic  valvular  disease  with  broken  compensation  its  action  cannot 
always  be  prophesied,  for  in  certain  cases  the  expected  effect  may  be  entirely 
absent.  This,  as  Mackenzie,  Lewis,  and  Windle  have  shown,  is  especially 
true  in  cases  of  mitral  stenosis  with  rapid,  regular  heart-rate,  in  which  most 
probably  the  vagi  are  paralyzed  and  atrophied  and  in  which  the  action  of 
digitalis  on  ventricular  tonicity  is  of  minor  importance. 

The  experiments  of  Cloetta  and  Gelbart  would  indicate  that  in  early 
aortic  lesions,  even  when  apparently  compensated,  a  prolonged  treatment 
with  digitalis,  lasting  several  months,  increases  the  strength  of  the  heart 
and  does  much  to  safeguard  it  against  overstrain.  It  is  most  important, 
however,  to  guard  against  any  great  cumulative  action  of  the  drug  in  such 
cases.  After  the  first  few  days  of  treatment  the  single  doses  should  be  small, 
and  the  pulse  should  be  carefully  watched  for  the  onset  of  bradycardia  or 
arrhythmia. 

Digitalis  in  Arrhythmia. — As  has  been  seen,  the  usefulness  of  digitalis 
depends  upon  the  nature  of  the  arrhythmia.  In  cases  of  respiratory  arrhyth- 
mia it  is  not  needed  unless  the  heart  is  definitely  dilated,  and  indeed  it 
tends  to  exaggerate  this  form  of  arrhythmia  itself  through  its  action  upon 
the  vagi. 

The  action  in  heart-block  will  be  discussed  in  a  later  chapter  (page  585), 
but  in  general  it  may  be  stated  that  digitalis  is  definitely  contraindicated  in 
partial  heart-block  or  in  cases  with  delayed  conduction  (a-c  interval  on  the 
venous  pulse  or  P-R  interval  on  the  electrocardiogram  prolonged).  In 
complete  block,  however,  where  the  impulses  from  the  auricles  and  the  influ- 
ence of  the  vagi  no  longer  reach  the  ventricle,  the  experiments  of  Erlanger 
with  digitalis  and  the  clinical  experience  of  Bachmann  with  strophanthin 
and  of  Hewlett  and  Barringer  with  digitalis  indicate  that  drugs  of  this  series 
increase  the  automaticity  of  the  ventricle  and  thus  tend  to  prevent  the  cessa- 
tion of  the  pulse.  Up  to  the  present,  however,  too  few  cases  of  this  sort  have 
been  reported  for  the  exact  sphere  of  its  usefulness  and  its  limitations,  its 
indications  and  contraindications,  to  be  definitely  defined,  and  in  all  such 
cases  the  drug  should  be  used  with  caution. 


256  DISEASES  OF  THE  HEART  AND  AORTA. 

In  cases  of  alternating  pulse  digitalis  is  usually  indicated  to  increase  the 
force  of  the  contractions,  of  which  the  alternating  is  in  itself  an  expression 
of  weakness. 

Though  extrasystoles  from  increased  irritability  may  be  brought  on  by 
digitalis,  extrasystoles  in  a  dilated  heart  are  usually  relieved  by  it  in  .propor- 
tion to  the  relief  of  the  dilatation. 

It  is  in  the  absolute  arrhythmia  from  auricular  fibrillation  (arrhythmia 
perpetua,  formerly  designated  by  Mackenzie  as  "nodal  rhythm"),  however, 
that  digitalis  exerts  its  most  favorable  influence  (Mackenzie,  Lewis,  Cushny, 
Edens,  Windle).  In  this  condition  it  has  the  same  action  as  pressure  on  the 
vagus  (Wenckebach).  It  does  not  remove  the  irregularity,  except  when  this 
is  in  itself  of  transitory  duration;  but  it  shows  the  rate  of  the  ventricles,  either 
indirectly  through  inhibiting  the  fibrillation  of  the  auricles  which  are  the 
pacemakers,  or  by  depressing  the  conductivity  of  the  His  bundle  so  that  the 
feebler  impulses  generated  in  the  auricles  no  longer  reach  the  ventricles  and 
only  the  greater  stimuli  become  active.  It  is  only  in  rare  cases,  formerly 
termed  by  Mackenzie  "essential  bradycardia"  or  "nodal  bradycardia," 
that  this  blocking  becomes  complete,  but  in  the  ordinary  cases,  slow  irregular 
heart-rate  following  the  administration,  the  impulse  for  each  contraction  of 
the  ventricles  still  arises  in  the  auricles. 

Mackenzie,  Lewis,  and  Windle  have  shown  that  the  beneficial  action 
is  often  greatest  when  the  pulse-rate  is  rendered  extremely  slow  (50  to  60 
per  minute). 

In  order  to  obtain  this  result  large  doses  may  have  to  be  administered 
for  a  considerable  period  of  time,  and  the  patient  may  entirely  miss  the 
benefits  if  half-hearted  therapy  is  resorted  to.  Windle  estimates  that  from 
five  to  eight  drachms  (20  to  30  c.c.)  of  the  tincture  may  have  to  be  adminis- 
tered in  fifteen-minim  (1-c.c.)  doses  during  a  period  of  about  ten  days  before 
the  maximal  slowing  sets  in. 

The  writer  has  found  that  with  doses  of  fifty  minims  of  the  tincture 
this  result  can  usually  be  obtained  in  two  or  three  days.  This  corresponds 
to  the  total  amount  given  by  Windle.  Eggleston  administers  half  the  entire 
amount  in  his  first  dose  and  then  gives  an  equal  amount  more  in  three  or 
four  doses  through  the  first  twenty-four  hours  and  obtains  the  effects  within 
twenty-four  hours. 

Certain  patients  whose  heart  muscles  have  undergone  too  great  degen- 
eration do  not  react  at  all  to  the  drug,  and  the  rapid  irregular  heart-rate 
continues  in  spite  of  its  use;  but  until  the  drug  has  been  pushed  to  its  limits 
it  is  very  difficult  to  foretell  whether  one  is  dealing  with  a  patient  who  would 
respond  to  a  sufficient  dose  or  one  in  whom  response  is  no  longer  possible. 

In  contrast  to  the  effects  obtained  in  broken  compensation  from  valvular 
disease,  which  depend  upon  increased  tonicity  and  increased  force  of  con- 
traction, the  effects  obtained  in  auricular  fibrillation,  which  depend  chiefly 
upon  the  slowing  of  the  heart  and  the  partial  blocking  of  the  impulses,  do 
not  outlast  the  period  of  administration,  but  the  tachycardia,  dyspnoea,  and 
weakness  are  often  resumed  within  a  couple  of  days  after  the  digitalis  is 
stopped.  The  drug  must,  therefore,  be  continued  even  after  the  patient 
is  up  and  about,  and  the  amount  then  given  is  determined  by  permitting  the 
patient  to  vary  his  own  dose  to  find  out  the  one  at  which  he  feels  most  vigorous. 


PLATE  XV. 


Heart-block  resulting  from  prolonged  use  of  digitalis  and  removed  by  atropine.  (Kindness  of  Dr.  R.  E. 
Morris.)  A,  electrocardiogram  taken  on  June  21,  1916,  showing  rapid  heart  rate  but  normal  sequence. 
B,  electrocardiogram  from  same  patient  taken  on  June  28  th,  after  prolonged  use  of  digitalis,  showing  complete 
heart-block.  C,  electrocardiogram  from  same  patient  on  June  28th,  one  hour  after  the  hypodermic  adminis- 
tration of  atropine  sulphate,  gr.  ^5,  showing  disappearance  of  the  heart-block.  Conduction  time  (P.-R. 
interval)  remains  long. 


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THE   EFFECTS  OF  DRUGS  IN  CARDIAC   DISEASE.       257 

CHOICE    OF    PREPARATIONS   AND   MODE    OF   ADMINISTRATION. 

So  many  preparations  of  digitalis  and  its  congeners  are  constantly  being 
placed  upon  the  market  that  some  difficulty  may  be  encountered  in  the  selec- 
tion of  the  preparation  best  suited  to  the  occasion,  as  well  as  in  its  mode  of 
administration. 

Albert  Fraenkel,  Mackenzie,  and  Worth  Hale  have  shown  that  a  good 
tincture  which  has  been  standardized  physiologically  (see  page  247)  is  about 
as  satisfactory  and  as  permanent  as  any  of  the  more  elaborate  and  costly 
preparations.1  As  Fraenkel  has  stated,  the  effect  depends  more  upon  the 
quantity  of  dose  than  upon  the  kind  of  drug  used. 

The  method  most  common  in  America  of  giving  1  c.c.  (15  minims)  of  the 
tincture  or  gr.  iss  of  the  powdered  digitalis  is  open  to  the  objection  that  it  is  too 
slow  when  the  patient  is  very  ill  and  a  prompt  action  of  digitalis  is  required. 
In  such  cases  more  prompt  effects  may  be  secured  by  a  few  larger  initial 
doses,  and  the  writer  has  found  it  more  satisfactory  to  administer  0.3  c.c.  (5 
minims)  of  the  fluid  extract  or  3  c.c.  of  the  tincture  every  four  hours  until  the 
pulse  rate  has  fallen  below  80,  "when  it  should  be  discontinued  by  the  nurse 
without  special  order"  and  smaller  doses  substituted  on  the  next  visit  of  the 
physician.  Albert  Fraenkel's  method  is  essentially  the  same,  giving  several  2 
c.c.  doses  of  tincture  every  four  hours  and  then,  to  prevent  cumulation,  drop- 
ping to  a  dose  of  one-quarter  this  amount.  A  similar  method  has  recently  been 
advocated  by  Gary  Eggleston( Arch.  Int.  Med.,  1915,  xvi.  1)  whose  exact  clinical 
study  controlled  by  modern  methods  of  precision  is  worthy  of  careful  perusal. 

Eggleston  standardizes  his  clinical  doses  in  "cat units"  (1  "cat  unit" 
=  mg.  digitalis  which  will  kill  1  Kg.  of  cat  when  slowly  and  continuously  in- 
jected into  a  vein).  He  administers  a  few  tremendous  doses  at  the  beginning 
of  treatment  (one-twentieth  to  one-eighth  cat  unit  per  pound  weight  of  pa- 
tient, 8  to  20  cubic  centimetres  of  the  tincture,  60  to 
150  cubic  centimetres  of  the  infusion,  1.0  to  1.75  mg.  crystalline  digitoxin.) 
He  finds  that  "it  is  possible  to  give  a  third  to  a  half  of  the  total  calculated 
therapeutic  dose  (5  to  15  c.c.  of  the  tincture)  at  a  single  administration :  to 
follow  this  in  four  to  six  hours  with  a  quarter  to  a  third  of  the  total  dose  and 
to  give  the  remainder  in  a  few  doses  of  smaller  size  at  intervals  of  four  to  six 
hours.  By  this  plan  of  administration  the  full  effects  can  be  secured  in  from 
twelve  to  thirty-six  hours  in  the  majority  of  cases." 

PRECAUTIONS   AND    METHODS   OF   ADMINISTRATION. 

Flavoring. — Gastric  disturbances,  such  as  nausea  and  vomiting, 
occasionally  result  from  the  administration  of  digitalis  preparations  or  deriva- 
tives. This  is  in  part  due  to  the  direct  irritating  action  upon  the  gastric  mucous 
membrane  and  in  part  to  the  extremely  unpleasant  taste  and  after-taste  of  the 
drug.  In  order  to  obviate  the  former  the  drug  should  always  be  given  in  a  large 
quantity  (at  least  half  a  tumbler)  of  water.  The  intensely  disagreeable  taste  of 
the  digitalis  and  strophanthus  preparations  may  be  disguised  by  the  addition  of 
bitter  orange  peel  (tinctura  aurantii  amari) ,  compound  tincture  of  either  gentian 
or  cardamom,  or  tincture  of  quassia  or  calumba.  It  may  also  be  given  in  albu- 
min water  flavored  with  lemon  so  that  its  taste  is  barely  noticeable. 

1  J.  H.  Pratt  (Boston  M.  and  S.  J.,  1910,  clxiii,  279)  finds  the  digitalis  of  Cesar  and 
Loretz  the  most  active  and  constant. 

17 


258  DISEASES  OF  THE  HEART  AND  AORTA. 

Sir  Clifford  Allbutt  recommends  that  it  be  given  in  an  iced  drink.  The  use  of 
any  of  these  disguises  frequently  minimizes  the  gastric  disturbances  resulting 
from  the  drug,  though  vomiting  of  central  origin  finally  results  (Hatcher). 

Rectal  Administration. — When  the  gastric  symptoms  persist  in  spite 
of  these  precautions,  the  drug  may  be  administered  per  rectum,  being  given 
in  100  c.c.  physiological  salt  solution  with  a  little  starch.  This  method  is 
very  satisfactory  (Janeway).  Dr.  Finley  informs  the  writer  that  he  has  seen 
the  pulse-rate  slowed  and  the  patient's  condition  greatly  improved  within 
two  hours  after  the  administration  of  digitalis  per  rectum,  whereas  the  effect 
rarely  follows  administration  by  mouth  in  less  than  twenty-four  hours. 

Intramuscular  and  Intravenous  Administration. — In  order  to  insure  very 
rapid  and  certain  absorption,  digitalis  tincture  or  the  more  elaborate  prepara- 
tions, such  as  digitalin,  digalen  or  digipuratum,  may  be  injected  into  the 
gluteal  or  lumbar  muscles.  The  injection  should  be  very  deep  and  the  site 
should  be  massaged  vigorously  for  ten  or  fifteen  minutes  afterwards  in  order  to 
insure  absorption,  for,  if  the  injection  remains  unabsorbed,  it  acts  as  an  irritant, 
and  not  only  intense  pain  but  the  formation  of  a  large  abscess  may  result.  It 
may  also  be  injected  into  the  vein  under  the  usual  aseptic  precautions. 

Inhalation  of  Digitalis  and  Strophanthus. — J.  Moczulski  (Wiener  Klin. 
Wchnschr.,  1914,  31)  has  obtained  excellent  and  prompt  results  by  inhalation 
of  1  c.c.  tincture  of  strophanthus  daily  administered  by  means  of  an  atomizer 
spray  under  pressure,  J.  Riegel  in  the  pharmacological  laboratory  of  the 
University  of  Minnesota  has  demonstrated  that  tincture  of  digitalis  adminis- 
tered intratracheally  in  this  way  to  animals,  acts  immediately,  but  the  writer 
has  found  it  so  irritating  that  in  rabbits  it  sets  up  a  bronchopneumonia. 

Period  of  Administration. — In  the  administration  of  digitalis  it  is  impor- 
tant to  obtain  a  definite  effect  and  yet  not  to  push  the  drug  beyond  the  first 
stage  of  its  activity — that  of  slowing  and  increase  in  size  of  the  pulse — and 
to  avoid  the  onset  of  the  second  stage,  i.e.,  of  irregularity.  Since  different 
hearts  vary  in  their  susceptibility  to  digitalis,  and  since,  on  the  other  hand, 
the  drug  begins  to  act  only  after  twenty-four  hours  and  may  have  a  cumula- 
tive effect,  this  task  is  by  no  means  easy.  To  avoid  the  onset  of  toxic  effects 
various  routine  methods  may  be  resorted  to.  Thus,  Professor  Osier  and 
other  authorities  recommend  giving  the  drug  in  "courses"  consisting  of 
eight  doses  of  15  minims  of  the  tincture  ( 0.1  Gm.  or  It  gr.  digitalis)  every 
four  hours.  The  course  is  to  be  repeated  if  necessary.  It  may  be  said  that 
this  method  often  falls  short  of  the  effect  or  brings  it  about  too  slowly.  The 
writer  has  found  it  very  satisfactory  to  order  "0.3  c.c.  (5  minims)  of  the 
fluidextract  three  times  a  day  until  the  pulse-rate  reaches  80,  when  it  should 
be  discontinued  without  the  necessity  of  a  special  order."  Albert  Fraenkel 
suggests  giving  several  strong  doses  equivalent  to  0.1  Gm.  (2  gr.)  of  powdered 
digitalis  (about  twice  the  usual  dose,  2  c.c.  or  30  minims  of  the  tinctura 
digitalis)  to  insure  prompt  effect  (slowing  of  the  pulse),  and  thereafter  drop- 
ping to  steady  dosage  of  .03  Gm.  (1  gr.,  0.5  c.c.  or  7i  minims  of  the  tincture) 
to  prevent  cumulative  but  retain  the  therapeutic  effect.  This  seems  to  be 
the  most  satisfactory  method,  since  it  insures  not  only  the  immediate  but  a 
permanent  effect.  Indeed,  in  many  chronic  cases  '  'the  strength  of  the  heart 
begins  to  fail  a  short  time  after  leaving  off  the  digitalis.  Here  the  continuous 
use  of  digitalis  (0.05  Gm.  or  1  gr.  digitalis),  as  recommended  by  Kussmaul, 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC   DISEASE.        259 

Naunyn,  and  Groedel,  for  months  and  even  years,  has  an  admirable  effect 
in  keeping  the  cardiac  activity  at  its  necessary  height"  (Romberg). 

Derivatives  of  Digitalis. — Although,  as  Fraenkel  has  shown,  the  purified 
glucosides  of  digitalis  have  no  great  advantage  over  the  crude  drug,  they 
have  enjoyed  considerable  vogue. 

Digitalin,  the  glucoside  first  introduced  into  practice,  still  enjoys  a 
certain  favor.  The  ordinary  digitalin,  or  ''German  digitalin"  of  commerce,  is 
a  very  variable  product,  and  it  is  only  the  purified  cligitaline  or  digitalinum 
verum  of  Kiliani  which  is  worthy  of  recommendation. 

Of  late  digitalin  has  been  largely  replaced  by  digitoxin,  especially  in  the 
form  of  the  digitaline  Nativelle  granules  (pure  digitoxin),  which  are  warmly 
recommended  by  Mackenzie  and  the  French  writers,  and  as  Cloetta's  '  'diga- 
len" (soluble  digitoxin)  or  in  Gottlieb's  digitonin-free  digipuratum  (digi- 
talis purified  from  digitonin).  The  claims  that  the  former  substance  does 
not  act  upon  the  stomach  and  also  that  it  is  a  preparation  of  great  stability 
have  both  been  largely  repudiated,  and  Hale  and  others  have  found  that  the 
samples  of  digalen  on  the  market  are  about  as  liable  to  deterioration  as  an 
ordinary  digitalis  preparation. 

Otfried  Muller  has  found  that  the  intravenous  injection  of  1  c.c.  (15 
minims)  of  digalen  has  no  influence  upon  the  vasomotor  nerves  of  the  arm  in 
man,  as  shown  by  the  plethysmography  and  very  little  effect  upon  the  blood- 
pressure.  He  believes  that  its  action  is  similar  to  that  of  strophanthin  intra- 
venously, only  that  it  is  less  powerful  and  less  rapid.  Albert  Fraenkel,  on 
the  other  hand,  regards  this  as  merely  a  matter  of  dosage,  but  believes  that 
strophanthin,  owing  to  its  more  definite  chemical  composition,  can  be  gauged 
more  accurately. 

In  digipuratum,  a  preparation  introduced  into  practice  by  Gottlieb  and 
Hoepffner  in  1908,  the  aims  sought  for  in  the  preparation  of  digalen  seem  to 
have  been  realized  to  a  much  greater  extent,  as  is  indicated  by  the  favorable 
comments  of  Mueller  and  Clemens  in  Germany,  Tissot  in  France,  Szinnei 
in  Austria,  and  Boos  and  his  associates  in  America.  The  writer's  experience, 
however,  does  not  bear  this  out,  and  Hatcher  has  produced  vomiting  move- 
ments by  intravenous  injection  in  gastrectomized  animals  with  digipuratum 
in  the  same  way  as  with  other  digitalis  preparations.1 

Digipuratum  is  usually  administered,  as  Hoepffner  suggested,  in  courses 
of  twelve  tablets  of  0.1  Gm.  (gr.  iss)  each. 

STROPHANTHIN. 

Where  rapid  intense  action  is  required,  as  in  a  badly  failing  heart  in 
which  an  immediate  result  is  required,  strophanthin  or  ouabain  is  the  drug 
of  choice,  and  should  be  administered  intravenously,  beginning  with  a  dose 
of  0.5  mg.  (gr.  xio)  of  the  amorphous  strophanthin,  or  0.25  mg.  (gr.  2T0")  of 
the  crystalline  ouabain ;  may  be  repeated  within  an  hour  if  no  effect  has  been 
noted.  Care  must  be  taken  to  be  certain  the  patient  has  not  been  taking 
digitalis  before  the  injection,  lest,  as  Fraenkel  has  observed,  a  sudden  cumula- 
tive action  set  in  whose  consequences  may  be  grave  or  even  fatal.  Otfried 
Muller  has  seen  a  cerebral  hemorrhage  set  in  in  a  patient  with  chronic  nephritis 

*R.  A.  Hatcher:  Personal  communication. 


260  DISEASES  OF  THE  HEART  AND  AORTA. 

following  an  intravenous  injection  of  strophanthin,  and  Fraenkel  warns 
against  its  use  in  cases  of  chronic  hypertension  for  fear  of  throwing  too  sudden 
a  strain  upon  the  heart.  On  the  other  hand,  hearts  whose  muscles  are  in 
good  condition  may  have  a  much  greater  tolerance  for  strophanthin;  and 
Liebermeister  has  given  as  much  as  4  mg.  (gr.  TV)  in  twenty-four  hours  to 
patients  with  pneumonia  without  any  ill  effects. 

In  ordinary  cases  the  intravenous  or  intramuscular  injection  of  strophan- 
thin is  reserved  for  emergencies,  and  especially  to  cover  the  period  during 
which  no  effect  could  be  expected  from  the  administration  of  digitalis  by  the 
mouth,  so  that  in  most  cases  the  oral  administration  of  digitalis  may  begin 
at  once,  allowing  its  effects  to  begin  about  the  time  that  those  of  the  strophan- 
thin wear  off.  In  patients  whose  condition  is  very  grave,  however,  and 
especially  in  those  in  whom  absorption  from  the  intestinal  tract  is  uncertain, 
it  is  better  to  rely  entirely  upon  the  strophanthin  and  make  daily  intra- 
muscular injections  of  a  single  dose,  leaving  the  digitalis  off  altogether  until 
the  period  of  emergency  of  uncertainty  is  over. 

DIGITALIS  AND   THE   NITRITES. 

As  has  been  stated,  the  drugs  of  the  digitalis  series  strengthen  the  force 
of  the  heart-beat  and  increase  its  tonicity,  and  thus  enable  the  dilated  heart 
to  empty  itself  better  into  the  blood-vessels  and  prevent  it  from  overfilling 
during  diastole.  This  in  itself  usually  suffices  to  return  the  circulation  to  its 
normal  state,  but  in  many  cases,  especially  in  acute  oedema  of  the  lungs  and 
in  failure  of  the  left  ventricle,  with  hypertension,  and  especially  in  the  attacks 
of  cardiac  asthma  of  aortic  insufficiency,  it  is  advisable  to  lighten  the  burden 
upon  the  heart  still  further  by  dilating  the  peripheral  arteries. 

The  best  drugs  for  this  purpose  are  those  of  the  nitrite  series  (amyl 
nitrite,  nitroglycerin,  sodium  or  potassium  nitrite,  erythroltetranitrate), 
whose  action  will  be  discussed  in  detail  in  a  later  section. 

In  using  these  drugs  in  conjunction  with  those  of  the  digitalis  series  it 
must  be  remembered  that  the  heart  does  its  best  work  when  the  general 
blood-pressure  is  high  enough  to  maintain  a  good  blood  flow  through  the 
coronary  arteries  and  the  respiratory  centre  in  the  medulla,  and  that,  owing 
to  varying  degrees  of  arteriosclerosis  and  arterial  elasticity,  the  optimum  will 
be  different  in  each  individual.  Nevertheless  a  certain  amount  of  relief  may 
be  afforded  to  the  majority  of  cases  provided  care  is  taken  not  to  pass  below 
the  optimum.  It  must  be  remembered,  moreover,  that  for  cases  of  increased 
intracranial  pressure,  apoplexy,  cerebral  sclerosis  in  which  the  vasoconstric- 
tion and  high  blood-pressure  are  the  result  of  an  attempt  at  physiological 
compensation,  this  optimum  pressure  may  lie  at  a  very  high  level,  and  at- 
tempts to  reduce  the  blood-pressure  may  actually  do  harm.  However,  in 
the  more  acute  conditions  of  high  pressure,  high-pressure  stasis,  reflex  eleva- 
tions of  pressure,  vasomotor  crises,  etc.,  these  phenomena  are  not  compensa- 
tory but  accessory  reflexes,  and  to  relieve  them  lessens  the  work  of  the  heart 
without  disturbing  any  essential  condition;  so  that  lowering  the  peripheral 
resistance  may  relieve  the  burden  on  the  heart  almost  as  much  as  increasing 
the  strength  of  the  latter,  and  the  optimum  is  attained  when  both  are  accom- 
plished at  once.  This  desirable  condition  is  further  enhanced  by  the  fact  that, 
as  Cameron  has  shown,  amyl  nitrite  and  nitroglycerin  augment  the  tonicity 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.         261 

of  the  heart  muscle,  and  thus  add  their  effect  to  that  of  the  digitalis;  the 
more  so  since,  in  accordance  with  a  well-known  pharmacological  principle, 
the  effect  of  two  drugs  exerting  the  same  action  administered  simultaneously 
is  greater  than  the  sum  of  the  two  components  acting  separately. 

The  ideal  combination  of  these  drugs  for  speed,  harmony,  and  intensity 
of  action  is  the  injection  of  strophanthin  and  nitroglycerin  simultaneously, 
for  the  former  exerts  little  action  upon  the  peripheral  vessels  and  both  sub- 
stances unfold  their  action  at  about  the  same  period  after  injection.  In 
attacks  of  cardiac  asthma,  particularly  in  cases  of  aortic  insufficiency,  this 
combination  of  drugs  may  give  great  relief.  Their  action  may  further  be 
strengthened  by  venesection  and  inhalation  of  oxygen,  according  to  the  method 
of  Hill  and  Mackenzie,  for  in  cases  of  severe  heart  failure  the  best  results  are 
obtained  by  firing  all  the  weapons  of  defence  in  one  broadside.  In  this  way 
the  excess  of  residual  blood  is  pumped  out  of  the  dilated  heart  and  the  latter 
allowed  to  return  to  normal  volume.  It  is  at  the  normal  volume  that  the 
heart  pumps  to  best  advantage.  If  it  is  still  possessed  of  any  recuperative 
power,  it  is  enabled  then  to  assert  itself,  far  better  than  if  the  same  measures 
were  applied  singly  at  long  intervals,  so  that  the  dilated  heart  is  depleted  a 
little  by  one  measure,  allowed  to  refill  to  the  original  degree  before  the  next 
is  applied,  responds  a  second  time  to  a  slight  degree  but  insufficient,  and, 
still  working  at  a  disadvantage,  again  becomes  dilated  as  it  was  before  the_ 
beginning  of  treatment. 

Contraindications  to  Digitalis. — However  valuable  the  substances  of 
the  digitalis  series  may  be  in  the  above-mentioned  conditions,  there  is  a  con- 
siderable group  of  cases  in  which  they  are  useless  or  positively  harmful.  This 
is  especially  true  for  hearts  in  acute  intoxications,  either 
from  acute  infectious  diseases  or  from  the  action  of  poisons 
or  from  acute  fatty  degenerations  from  other  causes. 

In  these  conditions  digitalis  usually  fails  to  exert  its  characteristic 
responses ;  partly  because  the  disturbance  in  the  circulation  lies  chiefly  in  the 
peripheral  vessels  rather  than  in  the  heart  itself;  partly  because  the  vagi  are 
less  active  than  normally  so  that  the  drug  cannot  exert  its  action  through 
this  channel;  and  partly  because  the  degenerated  heart  muscle  is  sensitive 
to  further  strains  upon  it. 

On  the  other  hand,  the  acutely  degenerated  heart  muscle  seems  hyper- 
sensitive to  digitalis  and  readily  passes  into  the  toxic  stages  of  digitalis  action 
(see  page  312).  This  may  be  analogous  to  the  fact,  demonstrated  by  Loeb 
and  Fleisher,  that  two  toxic  substances  acting  simultaneously  may  produce 
degenerations  of  the  heart  muscle  which  could  not  be  attained  by  either  of 
them  acting  alone,  for  the  toxic  agent  giving  rise  to  the  degeneration  repre- 
sents one  of  these  factors  and  the  digitalis  represents  the  other. 

Clinical  experience  is  in  harmony  with  these  results,  as  the  cases  cited 
on  pages  319  and  321  bear  witness;  and  in  such  cases  the  drugs  of  the  digitalis 
series  if  given  at  all  must  be  administered  with  extreme  caution. 

Another  condition  in  which  these  substances  are  contraindicated,  as 
stated  above,  is  partial  heart-block,  for  digitalis  is  likely  to  bring  on  complete 
block  suddenly  and  with  it  there  is  danger  of  an  attack  of  the  Adams-Stokes 
syndrome.  The  question  of  the  advisability  of  digitalis  in  complete  heart- 
block  is  still  an  open  one  and  is  discussed  on  pages  585  and  586. 


262  DISEASES  OF  THE  HEART  AND  AORTA. 

HALLUCINATIONS   FROM    DIGITALIS. 

Another  toxic  effect  of  digitalis  lies  in  the  production  of  mental  symp- 
toms, delirium  and  delusions,  through  its  action  on  the  central  nervous 
system  (Duroziez,  Hall,  see  page  228).  The  onset  of  these  symptoms  there- 
fore constitutes  a  contraindication  to  continuing  the  drug. 

STRYCHNINE. 

PREPARATIONS. 

Strychnine  (strychnina)  is  an  alkaloid  obtained  from  nux  vomica.  Tincture  nucis 
vomicae  contains  2  per  cent,  extract  of  nux  vomica  and  is  assayed  to  contain  0.1  per  cent, 
strychnine.  It  is  useful  more  as  a  stomachic  bitters  than  as  a  cardiac  stimulant.  Dose, 
1-2  c.c,  15  to  30  minims. 

Strychninse  sulphas  contains  5  molecules  of  water  of  crystallization  and  78  per  cent, 
of  strychnine,  soluble  in  3  parts  of  water.    Average  dose,  0.0015  Gm.  (^  gr.). 

Strychninse  nitras  is  soluble  in  42  parts  of  water  and  120  parts  alcohol.  Dose,  same 
as  sulphate. 

PHARMACOLOGICAL   ACTION    OF   STRYCHNINE. 

Effects  of  Strychnine  on  Cardiac  Tonicity. — P.  D.  Cameron  investigated 
the  effect  of  strychnine  upon  the  volume  of  the  dog's  heart  and  found  that 
in  doses  of  .03  mg.  per  kilo  (corresponding  to  2  mg.  for  a  man)  strychnine 
always  produces  a  small  diminution  in  the  volume  of  the  heart.  That  this 
is  probably  due  to  diminished  inflow  from  the  veins  secondary  to  general 
vasoconstriction,  rather  than  to  a  definite  increase  in  tonicity,  has  been 
shown  by  the  more  recent  unpublished  experiments  of  Messrs.  Larson, 
Mattson,  Lineer  and  Sprafka  in  the  Pharmacological  Laboratory  of  the  Uni- 
versity of  Minnesota.  These  observers  studied  the  effect  of  drugs  in  hearts 
dilated  by  a  slight  aortic  stenosis,  and  found  that  in  contrast  to  digitalis, 
the  effects  of  injections  of  strychnine  were  variable  and  uncertain. 

Absence  of  Clinical  Effects. — The  later  observations  of  W.  P.  Lucas, 
Edsall  and  Means  (Arch.  Int.  Med.,  1914,  xiv,  897)  and  of  L.  H.  Newburgh 
(Am.  Jour.  Med.  Sc,  1915,  cxcix,  696)  show  the  same  lack  of  positive  effect  of 
strychnine  in  clinical  doses  upon  any  of  the  important  phases  of  circulation. 

Since  the  rank  and  file  of  English  and  American  clinicians  entertain  an 
almost  superstitious  belief  in  the  efficacy  of  this  drug  it  is  evident  that  each 
man  must  convince  himself  by  following  a  few  cases  with  careful  determina- 
tions of  blood-pressure  but  only  one  set  of  observers  who  have  followed  the 
blood-pressure  carefully  has  come  to  any  different  conclusions. 

H.  W.  Cook  and  Briggs  working  in  the  early  days  of  the  narrow-cuffed 
Riva-Rocci  sphygmomanometer  and  whose  pioneer  observations  are,  there- 
fore, not  comparable  with  the  more  extensive  observations  of  the  later  obser- 
vers made  with  far  better  apparatus,  occasionally  found  rises  of  10  mm.  Hg 
following  injections  of  strychnine.  However,  this  apparatus  was  so  full  of 
experimental  errors  and  increases  of  10  mm.  Hg  are  so  likely  to  occur  from 
pain  sensations  like  the  prick  of  the  hypodermic  needle  that  their  question- 
able results  are  not  to  be  held  out  against  the  consensus  of  later  workers 
upon  larger  series  of  cases  with  better  apparatus. 

The  results  of  all  these  investigations  indicate,  therefore,  that  strychnine 
should  not  be  ranked  at  all  with  the  heart  stimulants  and  that  much  more 
harm  than  good  results  from  placing  any  reliance  whatever  upon  it  when  a 
real  heart  stimulant  is  needed. 

In  spite  of  the  effects  on  Cheyne-Stokes  breathing  reported  by  Eyster, 
Edsall  and  Means  (Arch.  Int.  Med.,  1914,  xiv,  897)  find  that  the  action  of 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE. 


263 


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Fig    133.— Chart  showing  effects  of  strychnine  and.  digitalis  in  a  case  of  continuous  irregularity. 
cig.   100.     oua  B^    H    Newburgh,  Am.  Jour.  Med.  Sci.,  191o,  cxhx,  701.) 


(After 


264  DISEASES  OF  THE  HEART  AND  AORTA. 

strychnine  upon  the  respiratory  centre  has  been  much  exaggerated,  and  that 
when  it  is  administered  in  therapeutic  doses,  no  effect  on  rate,  lung  ventila- 
tion or  alveolar  C02  could  be  discerned  although  under  similar  conditions 
atropine  gave  a  distinct  effect. 

It  is  questionable  whether  strychnine  has  any  direct  value  as  a  cardiac 
or  even  a  respiratory  stimulant,  and  it  can  be  definitely  stated  that  in  neither 
of  these  respects  does  it  compare  with  digitalis  or  atropine. 

The  action  of  the  heart  is  so  dependent  upon  the  activity  of  the  skeletal 
muscles,  however,  that  it  is  possible  that  doses  of  strychnine  sufficient  to 
increase  the  tone  of  the  skeletal  muscle  may  act  in  the  same  way  as  the  train- 
ing of  the  muscles  so  as  to  diminish  the  amount  of  effort  and  strain  which  a 
given  movement  or  exercise  induces;  and  in  that  way  the  drug  may  have 
some  effect  in  sparing  the  heart,  without  any  direct  effect  upon  the  circula- 
tory mechanism.  No  effect,  however,  could  be  expected  unless  the  doses 
employed  are  sufficient  to  cause  increased  reflexes. 

ATROPINE. 

Atropine  acts  by  paralyzing  the  nerve  endings  of  the  entire  automatic 
(parasympathetic)  nervous  system,  the  oculomotor  nerve,  chordi  tympani, 
the  vagus  and  the  pelvic  nerves  (see  page  19).  Its  effect  is,  therefore,  to 
dilate  the  pupils,  to  dry  the  mouth,  to  accelerate  the  heart  and  to  diminish 
or  abolish  any  partial  or  complete  heart-block  that  may  have  been  produced 
by  over-action  of  the  vagi.  It  is  in  this  latter  regard  that  it  is  most  useful  in 
cardiac  disease,  particularly  in  relieving  those  blocks  which  are  due  to  mild 
digitalis  poisoning  or  for  increasing  the  heart  rate  in  cases  in  which  the  pulse 
rate  has  been  brought  down  too  low  by  the  administration  of  digitalis. 

It  is  specific  for  the  disturbances  associated  with  the  clinical  symptoms 
of  vagotonic,  and  occasionally  may  cause  symptoms  of  palpitations  due  to 
that  syndrome  to  disappear. 

On  the  other  hand,  Edsall  and  Means  found  that  while  strychnine  and 
camphor  were  devoid  of  action  on  the  human  respiratory  centre,  and  caffeine 
exerted  variable  results,  atropine  caused  regularly  an  increase  in  lung  ventila- 
tion and  a  decrease  in  the  percentage  of  CO2  in  the  alveolar  air,  thus  proving 
itself  a  true  stimulant  of  the  respiratory  centre.  It  is  therefore  useful  in 
Cheyne-Stokes  respiration  in  morphine  poisoning,  and  in  the  attacks  of 
cardiac  asthma  which  are  precipitated  by  the  administration  of  morphine. 

On  the  other  hand,  atropine  antagonizes  the  good  effects  of  digitalis 
in  slowing  the  heart  in  auricular  fibrillation  (Mackenzie),  but  Hirschf elder 
(unpublished  experiments)  has  shown  that  it  does  not  diminish  the  beneficial 
effects  of  that  drug  in  increasing  cardiac  force  and  tonicity,  as  shown  in 
experimental  aortic  stenosis. 

The  good  effects  of  atropine  are  often  missed  because  it  is  administered 
in  too  small  doses.  Doses  of  \  mg.  (gr.  tto")  are  usually  without  sufficient 
effect  and  f  mg.  (gr.  gV)  or  1  mg.  (gr.  eV  )  must  be  resorted  to.  Unless  atro- 
pine has  been  used  in  doses  sufficient  to  cause  the  desired  effect  or  else  to 
cause  dryness  of  the  mouth  or  other  typical  symptoms,  one  cannot  be  certain 
that  an  efficient  dose  has  been  given. 

CAMPHOR. 

In  spite  of  the  wide  use  of  camphor  in  shock  and  in  pneumonia,  and 
in  spite  of   the   experiments  of    Winterberg,   Seligmann   and   Gottlieb   to 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE  265 

show  that  it  tended  to  inhibit  fibrillation  of  the  ventricle  in  excised  hearts, 
accurate  clinical  observations  have  shown  that  camphor  has  no  real  place 
among  the  clinical  stimulants  of  the  heart  and  vasomotor  centre.  Cameron 
was  unable  to  demonstrate  any  effect  on  cardiac  tonicity.  Brooks  and 
Heard  (Am.  Jour.  Med.  Sc,  1913,  cxlv,  238),  in  a  very  careful  experimental  and 
clinical  study,  have  been  unable  to  demonstrate  anyeffectupon  auricular  fibrilla- 
tion, and  Edsall  and  Means  have  found  it  likewise  without  effect  upon  the 
respiratory  centre.  Its  effect  upon  ingestion  is  probably  only  a  gastric  re- 
flex like  that  of  alcohol,  aromatic  spirit  of  ammonia  or  any  other  carminative. 
Camphor  is  a  white  substance,  soluble  in  alcohol,  ether,  and  chloroform, 
whose  structural  formula  is — 

CH2 CH CH2 


CH3 


Average  dose,  0.12  Gm.  (2  gr.),  best  given  as  linimentum  camphorse  (camphorated 
oil),  which  contains  20  per  cent,  of  camphor  dissolved  in  cotton-seed  oil.  Average  dose, 
0.75  to  2.0  c.c.  (11.25  to  30  minims),  available  for  hypodermic  use  or  by  mouth. 

Spiritus  camphorae,  a  10  per  cent,  solution  of  camphor  in  alcohol.  Dose,  1  c.c.  (15 
minims) . 

Camphor,  like  strychnine,  is  a  stimulant  to  the  vasomotor  centre, 
but,  according  to  Cameron,  does  not  seem  to  h  a  v  e  so  pronounced  an  effect  on  t  o  n  i  c- 
i  t  y  .  Like  strychnine  it  also  varies  in  its  effects  on  different  individuals.  Some  persons 
require  doses  twenty  times  as  large  as  do  others  before  an  effect  sets  in,  especially  when 
the  drug  is  given  by  mouth.  Camphor  is  most  important  for  its  use  in  shock.  It  is  given 
deeply  into  the  muscles  in  order  to  avoid  subsequent  inflammations.  It  is  not  so  valuable 
for  continuous  use.  As  recently  shown  by  Winterberg,  Seligmann,  and  Gottlieb  and 
Magnus,  camphor  has  also  a  very  distinct  action  upon  the  heart  muscle,  causing  the  fibril- 
lating  excised  heart  to  revive  from  fibrillary  contractions.  After  camphor  has  been  ad- 
ministered to  a  dog  the  ventricle  (in  situ)  can  be  thrown  into  fibrillary  contractions  by 
weak  faradic  stimuli  and  yet  recover.  On  the  other  hand,  a  direct  therapeutic  effect  upon 
the  heart  muscle  in  man  has  not  yet  been  proved. 

CALCIUM  SALTS. 
Calcium  chloride  and  other  salts  of  calcium  have  been  recommended  recently  as 
cardiac  stimulants  by  Lauder  Brunton  and  other  English  clinicians.  Although  the  action 
of  calcium  upon  the  excised  heart  is  indisputable,  its  effect  upon  the  heart  in  situ  has  been 
supposed  to  be  too  transitory  to  be  of  practical  value.  The  writer  has  been  unable  to  find 
any  effect  upon  the  maximal  and  minimal  blood-pressures  and  pulse-rates  of  a  number  of 
cases  of  typhoid  fever  who  were  receiving  calcium  lactate  in  sufficiently  large  doses  to 
hasten  coagulation.  Sladen  also  found  in  a  large  variety  of  cases  that  calcium  lactate  had 
no  effect  upon  pulse-rate  or  blood-pressure.  On  the  other  hand,  in  animals  calcium  chloride 
has  an  effect,  especially  upon  tonicity,  which  closely  simulates  that  of  strychnine.  Injec- 
tion of  considerable  quantities  directly  into  the  cavities  of  the  heart  revives  that  organ  as 
nothing  else  appears  to  do.  The  writer  has  found  that  in  some  cases  dogs'  hearts  that  had 
actually  stopped  beating  and  even  lost  their  mechanical  irritability  revived  to  such  an 
extent  as  to  resume  a  regular  rhythm  with  a  moderately  high  blood-pressure.  The  matter 
is,  however,  still  in  the  experimental  stage. 

CAFFEINE. 
From  the  results  of  experiments  upon    animals,   caffeine  would  take 
rank  next  to  digitalis  in  cardiac  therapy.     Like  digitalis  it  acts  upon  the 


266  DISEASES  OF  THE  HEART  AND  AORTA. 

cardiac  muscle,  increasing  the  size  and  force  of  the  contraction;  like  digitalis 
it  has  a  vasoconstrictor  action,  and  raises  the  blood-pressure  by  bringing 
about  constriction  of  the  peripheral  blood-vessels.  It  is  therefore  particularly- 
valuable  in  conditions  of  collapse  and  shock.  In  this  regard  it  is  more  reliable 
than  camphor  (Romberg)  or  strychnine. 

On  the  other  hand,  caffeine  does  not  exert  a  constricting  action  upon  the  coronary- 
arteries  (O.  Loeb),  and  hence  is  not  contraindicated  in  cases  of  coronary  sclerosis.  Upon 
the  pulse-rate  caffeine  exerts  a  variable  effect,  in  relatively  small  doses  (0.1  Gm.,  2  gr.) 
slowing  the  pulse  by  stimulating  the  vagi,  in  larger  doses  accelerating.  The  acceleration 
is  apparently  due  to  direct  action  upon  the  heart  muscle,  since  it  occurs  also  in  the  excised 
heart  when  caffeine  is  added  to  the  Locke's  solution.  However,  as  regards  the  effects  of 
a  given  dose,  there  is  the  greatest  variation  among  different  individuals,  some  persons 
being  extremely  sensitive  to  small  doses,  others  extremely  resistant.  Even  in  the  same 
individual  tolerance  varies.  L.  Taylor  (Arch.  Int.  Med.,  1914,  xiv,  769)  found  in  fifteen  cases 
of  heart  disease  treated  with  citrated  caffeine  (0.3  to  0.6  Gm.  t.i.d.),  usually  no  effect  on  blood- 
pressure,  but  sometimes  rise  and  sometimes  fall — diuresis  inversely  as  the  change  in  maxi- 
mal blood-pressure,  8  cases  of  insomnia,  7  of  nausea,  7  of  extreme  restlessness.  Thus,  in  a 
case  under  the  writer's  observation,  after  several  months  of  absolute  abstinence  from  coffee 
marked  palpitation,  tachycardia,  and  sleeplessness  resulted  from  a  single  cup  in  twenty- 
four  hours;  a  few  weeks  later  one  cup  and  after  a  few  months  two  cups  could  be  taken, 
without  any  apparent  effect. 

Unfortunately,  the  therapeutic  use  of  caffeine  is  often  accompanied  by 
palpitation,  sleeplessness,  and  even  nausea,  vomiting,  vertigo,  and  delirium, 
which  occur  with  particular  ease  in  cases  with  cardiac  disease.  The  palpita- 
tion and  discomfort  usually  set  in  at  about  the  same  point  as  the  therapeutic 
effects,  or  even  earlier;  but  there  are  certainly  many  cases  in  which  this  is 
not  the  case,  and  in  which  caffeine  is  a  valuable  therapeutic  agent. 

THEOBROMINE. 

Theobromine  has  a  much  less  effect  upon  the  cerebral  cortex  and  upon 
the  vasomotor  centre  than  caffeine,  but  has  a  very  strong  diuretic  action. 
As  shown  by  0.  Loeb  it  possesses  a  much  more  powerful  action  in  dilating 
the  coronary  arteries  of  the  excised  heart.  Upon  the  heart  in  situ  its  action 
does  not  seem  to  be  pronounced.  Indeed,  G.  S.  Bond,  in  the  writer's  labora- 
tory, has  been  unable  to  detect  any  effect  upon  the  outflow  from  the  coronary 
veins  as  the  result  of  intravenous  injection  of  agurin  (theobromine  sodium 
acetate).  The  stimulating  action  of  theobromine  upon  the  heart  muscle, 
though  not  as  intense  as  that  of  caffeine,  is  still  very  marked.  It  has  there- 
fore been  recommended  as  a  cardiac  stimulant,  particularly  by  the  French 
clinicians,  who  found  it  of  considerable  value  in  the  weak  hearts  of  fatty 
individuals.  Kaufmann  and  Pauli,  Brewer  and  v.  Leyden  recommended  the 
use  of  theobromine  in  attacks  of  angina  pectoris 
(stenocardia)  .  Pineles  advises  t  h  e  o  p  h  y  1 1  i  n  .  Pal  has  found 
that  theobromine  is  occasionally  useful  in  the  treatment  of  vasomotor  crises, 
but  that  it  often  fails  in  cases  where  iodine  and  potassium  thiocyanate  help. 
Romberg  is  not  able  to  detect  any  beneficial  action  of  theobromine  apart 
from  its  diuretic  action.  In  using  theobromine  it  is  preferable  to  use  those 
compounds  which  are  free  from  salicylates,  since  this  radical  has  a  certain 
depressant  action  upon  the  heart  and  an  irritant  action  on  the  kidneys. 
Acettheobromin  sodium  (''agurin'')  and  acettheocin 
sodium  are  therefore  preferable  to  theobromine  sodium  salicylate  ( "diuretin  "). 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.  267 

ACONITE. 
PREPARATIONS. 

Aconitura,  the  dried  tuberous  root  of  aconitum  napellus,  collected  in  autumn, 
and  yielding  not  less  than  0.5  per  cent,  aconitin.    Dose,  0.05  Gm.  (1  gr.j. 

Tinctura  aconiti,  U.  S.  P.,  now  represents  10  per  cent,  of  the  crude  drug, 
formerly  stronger.  It  is  the  most  certain  and  most  stable  of  all  the  aconite  preparations. 
Dose,  0.6  c.c.  (10  minims). 

Aconitina,  the  crystalline  alkaloid.  Dose,  0.00015  Gm.  (0.15  mg.  or  ?Jff  gr.). 
It  is  so  irritating  that  it  is  usually  preferable  to  prescribe  the  simple  tincture  of  aconite, 
since  this  is  assayed  according  to  the  last  pharmacopoeia. 

Pharmacological  Action.— Aconite  has  three  pharmacological  actions 
upon  the  circulatory  system:  (1)  It  stimulates  the  vagus  promptly  and  to 
a  high  degree;  (2)  it  diminishes  the  size  and  force  of  the  cardiac  contraction, 
and  also  accelerates  the  heart  when  this  organ  is  liberated  from  the  action 
of  the  vagus  centre;  (3)  it  slightly  stimulates  the  vasomotor  centre  in  very 
small  doses.  However,  it  also  diminishes  the  activity  of  the  respiratory 
centre,  and  may  thus  bring  on  dyspnoea.  In  experimental  aconite  poisoning 
in  animals  Cushny  has  been  able  to  produce  a  number  of  rather  unusual 
types  of  alterations  of  rhythm,  sudden  changes  in  the  rhythm  of  the  whole 
heart  of  varied  character,  with  heart-block,  pulsus  alternans,  auricular, 
ventricular,  or  auriculoventricular  extrasy stoles,  paroxysms  of  tachycardia 
resembling  the  idiopathic  paroxysmal  tachycardia  of  man,  and  reversal  of 
rhythm  in  which  the  cardiac  impulse  arises  in  the  ventricles  and  travels  up 
to  the  auricles.  In  the  latter  case  the  ventricles  may  beat  twice  as  fast  as 
the  auricles  (reversed  rhythm  with  partial  block). 

Therapeutic  Uses.— When  carefully  given  in  therapeutic  doses  aconite 
slows  the  heart  by  stimulation  of  the  vagus,  and  has  little  action  upon  the 
heart  muscle.  It  is  therefore  of  value  in  the  acceleration  of  the  pulse  in  fevers, 
where  the  heart  muscle  itself  needs  no  stimulation  and  the  heart  needs  slowing. 
Owing  to  the  variability  of  the  tincture  under  the  old  pharmacopoeia,  the 
use  of  aconite  has  fallen  into  disrepute,  and  enough  time  has  not  elapsed  since 
the  adoption  of  the  last  pharmacopoeia  (1900,  adopted  in  1905)  for  its  real 
utility  in  physiological  therapeutics  to  have  been  investigated.  There  is  no 
doubt  that  it  is  of  value  in  many  cases  of  tachycardia,  especially  those  of  ner- 
vous or  postfebrile  origin.  Da  Costa,  in  1864,  found  it  of  some  value  for  the 
tachycardia  of  acutely  overstrained  hearts,  but  particularly  useful 
when  given  with  digitalis.  This  combination  contains  two 
drugs;  both  stimulate  the  vagi,  the  one  tends  to  diminish,  the  other  to  increase 
the  force  of  cardiac  contraction.  The  recent  observations  of  Price,  quoted  by 
Cushny,  indicate,  however,  that,  in  spite  of  its  action  on  the  vagus,  aconite 
alone  does  not  affect  the  heart-rate  of  patients  with  auricular  fibrillation  who 
respond  readily  to  digitalis,  and  it  is  an  open  question  whether  the  results  ob- 
tained with  aconite  cannot  in  all  cases  be  obtained  better  with  other  drugs. 

EPINEPHRIN  (ADRENALIN). 
Epinephrin  (adrenalin,  suprarenin),  the  active  principle  of  the  supra- 
renal gland,  when  injected  subcutaneously  in  doses  of  1  mg.  exerts  a  stimulat- 
ing action  upon  the  entire  sympathetic  system,  and  causes  a  prompt  though 
very  transitory  elevation  of  the  blood-pressure.  This  is  brought  about  partly 
through  stimulation  of  the  myoneural  junction  of  the  vasoconstrictor  nerves, 
partly  by  direct  stimulation  and  partly  by  bringing  about  dilatation  of  the 


268  DISEASES  OF  THE  HEART  AND  AORTA. 

coronary  arteries.  This  dilatation  of  the  coronary  arteries  is  in  striking  con- 
trast to  the  intense  constriction  of  the  peripheral  vessels  and  is  in  harmony 
with  the  fact  that  stimulation  of  the  sympathetic  nerves  has  the  same  para- 
doxical effect. 

This  dilatation  of  the  coronaries  can  be  very  strikingly  demonstrated  upon 
the  exposed  heart  of  animals  operated  in  the  laboratory,  whose  vessels  can 
be  seen  to  dilate  enormously.  Vessels  previously  invisible  stand  out  in  bold 
lines  after  the  administration  of  adrenalin.  The  heart  beats  more  forcibly; 
its  systolic  output  and  tone  are  increased;  and  the  dilated  heart  soon  bails 
out  its  excess  blood  and  contracts  to  a  smaller  and  much  more  normal  size. 

These  properties  have  won  for  epinephrin  a  place  among  the  best  cardiac 
stimulants.  It  is  especially  useful  in  emergencies,  for  its  action  is  of  less  than 
five  minutes'  duration.  In  acute  heart  failure,  however,  this  may  be  sufficient 
to  relieve  a  threatened  failure  from  acute  dilatation,  and  Janeway  (Arch.  Int. 
Med.,  1914,  xiii,  378)  reports  that  injection  of  4  doses  of  1  mg.  adrenalin 
(1:1000  solution)  has  proved  life-saving  in  cases  of  pneumonia. 

It  is  also  of  benefit  because  it  acts  as  a  stimulator  of  the  whole  sympathetic 
nervous  system  and  of  the  suprarenal  gland,  and  its  stimulation  may  cause 
this  gland  in  turn  to  secrete  more  epinephrin  into  the  blood;  so  that  a  lasting 
beneficial  effect  may  be  obtained  due  in  part  to  the  epinephrin  injected,  in  part 
to  that  secreted  by  the  suprarenal  gland  which  it  has  awakened  into  activity. 

In  the  writer's  experience  it  has  occasionally  been  possible  to  revive  the 
hearts  of  dogs  and  rabbits  after  they  had  stopped  beating,  by  direct  intra- 
cardiac injection  of  adrenalin;  and  there  seems  to  be  no  reason  why  the  same 
method  should  not  be  applied  clinically. 

The  coronary  dilator  action  of  adrenalin  would  also  tend  to  render  it 
of  value  in  angina  pectoris,  particularly  if  given  along  with  the  nitrites,  so  as 
to  exert  a  synergistic  action  in  dilating  the  coronaries  but  an  antagonistic 
action  as  to  the  constriction  of  peripheral  arteries  and  the  raising  of  blood- 
pressure.  A  more  extended  clinical  test  is  necessary,  however,  before  the  use 
of  adrenalin  in  angina  pectoris,  with  or  without  nitrates,  can  be  recommended. 

All  in  all,  however,  epinephrin  is  a  drug  which  is  destined  to  come  into 
wider  clinical  use  than  has  heretofore  been  customary. 

Pituitary  Extract. — The  active  principle  of  the  infundibular  part  of 
the  hypophysis  cerebri  (pituitrin,  hypophysin,  etc.)  has  an  action  somewhat 
similar  to  that  of  epinephrin,  but  though  it  has  a  direct  action  upon  the  muscle 
in  the  walls  of  the  blood-vessels  as  well  as  upon  the  myoneural  junction,  its 
stimulating  effect  is  somewhat  less  constant  than  that  of  epinephrin,  and  falls 
of  blood-pressure  as  well  as  rises  may  be  encountered.  The  active  principle 
of  the  pituitary  has  not  been  isolated  chemically,  though  Fuhner  (Muenchen 
Med.  Wchnschr.,  1912,  lix,  852)  has  shown  that  it  belongs  to  the  same  group 
of  amines  derived  from  amino-acids  by  the  splitting  off  of  C02  as  do  epinephrin 
and  the  active  principles  of  ergot. 

ERGOT. 
Ergot  has  been  recommended  by  some  writers  for  its  vasoconstrictor 
action  exerted  through  stimulation  of  the  vasomotor  centre.  It  also  stimu- 
lates the  vagal  centre.  Cronyn  and  Henderson  have  found  that  these  effects 
are  very  uncertain  when  the  drug  is  given  by  mouth,  but  occur  quite  uni- 
formly when  it  is  given  intravenously.     Since  this  is  rarely  necessary,  the 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.  269 

use  of  ergot  may  be  confined  to  patients  with  vasomotor  failure,  in  which, 
like  adrenalin,  it  is  used  as  a  last  resort. 

NITRITES  AND  NITROGLYCERIN. 
PREPARATIONS.       (PHARMACOP03IAL,    U.  S.  P.J 
Amyl  nitrite  (amylis  nitris),  a  liquid  containing  about  80  per  cent,  of  amyl  nitrite. 
Average  dose,  0.2  c.c,  3  minims  (inhaled).   Usually  to  be  had  in  pearls,  each  pearl  contain- 
ing one  dose. 

Nitroglycerin  CH2ON02 

CHONO2 

CH2ONO2 

is  sold  in  tablets  of  varying  size,  usually  one  tablet  containing  y^  gr.  (0.6  mg.).  However, 
in  tablet  form  the  nitroglycerin  may  undergo  more  or  less  rapid  deterioration,  and  hence 
administration  in  this  form  is  unreliable.  It  is  best  given  as  spirit  us  gly  eery  lis  nitratis 
(spiritus  glonoini),  a  1  per  cent,  solution  of  nitroglycerin  in  alcohol,  which  should  be  freshly 
prepared  from  a  10  per  cent,  stock  solution.  Initial  dose,  0.05  c.c.  (1  minim),  increasing, 
if  necessary,  1  minim  at  a  time. 

Sodii  nitris  (sodium  nitrite),  NaN02,  a  white  fused  mass,  very  deliquescent  and  slowly 
becoming  oxidized  to  sodium  nitrate  on  exposure  to  the  air,  thus  becoming  useless.  Dose, 
0.06-0.12  Gm.   (gr.  i-ii). 

There  are  also  several  non-pharmacopceial  nitrates  which  are  very- 
satisfactory.  Erythrol  tetranitrate,  CH2ON02-CHON02- 
CHONO2-CH2ONO2,  has  about  the  same  action  as  nitroglycerin,  except  that 
it  acts  more  slowly  (action  lasting  three  to  four  hours).  Sold  as  tablets,  each 
containing  .03  Gm.  (-|-  gr.).  Dose,  one  or  two  tablets  every  four  to  six  hours. 
In  the  cases  in  which  the  writer  has  used  it,  erythrol  tetranitrate  has  been 
very  efficient  and  satisfactory. 

ACTION    OF   THE    NITRITES. 

In  practical  therapy  the  nitrites  are  drugs  of  great  importance.  In 
animals  they  are  found  to  act  upon  the  muscles  and  nerves  of  the  blood- 
vessels to  bring  about  an  intense  vasodilatation,  thereby  diminishing  the 
resistance  to  blood  flow  and  lessening 

the  resistance  to  the  action  of  the  heart.     ^  g      min.  hours 

Francois-Franck  first  observed  that  the 
coronary  arteries  of  the  exposed  dog's 
heart  could  be  seen  to  dilate  markedly 
after  the  adrninistration  of  nitrites  and 
the  writer  has  been  able  to  confirm 
this  observation  on  numerous  occa- 
sions, even  when  the  general  blood  has  Fm.  134.— Effects  of  drugs  of  the  nitrite 

-   ,,  m,  .  ,  £      r\  11        series  upon  the  blood-pressure  in  man.    (Schema 

fallen.         Ihe     experiments     OI       USWald        repre8enting  the  findings  of  Hewlett  and  Mat- 

Loeb  on  the  excised  heart  and  of  G.  S.     tiww».)   min,  minutes. 

Bond  on  the  outflow  from  an  incised 

coronary  vein  are  negative.    The  beneficial  effects  of  nitrites  in  angina  pectoris 

seem  therefore  to  be  due  to  dilatation  of  the  coronary  arteries. 

The  relation  of  the  various  nitrites  to  one  another  as  regards  rapidity  of  ac- 
tion is  shown  in  Fig.  134.  The  effect  of  amyl  nitrite  sets  in  within  a  minute  and 
passes  off  within  five  minutes ;  that  of  nitroglycerin  lasts  from  about  the  seventh 
to  the  twentieth  minute  after  administration,  sodium  nitrite  from  the  fifteenth 
to  the  thirty-fifth,  while  erythrol  tetranitrate  begins  to  exert  an  effect  only 
after  about  fifteen  to  thirty  minutes,  but  this  continues  for  three  to  four  hours. 


270 


DISEASES  OF  THE  HEART  AND  AORTA. 


Amyl  Nitrite. — Hewlett  has  recently  made  a  careful  clinical  study  of  the  effects  of 
amyl  nitrite  inhalation,  and  found  (1)  an  immediate  fall  of  maximal  pressure, 
average  13  mm.  Hg,  lasting  less  than  forty  seconds,  and  accompanied  by  a  less  fall  of 
minimal  pressure  and  an  increase  of  pulse-rate.  This  is  followed  by  a  secondary, 
rise  (about  28  mm.)  of  maximal  pressure  to  considerably  above  the  original  height, 
accompanied  by  a  less  marked  rise  of  the  minimal  pressure  and  by  a  return  of  pulse-rate 
to  the  normal.  These  changes  in  blood-pressure  correspond  to  an  increased  sys- 
tolic output  and  increased  force  of  heart-beat  (augmentor  effect),  and  Hewlett  was 
able  to  see  with  the  fluoroscope  that,  "as  the  action  of  the  heart  slowed  down  the  excur- 
sions of  the  left  ventricle  became  wider  by  one-half  centimetre,  but  they  soon  returned  to 
normal."  In  other  words,  besides  being  a  vasodilator  amyl  nitrite  is  a  very 
active  cardiac  stimulant,  more  rapid  than  any  except  adrenalin.  These 
findings  accord  well  with  the  results  of  Cameron  on  dogs,  that  nitroglycerin  both  i  n  - 
creases  cardiac  output  and  cardiac  tonicity  to  a  marked  degree. 
Relaxation  of  the  peripheral  blood-vessels  under  the  influence  of  the  amyl  nitrite,  as  shown 
by  the  plethysmograph,  was  present  throughout  all  Hewlett's  experiments  in  spite  of  the 
peculiar  variations  of  blood-pressure.  The  vasodilatation  reaches  its  maximum  within 
the  first  minute  and  very  gradually  subsides  after  the  second,  but  a  definite  effect  is  still 
noticeable  ten  or  twelve  minutes  after.  In  older  persons  Hewlett  found  that  the  pulse- 
rate  often  did  not  change,  probably  owing  to  the  absence  of  the  tonic  activity  of  the  vagus. 

The  following  represent  typical  effects  in  normal  men  as  obtained  in  the 
very  careful  clinical  investigations  of  Hewlett  and  Matthew: 


Dose. 

Time  when 
action  begins. 

Average 
fall  inB.P. 

Maximal 

fall 
occurs  in 

Duration. 

Amyl  nitrite  (Hewlett) 

15  sec. 
1    min. 
5    min. 
5|  min. 
12 

20  mm. 

28' 

32 

35 

35 

1    min. 
4§  min. 
14  min. 
22  min. 
100  min. 

10  min. 

Nitroglycerin  .05-.  1  c.c.  (n\,  i-ij) 

Sodium  or  potassium  nitrate  .15  Gm.  (gr.  ij). .  . 

Erythrol  tetranitrate  .03-06  Gm.  (gr.  §-i) 

Manitol  tetranitrate  .06  Gm.  (gr.  i) 

^hr. 

Nitroglycerin.— As  to  nitroglycerin,  there  is  tremendous  variation  in  its  effects  upon 
different  individuals,  A.  Loeb  having  reported  a  case  of  collapse  after  0.6  mg.  (T£7  gr.), 
whereas  J.  Stewart  has  given  20  grains  a  day  to  a  single  patient. 

In  some  cases  it  is  impossible  to  obtain  a  fall  of  pressure  with  any  ordinary  doses. 
The  writer's  experience  agrees  with  that  of  Matthew,  that  the  effects  are  often  lacking  in 
cases  of  nephritis  in  which  blood-pressure  has  persisted  for  some  time.  To  this  might 
also  be  added  a  certain  group  of  arteriosclerotics  in  which  the  renal  symptoms  do  not  pre- 
dominate, although  it  is  possible  that  arteriosclerotic  changes  may  be  present  in  the  kidney. 

In  Prof.  J.  O.  Hirschfelder's  wards  it  was  customary  to  begin  with  a 
dose  of  1  gtt.  (-5V  c.c,  |  minim)  every  half  hour,  increasing  1  gtt.  at  every 
third  dose  until  palpitation,  headache,  or  buzzing  in  the  ears  warned  that  the 
physiological  limit  had  been  reached.  The  next  dose  was  then  omitted  and 
a  permanent  dosage  of  1  gtt.  less  than  the  dose  last  given  was  then  kept  up. 
In  some  cases  as  much  as  1  c.c.  (15  minims)  of  the  1  per  cent,  solution  was 
given  every  half  hour  with  only  the  mildest  subjective  symptoms,  the  average 
permanent  dose  being  0.3  to  0.6  c.c  (5  to  10  minims).  The  effect  of  these 
doses  is  very  variable. 

Effect  on  the  Circulation. — A  fall  in  minimal  blood-pressure  is  the  most 
constant,  usually  accompanied  by  a  rise  in  pulse-pressure,  and  the  maximal 
pressure  sometimes  rising,  sometimes  falling.  Hewlett  thinks  that  there  is 
combined  dilatation  of  the  blood-vessels  and  increased  systolic  output  of 
the  heart.  In  a  series  of  observations  upon  the  fluctuations  of  blood-pressure 
after  the  administration  of  these  drugs,  made  with  the  Erlanger  apparatus 
.independently  of  and  some  years  before  those  of  Hewlett,  the  writer  had 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.  271 

noticed  effects  quite  similar  to  those  above  mentioned.  There  seems  no  doubt, 
therefore,  that,  as  stated  by  Hewlett,  the  beneficial  effects  of  the  nitrites  in 
man  are  due  to  something  more  than  a  simple  vasodilatation,  and  indeed 
it  is  possible  that  the  latter  may  play  often  even  a  minor  role.  Certain  it  is 
that  in  many  cases  they  are  ideal  drugs  to  relieve  the  work  of  the  heart  over 
short  periods  when  the  blood-pressure  is  not  already  too  low  to  admit  of  their 
use.  However,  it  must  be  borne  in  mind  that  individual  susceptibilities  vary, 
and  the  patient  should  be  tested  with  amyl  nitrite,  whose  effects  can  be  con- 
trolled, before  any  other  nitrite  should  be  given.  When  used  over  long  periods 
of  time,  moreover,  the  production  of  methsemoglobin  in  the  blood  may  be 
brought  on  (shown  by  the  spectroscope,  or  by  a  chocolate  tint  in  the  blood), 
which  is  distinctly  harmful  and  a  sign  for  immediately  stopping  the  use  of 
the  drug. 

VASOTONIN  (YOHIMBIN-URETHANE). 

Franz  Miiller  and  Bruno  Fellner  have  recently  taken  advantage  of  the 
vasodilator  action  of  the  salts  of  yohimbin  to  introduce  a  derivative  of  the 
latter  into  medical  practice.  In  order  to  obviate  the  aphrodisiac  action 
and  the  effect  upon  the  respiratory  centre,  they  have  combined  yohimbin 
nitrate  with  urethane,  by  which  they  claim  a  definite  double  salt  of  yohim- 
binurethane  is  formed,  to  which  they  have  given  the  trade  name  of  vaso- 
tonin. The  claim  that  'Vasotonin"  represents  a  definite  chemical  combi- 
nation, rather  than  a  mixture  of  the  two  drugs,  has  been  sharply  criticised 
by  Spiegel  and  cannot  be  regarded  as  definitely  settled.  On  the  other  hand, 
Miiller  has  shown  that  the  physiological  effects  of  yohimbin  are  greatly 
changed  by  the  presence  of  the  urethane,  so  that  the  desired  effect  of  removing 
the  aphrodisiac  and  respiratory  effects  seems  to  have  been  accomplished. 

Miiller  has  shown  experimentally  upon  animals  that  it  lowers  the  blood- 
pressure  by  producing  dilatation  of  the  blood-vessels  of  the  limbs  and  also 
a  certain  amount  of  dilatation  in  the  blood-vessels  of  the  brain,  but  that  the 
vessels  of  the  splanchnic  area  are  constricted.  He  showed  by  means  of  the 
cardiometer,  as  Cameron  had  shown  for  the  nitrites,  that  in  ordinary  doses 
it  increases  the  tonicity  of  the  heart  muscle. 

His  results  were  at  once  applied  clinically  by  B.  Fellner  in  a  series  of 
fifteen  cases. 

Fellner  found  that  in  man  the  subcutaneous  administration  of  1  c.c.  (15 
minims)  of  vasotonin  (containing  10  mg.  yohimbin  nitrate  or  8  mg.  yohimbin) 
exerted  about  the  same  effects  as  Miiller  had  observed  in  animals,  and  gave  rise 
to  a  dilatation  of  the  arteries  with  a  fall  of  maximal  blood-pressure  often  amount- 
ing to  50  mm.  Hg.  The  minimal  blood-pressure  was  affected  to  a  less  degree; 
the  pulse-pressure  usually  diminished.  With  a  single  injection  daily  or  even 
upon  alternate  days  these  effects  persisted  and  in  many  cases  gave  the  desired 
result.  His  observations  have  been  confirmed  by  Staehelin  and  by  Rosendorff. 

Fellner  recommends  the  drug  in  the  following  classes  of  cases: 

1.  Transitory  hypertension,  such  as  attacks  of  angina  pectoris,  various 
forms  of  asthma,  vasomotor  crises  and  conditions  of  increased  vasomotor 
irritability,  intermittent  claudication,  etc. 

2.  More  lasting  hypertension,  as  in  arterioscleroses,  the  toxic  hyper- 
tension of  lead  and  nicotine  poisoning,  and  also  in  chronic  nephritis. 

Aneurism  might  also  be  added  to  this  list. 


272  DISEASES  OF  THE  HEART  AND  AORTA. 

As  regards  the  clinical  phase  of  the  question,  it  must  be  said  that,  regard- 
less of  whether  vasotonin  is  a  definite  chemical  combination  or  merely  a 
mixture  of  two  drugs,  the  results  obtained  by  these  observers  merit  serious 
considerations,  and,  while  they  do  not  seem  superior  to  those  obtained  with 
the  nitrites,  compare  very  favorably  with  the  latter. 

POTASSIUM  IODIDE. 

Potassium  iodide  is  the  drug  which  is  most  widely  used  in  the  treatment 
of  all  forms  of  arteriosclerosis,  and  the  clinical  results  are  so 
definite  as  to  render  its  usefulness  certain.  The  manner  in  which  it  exerts 
this  beneficial  action  is,  however,  much  less  definitely  known.  It  was  at 
first  supposed  by  Potain  and  others  to  lower  the  blood-pressure  by  some 
direct  action  upon  the  vasomotor  or  cardiac  mechanisms,  but  this  action  is 
slight  if  any,  and  the  writer  does  not  recall  ever  having  seen  high  blood-pressure 
depressed  by  potassium  iodide  without  the  intervention  of  some  other  factor. 
It  was  then  supposed  to  have  some  effect  in  diminishing  the  viscosity  of  the 
blood,  as  was  claimed  by  Otfried  Muller  and  Inada  in  Romberg's  clinic.  A 
careful  perusal  of  their  statistics  shows  that  the  results  were  absolutely 
negative  in  about  half  of  their  cases  and  within  the  limits  of  observational 
error  in  the  others.  Determann,  who  repeated  their  experiments,  found  the 
effect  upon  viscosity  entirely  negative. 

It  was  then  claimed  by  Koranyi  and  others  that  potassium  iodide  prevented 
the  production  of  adrenalin  arterionecrosis,  but  this  claim  also  fell  to  the  ground 
when  tested  upon  a  very  large  series  of  animals  by  Leo  Loeb  and  Githens. 

The  pharmacological  action  of  potassium  iodide  is  therefore  still  to  be 
classed  among  those  mysterious  actions  termed  "alterative." 

Some  light  is  thrown  upon  the  action  of  potassium  iodide  by  the  recent  studies  of 
Collins  and  Sachs  and  Longcope  upon  the  vascular  changes  due  to  syphilis.  These  ob- 
servers obtained  a  positive  Wassermann  reaction  in  many  cases  of  aortic  insufficiency 
in  which  there  was  no  other  sign  of  active  luetic  lesion.  In  these  cases  and  also  in  simple 
arteriosclerosis  of  luetic  origin,  the  potassium  iodide  probably  facilitates  the  removal  of 
the  luetic  exudations  and  thus  diminishes  the  ill  effects  of  the  arterial  lesion.  This  would 
explain  why  no  action  can  be  detected  upon  the  healthy  vessel  or  upon  the  mechanical 
factors  in  the  circulation. 

It  must  be  admitted  that  the  mode  of  action  is  entirely  unknown;  but, 
on  the  other  hand,  administration  of  potassium  iodide  does  lessen  the  symp- 
toms of  stenocardia  and  other  painful  and  disagreeable  symptoms  in  many 
cases  of  arteriosclerosis,  and  may  even  cause  them  to  disappear  permanently. 
It  may  therefore  be  administered  with  advantage  in  all  cases  in  which  the 
above-mentioned  symptoms  arise  or  even  where  they  are  threatened. 

Potassium  iodide  is  best  given  after  meals  in  large  amounts  (half  glassful 
or  glassful)  of  water  or  milk.  The  unpleasant  taste  may  be  disguised  by  a 
little  sherry,  elixir  aromaticum  or  gentian.  Dose  potassii  iodidi  0.3  to  2.0  Gm. 
(gr.  v  to  xxx)  (reached  by  increasing  doses). 

When  not  well  borne  by  the  stomach  or  when  the  heart  is  very  weak, 
sodium  iodide,  the  iodized  fatty  acid  "  iodipin,"  or  new  iodized  organic  acid 
"safodin"  may  be  substituted.     Their  action  does  not  seem  to  differ  much 

from  that  of  potassium  iodide. 

SAJODIN. 

Sajodin  (calcium  monoiodobehenate,  (C2iH42ICOO)2Ca),  is  a  colorless, 
tasteless  powder  yielding  iodine  on  decomposition.     It  contains  26  per  cent. 


THE  EFFECTS  OF  DRUGS  IN  CARDIAC  DISEASE.  273 

of  iodine.    Dose,  1  to  3  Gm.  (gr.  xv  to  xlv)  daily,  best  in  powders  or  capsules, 
half  an  hour  after  meals. 

Sajodin  has  all  the  pharmacological  actions  of  potassium  iodide,  except 
for  the  fact  that,  since  the  iodine  is  split  off  more  slowly,  the  action  upon 
the  stomach  and  the  tendency  to  produce  iodine  rashes  are  far  less  marked 
and  less  rapid  in  development.  On  the  other  hand,  the  desired  effects  of  the 
iodine  seem  to  appear  with  equal  rapidity  and  from  somewhat  smaller  doses, 
and  in  many  cases  this  drug  can  be  administered  over  much  longer  periods 
of  time  than  the  iodide.  Excellent  effects  are  therefore  obtained  in  myocar- 
ditis, arteriosclerosis,  angina  pectoris,  and  aneurism  by  its  use  (Kuttelwascher, 
Vigorelli). 

SALVARSAN— "  606." 

The  exact  role  to  be  played  by  salvarsan,  Ehrlich's  great  antisyphilitic,  in 
the  treatment  of  luetic  diseases  of  the  circulation,  is  still  somewhat  undecided. 

As  shown.by  Hering,  Camus,  Hoke,  and  Rihl,  salvarsan,  ideal  and  hyper- 
ideal  when  injected  into  animals,  produces,  as  do  most  other  preparations  of 
arsenic,  an  intense  fall  in  blood-pressure.  That  this  is  due  chiefly  to  a  paralysis 
of  the  abdominal  vessels  is  shown  by  the  fact  that  the  blood-pressure  can  no 
longer  be  raised  by  injection  of  adrenalin,  although  it  can  be  raised  to  a 
considerable  height  by  clamping  the  descending  aorta.  Hoke  and  Rihl  have 
interpreted  the  latter  phenomenon  as  evidence  that  the  strength  of  the  heart 
is  unimpaired,  but,  as  has  been  shown  in  other  chapters,  in  persons  with  a 
normal  circulatory  system  this  fall  in  blood-pressure  amounts  to  from  25  to 
45  mm.  Hg  (30  to  60  cm.  H20)  and  lasts  from  one  to  three  days,  when  it  may 
be  followed  by  a  transient  rise.  There  is  probably  some  weakening  of  the 
heart  as  well,  but  this  is  not  a  source  of  danger  to  the  normal  circulatory 
system.  In  persons  with  diseases  of  the  heart,  aorta,  and  kidneys  these 
effects  are  dangerous ;  and  a  considerable  number  of  deaths  have  been  reported. 
These  cases  have  been  subjected  to  a  critical  review  by  Ehrlich  and  Martius 
of  Frankfurt,  who  call  attention  to  seven  reported  deaths  which  seem  to 
have  been  due  entirely  to  the  action  of  the  drug.  Several  of  these  patients 
were  in  excellent  condition  at  the  time  that  the  injections  were  made.  In 
five  out  of  these  seven  cases  the  triad  luetic  aortitis,  coronary 
sclerosis,  and  myocarditis  were  found  at  autopsy,  but  in  four 
of  these  five  they  were  not  recognizable  clinically. 

Death  in  these  cases  sometimes  occurred  from  collapse  within  a  few 
hours  after  the  injection,  as  in  the  case  reported  by  Spiethoff,  and  sometimes 
occurred  suddenly  several  days  later.  Ehrlich  has  accordingly  advised  against 
its  use  in  "persons  who  have  very  irritable  cardiac  nerves,  or  heart  disease, 
arterial  degenerations,  aneurisms,  or  cerebral  hemorrhage,  old  persons,  ne- 
phritics,  diabetics,  and  patients  with  gastric  ulcer."  This  conservative 
expression  is  voiced  by  Martius,  Sieskind,  and  other  subsequent  observers, 
and  if  rigidly  followed  would,  of  course,  exclude  salvarsan  entirely  from  the 
therapeutics  of  the  circulation.  Nevertheless,  it  must  by  no  means  be  assumed 
that  every  case  or  even  a  very  large  percentage  of  cases  of  cardiovascular 
disease  suffers  from  treatment  with  salvarsan.  Thus,  Martius  writes  that 
"Numerous  reports  have  been  made  of  favorable  experiences  in  angina 
pectoris,  and  the  most  astonishing  results  were  obtained  in  just  those  cases 
with  the  most  severe  and  most  dangerous  attacks.  But  these  patients  were 
18 


274  DISEASES  OF  THE  HEART  AND  AORTA. 

always  persons  with  intact  heart  and  in  whom  no  really  severe  lesion  of  the 
heart  or  vessels  was  suspected." 

The  danger  of  collapse  from  cardiac  failure  resulting  from  the  use  of 
large  doses  of  salvarsan  intravenously  may  indeed  be  obviated  to  a  great 
extent  by  the  use  of  smaller  doses,  and  the  37  cases  reported  by  Wechselmann 
and  Nicolai  without  cardiac  failure  did  not  receive  doses  larger  than  0.5  Gm. 
Still  smaller  doses  (0.2  to  1.2  Gm.  intravenously)  may  be  given  repeatedly 
(at  intervals  of  about  a  week)  with  still  less  danger  at  the  time  of  injection, 
but,  as  Kromayer  has  stated,  the  danger  of  severe  recurrence,  and  especially 
of  lesion  to  the  nervous  system,  is  particularly  great  after  the  use  of  repeated 
small  doses.  In  cardiac  and  arterial  disease,  however,  it  must  be  remembered 
that  merely  bringing  about  the  subsidence  of  the  luetic  lesion  temporarily  may 
enable  the  circulation  to  regain  its  function,  so  that  at  a  later  period  larger 
doses  may  be  given  before  the  new  crop  of  lesions  has  had  time  to  form.  The 
use  of  salvarsan  in  such  doubtful  cases  is  at  present  in  a  transition  stage,  the 
final  development  of  which  will  require  several  years  of  investigation  to  decide. 

POTASSIUM  THIOCYANATE. 
Another  drug  which  tends  to  lower  the  blood-pressure  greatly  is  potassium  thiocya- 
nate  (KCNS).  The  use  of  this  drug  as  a  sedative  to  the  nervous  system  was  first  suggested 
by  W.  Pauli  (1903),  who  believed  that  he  obtained  some  excellent  results  in  eleven  arterio- 
sclerotics and  in  two  cases  of  heart  failure.  It  was  used  more  carefully  by  J.  Pal  (1905), 
who  writes:  "I  have  been  able  to  obtain  a  good  effect  from  thiocyanate  preparations  in 
some  cases  in  which  even  potassium  iodide  was  without  effect.  This  cyanate  often  grad- 
ually reduces  a  high  blood-pressure,  but  often  brings  on  symptoms  of  intoxi- 
cation in  arteriosclerotics,  especially  in  those  with  renal  complications.  These  toxic 
symptoms  are  erythemata  and  mental  confusion,  which  disappear,  as  I 
have  found,  when  the  thiocyanate  is  left  off  and  opium  given.  .  .  .  Diuretin  and  iodide  or 
thiocyanate  are  of  value  (in  vasomotor  crises)  only  when  administered  over  long  periods." 

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innere  Med.,  Wiesb.,  1901. 

Aconite. 

Matthews,  S.  A.:  A  Study  of  the  Action  of  Aconitin  on  the  Mammalian  Heart  and  Cir- 
culation, J.  Exp.  Med.,  Baltimore,  1897,  ii,  593. 

Cushny,  A.  R.:  The  Irregularities  of  the  Mammalian  Heart  Observed  under  Aconitine 
and  on  Electrical  Stimulation,  Heart,  Lond.,  1909-1910,  i,  1. 

Da  Costa,  J.  M.:  On  Irritable  Heart,  Am.  J.  M.  Sci.,  Phila.,  lxi,  17. 

Hirschfelder,  A.  D.:  Observations  upon  Paroxysmal  Tachycardia,  Bull.  Johns  Hopkins 
Hosp.,  Bait.,  1906,  xvii,  337. 

Adrenalin. 

Straub,  W.:  Die  pharmakologische  Grundlagen  der  Adrenalintherapie,   Munchen.  med. 

Wchnschr.,  1911,  lviii,  1388. 

Caffeine. 
Wagner:  Experimentelle  Untersuchungen  ueber  den  Einfluss  des  Kaffeins  auf  Herz  und 

Gefassapparat,  In.  Diss.,  Berl.,  1885. 
Glupe:  Ueber  die  Wirkung  der  Kaffeinsalze  bei  Herzkrankheiten,  In.  Diss.,  Berl.,  1884. 
Cushny  and  van  Naten:  On  the  Action  of  Caffeine  on  the  Mammalian  Heart,  Arch.  int.  de 

Pharmacodyn.,   1901,  ix,   169. 
Cushny,  A.  R.:  A  Contribution  to  the  Pharmacology  of  the  Mammalian  Heart,  Brit.  M.  J., 

1898,  i,  1068. 
Fraenkel:  Klinische  Untersuchungen  ueber  die  Wirkung  von  Kaffein,  Morphium,  Secale 

cornutum  und  Digitalis  auf  den  arteriellen  Blutdruck,  Deutsch.  Arch.  f.  klin.  Med., 

Leipz.,  1889-1890,  xlvi,  542. 
Bock:  Ueber  die  Wirkung  des  Kaffeins  und  Theobromins  auf  das  Herz,  Arch.  f.  exper. 

Pathol,  u.  Pharmakol.,  Leipz.,  1900,  xliii,  367. 

Calcium  Salts. 
Brunton,  T.  Lauder:  Use  of  Calcium  Salts  as  Cardiac  Tonics  in  Pneumonia  and  Heart 

Disease,  Brit.  M.  J.,  1907,  i,  616. 
Stark,  J.:  Calcium  Salts  as  Cardiac  Tonics,  Lancet,  Lond.,  1907,  i,  1701. 
Barr,  J. :  On  the  Use  of  Calcium  Salts  as  Cardiac  Tonics  in  Pneumonia  and  Heart  Disease, 

Brit.  M.  J.,  Lond.,  1907,  i,  717. 
Sladen:  Personal  communication. 
Boggs,  T.  R.:  Variations  in  the  Calcium  Content  of  the  Blood  Following  Therapeutic 

Measures,  Johns  Hopkins  Hosp.  Bull.,  Baltimore,  1908,  xix,  201. 


278  DISEASES  OF  THE  HEART  AND  AORTA. 

Nitrites. 
Brunton,  T.  L.    Quoted  on  page  253. 
Hewlett,  A.  W. :  The  Effect  of  Amyl  Nitrite  Inhalations  upon  the  Blood-pressure  in  Man, 

J.  Med.  Research,  Bost.,  1906,  xv,  383. 
Cameron.    Quoted  on  page  201. 

Matthew:  Vasodilators  in  High  Blood-pressure.    Quart.  J.  M.,  Oxford,  1909,  ii. 
Loeb,  A.:  Klinische  Untersuchungen  ueber  den  Einfluss  von  Kreislaufsaenderungen  auf 

die  Urinzusammensetzung,  Deutsches,  Arch.  f.  klin.  Med.,  Leipz.,  lxxxiv,  579. 
Stewart,  J.:  Tolerance  to  Nitroglycerin,  J.  Am.  M.  Assoc,  Chicago,  1905,  xliv,  1678. 

Potassium  Iodide. 

Potain:  La  clinique  medicale  de  la  Charite,  Par.,  1894. 

Muller,  O.,  and  Inada:  Zur  Kenntniss  der  Iodwirkung  bei  der  Arteriosklerose,  Deutsche 

med.  Wchnschr.,  Leipz.,  1904,  xxx,  1751. 
Determann.    Quoted  on  page  61. 
Koranyi,  Loeb  and  Githens.    Quoted  on  page  259. 

Potassium  Thiocyanate. 

Pauli,  W.:  Ueber  Ionenwirkung  und  ihre  therapeutische  Verwendung,  Miinchen.  med. 

Wchnschr.,  1903,  1,  153. 
Pal,  J.:  Die  Gefasskrisen,  Leipz.,  1905. 

Sajodin. 

Kuttelwascher,  W.:  Erfahrungen  mit  Sajodin,  Prager  med.  Wchnschr.,  1907,  546. 
Vigorelli,  A.:  Alguni  Experimenti  golla  Sajodina,  Poliambulanza  di  Milano,  1908,  No.  10, 
quoted  from  Zentralbl.  f.  d.  ges.  Physiol,  u.  Path.  d.  Stoffw.,  Berl.,  1909,  N.  F.,  iv,  639. 

Salvarsan  ("606"). 

Hering,  H.  E. :  Experimented  Erfahrungen  ueber  die  letale  Dosis  der  sauren  Losung  von 

Ehrlich-Hata  606.     Miinchen.  med.  Wchnschr.,  1910. 
Camus,  J.  and  L.:  Recherches  experimentales  sur  le  "606,"  Paris  medical,  Dec,  1910, 

quoted  from  Sieskind. 
Hoke,  E.,  and  Rihl,  J. :    Experimented  Untersuchungen  ueber  die  Beeinflussung  der  zir- 

kulationsorgane  und  der  Atmung  durch  das  Salvarsan,  Verhandl.  d.  Kong.  f.  innere 

Med.,  Wiesb.,  1911,  xxviii,  242,  and  discussions  by  Hering,  Schreiber,  Nicolai,  and 

Benario. 
Sieskind,  R.:  Das  Verhalten  des  Blutdrucks  bei  intra venoser  Salvarsaninjektionen,  Miin- 
chen. med.  Wchnschr.,  1911,  lviii,  568. 
Ehrlich,    P.:    Die    Salvarsantherapie,     Ruckblicke    und     Ausblicke,     Miinchen.     Med. 

Wchnschr.,  1911,  lviii,  1. 
Martius,  K. :  Ueber  Todesfalle  nach  Salvarsaninjektionen  bei  Herz  und  Gefasskrankheiten, 

ibid.,  1911,  lviii,  1067. 
Spiethoff,  B.:  Salvarsan  bei  Syphilis,  ibid.,  1911,  lviii,  192. 
Wechselmann  and  Nicolai:  Action  du  dioxydiamidoarsenobenzol  d'Ehrlich  sur  le  ceeur, 

Arch,  des  Malad.  du  cceur  et  des  vaiss.,  Par.,  1910,  iii,  730. 
Kromayer:  Chronische  Salvarsanbehandlung  bei  Syphilis,    Deutschen  med.  Wchnschr., 

Leipz.,  1911,  xxxvii,  1547. 

Vasotonin. 

Muller,  Fr.,  and  Fellner,  B.:  Ueber  "Vasotonin,"  ein  neuesdruckherabsetzen  des  Gefass- 

mittel,  Therap.  Monatsh.,  Berl.,  1910,  xxiv,  285. 
Muller,  Fr.:  Erwiderung  auf  die  Bemerkungen   des    Herrn  Prof.  L.  Spiegel  im  Juliheft 

dieser  Zeitschrift,  ibid.,  1910,  xxiv,  439;  Ueber  Vasotonin,  Zweite  Erwiderung  an  Herrn 

Prof.  L.  Spiegel,  ibid.,  1910,  xxiv,  546. 
Spiegel,  L.:  Ueber  Vasotonin,  ibid.,  1910,  xxiv,  365;  also  Nocheinmal  das  "Vasotonin," 

ibid.,  1910,  xxiv,  544. 
Heubner,  W.:  Zur  Vasotoninfrage,  ibid.,  1910,  xxiv,  549. 
Staehelin,  R.:  Erfahrungen  mit  Vasotonin,  ibid.,  1910,  xxiv,  477,  521. 
Rosendorff :  Ueber  Erfahrungen  mit  Vasotonin,  ibid.,  1911,  xxv,  148. 


VI. 

GYMNASTICS  AND  HYDROTHERAPY. 

GYMNASTICS. 
FUNDAMENTAL    PRINCIPLES. 

During  recent  years  gymnastic  exercises  have  come  to  play  a  major 
role  in  the  treatment  of  cardiac  diseases.  Although  this  treatment  was 
introduced  empirically,  its  physiological  basis  is  found  in  the  fact,  shown 
by  Frank  and  Hirschfelder,  that  a  strain  upon  the  ventricles  which  does 
not  exhaust  them  tends  to  act  as  a  stimulus  which  gives  rise  to  more  forci- 
ble contractions,  increases  their  tonicity,  and  causes  the  residual  blood 
(and  hence  the  d'latation)  to  decrease.  The  guiding  principle  is  further 
given  by  the  experimental  evidence  produced  by  these  writers,  that  when 
the  strain  was  excessive  it  had  the  opposite  effect,  and  caused  weakening 
of  the  contractions,  diminished  tonicity,  and  dilatation  of  the  heart.  (See 
Fig.  119.) 

In  dealing  with  normal  individuals  it  is  observed  that  the  strengthen- 
ing of  every  normal  individual,  the  training  of  every  athlete  or  laborer  con- 
sists in  the  habituation  of  the  body,  and  particularly  of  the  heart,  to  gradu- 
ally increasing  muscular  effort  and  exercises.  (See  page  206.)  To  a  great 
extent,  as  has  been  seen,  page  204,  this  consists  in  securing  a  greater  increase 
in  output  of  blood  at  each  beat  without  calling  upon  any  of  the  accessory 
nervous  mechanism  to  bring  this  about.  Such  exercises  have  also  been 
used  with  great  success  in  the  treatment  of  patients  with  heart  failure.  It 
stands  to  reason  that  they  should  not  be  used  at  once  when  the  patient  is 
brought  in  with  an  acute  heart  failure;  but  after  a  sufficiently  long  period 
of  rest,  when  the  acute  condition  has  passed  off  and  he  can  sit  up  in  bed 
without  discomfort,  a  few  of  the  mildest  arm  movements  may  be  begun 
with  great  advantage.  It  is  often  better  to  train  the  patient  by  a  few  mild 
passive  or  resisted  movements  while  he  is  still  in  bed  than  to  subject 
him  at  once  to  the  strain  of  getting  up  for  an  hour  or  so  after  his  sojourn 
in  bed.  Moreover,  many  other  muscles  may  be  kept  in  tone,  the  blood- 
vessels in  the  muscles  may  be  kept  dilated,  and  the  resistance  to  blood 
flow  may  thus  be  diminished. 

SYSTEMS    OF    EXERCISE. 

In  accordance  with  these  facts  several  systems  of  exercises  have  been 
developed  for  assisting  in  the  training  of  the  heart.  In  all  of  them  the  cru- 
cial point  lies  in  the  avoidance  of  the  slightest  fatigue,  holding  of  the  breath, 
or  increased  breathing.  Hence  the  actual  result  obtained  depends  more 
upon  the  vigilance  and  intelligence  of  the  physician,  nurse,  or  attendant 
who  supervises  the  exercises  than  upon  the  exercises  themselves. 

279 


280  DISEASES  OF  THE  HEART  AND  AORTA. 

Ease  of  mind  and  mental  distraction  are  as  important  as  any  other  points 
in  carrying  out  the  exercise,  and  the  writer  has  seen,  numerous  patients  to 
whom  a  given  exertiDn  was  difficult  or  impossible  until  their  minds  were  di- 
verted, when  it  was  performed  subconsciously,  without  the  slightest  strain. 
Dr.  R.  E.  Morris  has  adopted  the  habit  of  keeping  a  graphophone  playing  to 
divert  the  patient's  mind  throughout  the  exercise. 

In  general  the  exercises  may  be  divided  into  four  classes:  (1)  Passive 
movements.  (2)  Contraction  of  antagonistic  muscles.  (3)  Resisted  move- 
ments    (4)  Mechanical  gymnastics. 

Passive  Movements. — These  are  the  mildest  possible  forms  of  exercise. 
The  attendant  grasps  the  patient  by  the  hands  or  feet  and  moves  these 
members  gently  and  slowly  about,  while  the  patient  makes  no  effort  at 
contraction  whatever.  Such  movements  have  the  effect  of  increasing 
the  circulation  of  lymph,  the  absorption  of  oedema,  and,  to  a 
certain  extent  also,  of  increasing  the  rapidity  of  blood  flow.  It  is  impor- 
tant to  avoid  all  exercises  in  which  the  arms  are  raised  high  above  the 
head,  since  this  hydrostatically  increases  the  pressure  in  the  vena  cava  and 
may  cause  momentary  dilatation  of  the  heart. 

The  following  exercises  or  modifications  of  them  may  be  carried  out 
while  the  patient  is  still  in  bed,  provided  the  greatest  precaution  is  used 
in  their  execution. 

(1)  Arms  horizontal,  to  the  front  and  back  to  the  line  of  the  shoulders. 

(2)  Arms  horizontal  in  line  of  shoulders,  thence  down  to  the  sides  of  the  body. 

(3)  Arms  horizontal,  describe  circles  with  hands. 

(4)  Arms  vertically  dependent  at  sides,  flex  and  extend  elbows. 

(5)  Arms  dependent  at  sides,  pronate  and  supinate  alternately. 

(6)  Clinch  and  open  fists. 

(7)  Legs  straight,  abduct;  then  adduct  thighs. 

(8)  Flex  and  extend  knee  at  side  of  couch,  never  raising  knee  above  level  of  body. 

(9)  Flex  and  extend  foot  at  ankle-joint. 

(10)  Rotate  thighs  internally  and  externally. 

(11)  Execute  small  circles  with  feet  without  raising  them  more  than  one  foot;    legs 

straight. 

Contraction  of  Antagonistic  Muscles. — Substantially  the  same  exercises 
may  be  carried  out  by  allowing  the  patient  himself  slowly  and  simultane- 
ously to  contract  both  the  muscles  concerned  in  the  movement  and  those 
which  antagonize  them, — i.e.,  biceps  and  triceps,  flexors  and  extensors  of 
wrist,  etc.  In  this  way  little  movement  is  made,  the  pulse-rate  is  slowed 
rather  than  accelerated,  and  yet  a  good  deal  of  energy  may  be  expended. 
The  blood-pressure  is  raised,  however.  If  the  patient  can  be  trained  to 
avoid  all  difficulty  in  breathing  and  all  discomfort,  a  good  deal  of  improve- 
ment in  muscular  strength  and  in  cardiac  tonicity  may  be  obtained  by 
this  method.  Its  main  drawback  lies  in  the  fact  that  the  intensity  of  the 
exercise  is  controlled  not  by  the  attendant  but  by  the  patient,  and  that 
the  latter  is  most  likely  to  do  more  than  is  beneficial. 

RESISTED    MOVEMENTS.       (SCHOTT    MOVEMENTS.) 

Probably  the  most  widely  used  of  all  the  cardiac  gymnastics  are  the 
passive  movements  introduced  by  August  Schott  of  Nauheim.  These  are 
generally  used  in  connection  with  the  Nauheim  baths.     This  combination 


GYMNASTICS  AND  HYDROTHERAPY.  281 

is  particularly  advantageous  and  permits  at  once  of  all  the  advantages  of 
mild  exercise,  of  baths,  of  rest  and  stimulation  to  sleep,  of  psychic  sedative, 
and  of  the  psychic  suggestion  to  the  patient  that  a  great  deal  is  being  done 
and  a  great  effort  is  being  made  for  his  welfare. 

The  Schott  movements  consist  of  practically  the  exercises  described 
above  carried  out  by  the  patient  himself,  but  with  an  attendant  who  makes 
a  slight  resistance  to  each  movement.  The  resistance  should  be  just  enough 
to  prevent  the  movement  from  being  made  rapidly,  and  at  no  time  should 
it  cause  the  patient  any  apparent  effort  or  increase  his  respirations.  Each 
day  the  resistance  may  be  increased  slightly,  so  that  in  a  short  time  the 
patient  may  be  doing  a  good  deal  of  work  without  realizing  it.  In  exe- 
cuting the  resistance  the  attendant's  mind  is  kept  fixed  upon  the  condition 
of  the  patient,  and  he  is  consequently  more  likely  to  notice  over-exertion 
in  the  latter  than  if  he  were  merely  supposed  to  watch  him  without  doing 
anything  himself.  In  carrying  out  the  Schott  movements  the  following 
rules  are  prescribed.1 

Precautions  for  Schott  Exercises. — (1)  Each  movement  is  to  be  performed  slowly 
and  at  uniform  rate. 

(2)  No  movement  is  to  be  repeated  twice  in  succession  in  the  same  limb  or  group 
of  muscles. 

(3)  Each  single  or  combined  movement  is  to  be  followed  by  an  interval  of  rest. 

(4)  The  movements  are  not  to  be  allowed  to  accelerate  the 
patient's  breathing,  and  the  operator  must  watch  the  face  for  the  slightest 
indications  of  (a)  dilatation  of  the  nostrils,  (b)  drawing  of  the  corners  of  the  mouth,  (c) 
duskiness  or  pallor  of  the  cheeks  or  lips,  (d)  yawning,  (e)  sweating,    (/)  palpitation. 

(5)  The  appearance  of  any  one  of  the  above  signs  of  distress  should  be  the  signal 
for  immediately  interrupting  the  movement  in  process  of  execution,  and  for  either  sup- 
porting the  limb  which  is  being  moved  or  allowing  it  to  subside  into  a  state  of  rest. 

(6)  The  patient  must  be  directed  to  breathe  regularly  and 
uninterruptedly,  and,  should  he  find  any  difficulty  in  doing  so,  or  for  any  reason 
show  a  tendency  to  hold  his  breath,  he  must  be  instructed  to  continue,  counting  in  a 
whisper  throughout  the  progress  of  each  movement. 

(7)  No  limb  or  portion  of  the  body  of  the  patient  is  to  be  so  constricted  as  to  compress 
the  vessels  and  check  the  flow  of  blood. 

Schott  Exercises. — The  following  is  a  list  of  Schott  exercises  in  the 
order  in  which  they  are  given.  The  resistance  is  moderate  and  steady,  the 
operator's  hand  always  being  applied  upon  the  surface  of  the  extremity 
toward  which  the  movement  is  made,  even  if  that  entails  gliding  around 
it  gently  during  the  movement.  Usually  the  operator's  hand  is  at  one  side 
of  the  patient's  limb  at  one  phase  of  the  exercise  and  at  the  opposite  when 
the  movement  is  reversed. 

1.  Arms  extended  in  front,  palms  facing  each  other.  The  operator's  palms  rest  upon 
the  backs  of  the  patient's  hands.  Patient's  arms  carried  backward  to  line  of  shoulders, 
the  movement  being  gently  resisted  by  operator  (Fig.  135).  The  operator's  palms  are  then 
rested  against  those  of  the  patient,  and  the  return  of  the  arms  in  front  of  the  chest  is  re- 
sisted. 

2.  One  arm  at  side,  elbow-joint  flexed  upward  to  shoulder,  then  extended  to  original 
position. 

3.  Arms  at  side,  raised  outward  till  thumbs  meet  over  the  head,  then  brought  back 
to  the  original  position. 

1  Quoted  from  W.  Bezly  Thome. 


282 


DISEASES  OF  THE  HEART  AND  AORTA. 


4.  Hands  at  level  of  pelvis  in  midline,  fingers  slightly  flexed.    Arms  raised  to  the 
vertex  of  the  head,  then  back. 


Fig.  135.— Schott  resisted  movements.  (Modified  from  W.Bezly  Thome.)  The  attendant's  hands  are  indi- 
cated in  black;  the  direction  of  the  movement  made  by  the  patient  is  indicated  by  the  black  arrows. 


5.  Arms  at  sides,  then  raised  forward  in  parallel  planes  until  they  are  vertical,  then 
moved  back.  The  hand  of  the  operator  must  glide  around  the  wrist  so  that  it  is  always 
applied  to  antagonize  the  movement. 

6.  Trunk  flexed  on  hips,  knees  straight;  trunk  then  extended. 

7.  Trunk  rotated  without  movement  of  the  feet.  Operator  exerts  resistance  against 
the  shoulders. 


GYMNASTICS  AND  HYDROTHERAPY.  283 

8.  Trunk  flexed  laterally,  first  to  one  side  then  to  the  other,  the  movement  being  an- 
tagonized by  resistance  applied  in  the  axilla,  the  operator's  other  hand  resting  on  the  hip. 

9.  Movement  like  No.  2;  fists  clinched. 

10.  Same,  but  palmar  surface  of  fist  turned  outward. 

11.  Arm  extended  from  side,  palm  down,  raised  forwards  and  upwards  describing 
a  semicircle  until  it  is  raised  vertically  alongside  of  the  ear.     The  movement  is  then  reversed. 

12.  Arms  at  sides,  palms  inward,  moved  upwards  and  backwards  in  parallel  planes. 

13.  Patient  rests  one  hand  on  chair  or  table,  raises  knee  to  horizontal,  flexing  at  hip 
and  knee. 

14.  With  one  hand  resting  on  table,  patient  swings  extended  leg  forward  and  back- 
ward from  the  hip-joint. 

15.  Resting  with  both  hands  on  chair  in  front,  raises  foot  by  flexing  knee  without 
movement  at  hip. 

16.  Resting  one  hand  on  chair  at  side,  patient  swings  opposite  extended  leg  out- 
ward from  hip-joint,  then  returns  to  normal. 

17.  Arms  rotated  outwards  and  inwards  from  shoulder-joint,  operator  grasping  the 
metacarpal  portion  of  the  hand. 

18.  Wrist-joint  flexed  and  extended. 

19.  Ankles  dorsoflexed  and  extended  alternately. 

In  advising  the  patient  either  to  resort  to  such  gymnastic  exercises  at 
home  or  to  pay  a  visit  to  one  of  the  spas  or  sanitoria  at  which  they  are  given 
the  physician  should  bear  in  mind  that  the  exercises  are  to  be  regarded  as  a 
form  of  training  for  hearts  with  reserve  power  rather  than  as  a  panacea  for 
regenerating  a  diseased  heart  already  working  at  its  utmost.  In  such  cases, 
notably  in  persons  with  severe  arteriosclerosis,  hypertension,  severe  myo- 
carditis, and  badly  broken  compensation,  much  harm  may  be  done.  It  is 
unfortunate  that  certain  spa  physicians  are  liable  to  become  over-enthusiastic 
in  the  use  of  one  method  and  to  employ  it  in  all  cases  regardless  of  the  con- 
traindications, and  deaths  under  treatment  sometimes  result. 

MECHANOGYMNAST1CS. 

Movements  may  also  be  carried  out  by  means  of  the  elaborate  and 
ingenious  apparatus  devised  by  Zander  for  regulating  them  in  direction 
and  intensity.  In  these  exercises  the  movements  are  semi-passive,  being 
determined  to  a  great  extent  and  carried  on  by  the  apparatus.  Hence  it 
becomes  more  difficult  to  control  them  accurately  than  is  the  case  with  the 
resistance  movements.  It  is  unquestionable  that  excellent  results  have  been 
obtained  by  this  method,  especially  in  cases  where  there  is  mild  dilatation 
but  no  serious  heart  lesion;  but  it  is  certain  that  the  limits  of  the  patient's 
strength  are  too  readily  overstepped;  and  equally  certain  that,  in  the  large 
institutions  where  this  is  carried  out,  the  superintendents  usually  pay  so 
little  attention  to  the  individual  patient  that  these  exercises  very  frequently 
do  distinct  harm. 

Budingen  has  recently  devised  an  apparatus  for  passive  motion  of  the 
legs,  which  consists  of  a  horizontally  moving  treadle  run  by  a  motor  and  can 
be  brought  to  the  patient's  bed.  He  claims  that  it  relieves  oedema  and 
strengthens  the  legs.  However,  mild  active  or  passive  movements  of  the  feet 
and  legs  are  excellent  substitutes  for  these  mechanical  devices. 

WALKING   AND    CLIMBING. 

The  question  of  walking  involves  not  only  an  important  form  of  exer- 
cise treatment  but  also  the  regulation  of  the  convalescent's  daily  life.  As 
has  been  stated  above,  walking  up  and  down  stairs  frequently  introduces 


284  DISEASES   OF  THE   HEART   AND    AORTA. 

the  greatest  strain  upon  the  patient's  heart.  It  is  most  important  that  this 
strain  should  be  minimized.  This  may  be  done  by  causing  him  to  rest  upon 
each  step  long  enough  to  count  five,  ten,  or  twenty,  thus  insuring  him  against 
hurry  and  breathlessness  (J.  O.  Hirschfelder) .  Another  method  which  has 
been  found  useful  was  suggested  by  the  writer's  wife  while  climbing  moun- 
tains in  the  Sierra  Nevadas.  She  noticed  that  she  could  climb  quite  steadily 
up  the  steepest  trails  provided  she  took  a  deep  or  normal  inspiration  each 
time  the  same  foot  touched  the  ground.  In  this  way  a  relation  was  estab- 
lished between  speed  and  respiration,  the  former  was  regulated  by  the 
latter,  and  a  certain  balance  maintained  between  the  rate  at  which  oxygen 
was  used  up  and  that  at  which  it  was  supplied.  As  the  pulse-rate  is  often 
some  definite  multiple  of  the  respiratory  rate,  this  procedure  also  tends  to 
regulate  the  former.  This  rhythm  is  one  which  is  very  satisfactory  for 
patients  with  heart  disease.  It  is  readily  acquired,  and,  having  once 
become  habitual,  does  much,  automatically,  to  keep  the  patient  within  his 
physiological  limits,  thus  enhancing  the  beneficial  effect  of  the  exercise 
while  establishing  a  safeguard  against  overstrain. 

OertePs  Mountain  Climbing. — Long  walks  and  mountain  climb- 
ing were  introduced  as  an  after-treatment  in  cardiac  disease  by  0  e  r  t  e  1 . 
Oertel  found  that  patients  convalescent  from  heart  failure,  and  especially 
those  suffering  from  fatty  infiltration  of  the  heart,  were  much  benefited 
by  long  walks  taken  slowly,  interrupted  by  frequent  rests.  Walks  along 
gradually  sloping  paths  in  the  mountains  were  most  beneficial,  and  in  fact 
became  a  feature  of  the  method.  This  is  designed,  however,  only  to  put 
the  finishing  touches  upon  the  treatment,  and  to  fit  the  patient  whose  heart 
is  already  in  good  working  order  for  the  more  strenuous  life  to  be  pursued 
after  his  discharge. 

CHOICE    OF    EXERCISE. 

As  regards  the  choice  and  use  of  exercise  in  treatment,  the  following 
general  principles  may  be  laid  down: 

(1)  No  exercise  should  be  begun  until  the  patient  has  been  under 
observation  for  a  few  days,  so  that  his  general  condition  is  thoroughly 
understood. 

(2)  If  the  patient  is  not  improving  under  absolute  rest,  exercises 
would  only  increase  the  work  imposed  upon  the  heart  and  would  do  harm. 

(3)  If  the  patient  has  improved  under  absolute  rest,  he  may  be  given 
one  or  two  passive  movements  (each  carried  out  five  or  ten  times)  two  or 
three  times  a  day,  and  the  exercises  very  carefully  increased  in  number 
and  intensity  each  day  before  allowing  him  to  get  out  of  bed.  Even  a  few 
mild  resisted  arm  exercises  may  be  tried,  bearing  in  mind  the  same  princi- 
ples, for  it  must  be  remembered  that  the  patient  may  obtain  much  more 
complete  and  immediate  rest  after  these  exercises  while  in  bed  than  when 
out  of  it,  and  also  that  he  is  not  at  the  same  time  subjected  to  the  strain 
of  standing.1 

1  The  relative  mildness  of  such  exercises  in  patients  still  bed-ridden  is  seen  in  the 
fact  that  their  pulse-rate  and  respiration  return  at  once  to  normal  on  cessation  of  the  exer- 
cise. Physiologically,  to  exercise  in  the  horizontal  posture  increases  the  systolic  output 
more  and  changes  the  pulse-rate  less  than  in  the  erect  posture  (Erlanger  and  Hooker). 


GYMNASTICS  AND    HYDROTHERAPY.  285 

Once  out  of  bed  the  patient  should  at  first  be  given  a  day  or  two  of 
complete  rest  to  accommodate  himself  to  the  new  position.  Then  he  may 
be  allowed  to  begin  gradually  with  a  few  of  the  resisted  movements,  if  a 
competent  attendant  or  physician  can  supervise  them;  if  this  is  not  avail- 
able, he  may  be  allowed  to  practise  a  few  exercises  in  contracting  antago- 
nistic muscles  (Selbsthemmungsbewegungen) ,  at  first  under  the  direction 
of  the  physician,  later  under  the  observation  of  a  skilled  attendant,  or  of  some 
reliable  member  of  the  family  who  has  been  carefully  instructed  in  the  pre- 
cautions given  above.    About  this  stage  the  bath  treatment  may  be  begun. 

(4)  Mechanical  gymnastics  (with  the  Zander  apparatus  or  modifica- 
tions thereof)  can  be  recommended  only  when  supervised  by  persons  of 
great  experience  and  excellent  judgment. 

Training  at  End  of  Treatment. — (5)  When  the  patient  has  recovered 
somewhat,  but  not  sufficiently  to  withstand  the  wear  and  tear  of  daily 
life,  he  should  be  encouraged  to  take  short  walks,  gradually  lengthening 
the  space  covered,  at  first  about  the  hospital  grounds,  later  about  the 
city  or  country,  keeping  records  of  the  distance  traversed  each  day.  He 
may  then  be  allowed  to  walk  up  hill.  Pari  passu  with  this  the  resisted 
or  antagonized  movements  and  the  baths  should  be  given.  Before  dis- 
charging the  patient,  he  should  be  compelled  to  take  some  regular  gym- 
nastic exercises  every  day  and  made  to  do  work  at  least  as  strenuous  as 
that  which  will  form  the  routine  of  his  daily  life  after  passing  from  under 
the  physician's  care.  It  is  no  more  fair  to  the  convalescent  to  put  him 
directly  back  from  the  sedentary  life  of  the  bedroom  or  the  hospital  to  the 
deadly  struggle  for  existence  outside  than  it  would  be  to  match  the  average 
citizen  against  a  prize-fighter.  He  must  be  gradually  trained  for  the  effort. 
This  principle  was  very  well  recognized  by  da  Costa  during  the  Civil  War. 
Before  sending  his  patients  back  to  their  regiments  where  they  were  subject 
to  heavy  field  duty,  forced  marches,  etc.,  he  kept  them  at  lighter  duties 
about  the  hospital,  upon  local  guard  duty,  etc.,  and  from  time  to  time 
during  this  period  subjected  them  to  tests  of  increasing  severity  (running 
races,  etc.)  until  he  was  quite  certain  of  their  ability  to  stand  the  strain. 
The  magnificent  results  which  he  reports  from  his  large  series  of  cases 
treated  under  otherwise  unfavorable  conditions  constitute  a  fitting  monu- 
ment to  one  of  America's  greatest  clinicians,  and  merit  the  careful  study 
of  all  who  would  learn  how  cures  should  be  obtained  in  heart  diseases. 

Treatment  and  Occupation. — On  the  other  hand,  the  training  to  which 
the  patient  need  be  subjected  should  be  suited  to  the  life  that  he  leads.  It 
would  be  unnecessary  to  train  a  clerk  in  a  store  up  to  the  point  of  muscular 
strength  that  is  necessary  for  the  ordinary  laborer.  But  it  is  necessary 
that  he  should  not  be  exhausted  by  a  few  hours'  standing  lest  the  cardiac 
overstrain  return.  On  the  other  hand,  when  restitutio  ad  integrum  has  not 
been  possible,  the  patient's  life  must  net  be  the  same  as  it  was  before  his 
illness.  His  work  must  be  cut  down.  This  may  often  be  done  in  the  more 
well-to-do  without  changing  the  business  by  employing  assistants  to  attend 
to  all  except  the  more  essential  affairs.  Poorer  persons  must  change  their 
occupations.  It  is  as  much  the  duty  of  the  physician  to  see 
that  this  is  done  after  the  recovery  as  it  was  his  duty 
during    the    height    of    the    illness    to    give    correct    treat- 


286  DISEASES   OF   THE   HEART   AND    AORTA. 

m  e  n  t .  Otherwise  he  has  merely  prepared  the  patient  for  another  break- 
down. The  difficulty  in  finding  suitable  occupation  and  the  acumen  neces- 
sary in  meeting  changed  conditions  increase  rather  than  decrease  the 
responsibility  of  the  physician  in  this  regard.  He  must  see  to  it  that,  as 
stated  by  Professor  Osier,  "  the  patient  must  always  live  within  his  income 
of  cardiac  energy."  His  mode  of  life,  and  especially  the  speed  of  his  move- 
ments and  the  intensity  of  his  efforts,  should  be  so  regulated  that  he  no 
longer  feels  at  any  time  palpitation,  shortness  of  breath,  or  precordial  pain. 

HYDROTHERAPY  IN  THE  TREATMENT  OF  HEART  DISEASES. 

Although  the  healing  power  of  mineral  springs  and  baths  was  thought 
by  the  older  physicians  to  be  well-nigh  universal,  the  scientific  application 
of  hydrotherapy  to  heart  disease  is  due  largely  to  the  studies  of  a  small 
group  of  men  at  Bad  Nauheim,  Germany.  Benecke,  in  1870,  noted  the 
favorable  action  of  baths  at  this  watering-place,  but  it  is  to  August  Schott 
that  is  due  the  real  credit  for  introducing  into  cardiac  therapy  what  is 
really  a  very  valuable  method  of  treatment. 

PHYSIOLOGICAL    ACTION    OF    BATHS. 

Physiologically  it  has  been  found,  especially  by  Erlanger  and  Hooker, 
and  a  little  later  by  Jacob  and  Strasburger,  that  all  baths  given  at  about 
the  temperature  at  which  the  body  neither  gives  off  nor  loses  heat  (92°  F., 
33°  C.)  increase  the  pulse-pressure  and  slow  the  pulse-rate.  Strasburger 
found  this  to  be  particularly  true  as  regards  baths  of  the  same  composition 
as  those  at  Nauheim,  or  indeed  any  other  baths  in  which  C02  is  effervescing; 
and  ascribes  this  action  to  the  dilatation  of  the  vessels  in  the  skin  over  the 
whole  body,  as  well  as  to  the  cardiac  reflexes  from  stimulation  of  the  sensory 
nerves  by  the  prickling  sensation  of  the  C02  (see  page  242).  These  effects  in 
themselves  would  be  sufficient  upon  a  priori  grounds  to  indicate  a  probable 
value  of  such  baths  on  weakened  hearts.  Schott's  treatment  has,  however, 
long  antedated  these  explanations.  Schott,  Thorne,  Schminke,  and  a  host  of 
other  observers  have  demonstrated  that  the  area  of  cardiac  dulness  and 
the  X-ray  shadow  of  the  heart  diminished  after  such  a  bath  (cardiac  tonicity 
increased). 

An  excellent  treatise  of  his  results  and  those  obtained  by  other  ob- 
servers is  given  in  extenso  in  English  in  the  monograph  of  W.  Bezly  Thorne, 
to  which  the  reader  is  referred  for  details  of  the  method.  Other  excellent 
accounts  are  given  by  Satterthwaite,  P.  K.  Brown,  et  al. 

PRECAUTIONS. 

The  baths  should  not  be  given  to  patients  who  are  in  the  extreme 
stages  of  cardiac  break-down,  nor  indeed  to  any  very  weak  patients,  until 
they  have  been  prepared  for  the  slight  strain  which  accompanies  them  by 
some  course  of  mild  exercises,  preferably  resistance  exercises  (see  page  268). 
They  should  never  be  taken  less  than  one  or  two  hours  after  a  light  meal 
or  four  to  five  hours  after  a  heavy  one,  and,  on  the  other  hand,  should  not 
be  given  upon  an  absolutely  empty  stomach. 


GYMNASTICS   AND   HYDROTHERAPY.  287 


NATURAL    AND    ARTIFICIAL    NAUHEIM    BATHS. 

The  Nauheim  baths  are  obtained  from  several  mineral  springs  of  different  com- 
position. A  course  of  baths  is  begun  in  the  Great  Sprudel  (composition  H20  1000,  NaCl 
2.18,  KC1  0.5,  CaCl2 1.7,  MgCl2  0.4,  calcium  bicarbonate  2.3,  CO,  3.17;  temperature  31.6°  C, 
88.8°  F.),  most  of  the  C02  being  allowed  to  escape  before  immersion  of  the  patient. 

The  effect  of  the  Nauheim  baths  can  be  imitated  at  home  or  in  the  hospital  by  add- 
ing the  same  salts  to  the  water  in  the  bath-tub.  A  great  variety  of  such  artifi- 
cial Nauheim  salts  are  on  the  market,  put  up  in  packages  ready  for  use.  The 
most  satisfactory  known  to  the  writer1  contains: 

Grammes.     Pounds.     Per  cent. 

Sodium  chloride 3500  8  2.2 

Calcium  chloride  (magnesium  chloride) 900  2  0.53 

Sodium  bicarbonate 800  If  0.1 

Sodium  bisulphate  yielding  C02 1000  2\  0. 29 

In  order  to  prevent  the  bisulphate  from  injuring  the  tub  it  is  advisable  to  cover  the 
walls  and  floor  of  the  latter  with  a  large  sheet  of  rubber  cloth  about  6  x  8  ft.  in  size.  The 
bath  is  filled  with  warm  water,  90°-95°  F.  (a  good-sized  bath  requires  40  to  45  gal. — 150  to 
175  litres)  and  the  salts  added — first  the  sodium  chloride,  then  the  calcium  chloride,  then 
the  sodium  bicarbonate,  and  lastly  the  acid  sulphate  (NaHC03  +  NaHS04  =  Na2S01  +  C02  + 
H20).     The  effervescence  continues  throughout  the  bath. 

CAUTIONS   IN    GIVING    BATHS. 

In  preparing  the  first  bath  it  is  better  to  begin  with  half 
strength  of  the  salts  or  even  less.  The  patient  is  allowed  to  remain  in 
this  bath  not  longer  than  fifteen  minutes,  being  watched  care- 
fully during  this  time  and  removed  at  once  if  there  is  the  slightest 
increase  in  cyanosis  or  real  discomfort  of  any  kind- — flushing, 
excitement,  or  syncope.  "The  immediate  effect  of  the  first  few  baths  is  to 
produce  a  sense  of  oppression  at  the  precordium,  under  the  influence  of 
which  the  patient  breathes  slowly  and  deeply  for  two  or  three  minutes. 
Respiration  then  becomes  easy  and  continues  slower  by  from  two  to  four 
breaths  a  minute/'  after  which  the  symptoms  subside.  In  general  the  effect 
should  be  similar  to  that  in  the  following  case  quoted  from  Thorne: 

"A  patient,  aged  46,  whose  health  had  been  declining  for  years,  was  found  to  have 
a  pulse  of  80  in  the  recumbent,  and  of  88  in  the  sitting,  position.  While  he  stood  it  varied 
from  100  to  104,  and  if  he  walked  ten  paces  it  rose  from  120  to  130.  The  apex  was  found 
to  beat  an  inch  outside  the  nipple  line.  Within  two  minutes  of  immersion  in  his  first 
thermal  bath  the  pulse  had  fallen  to  70,  and  judged  by  the  finger  appeared  to  have  doubled 
its  volume;2  at  the  end  of  four  minutes  k  was  68,  in  six  minutes  66,  in  eight  minutes  68, 
and  while  standing  after  the  bath  it  was  90.  Before  he  left  the  bath  after  an  immersion 
of  ten  minutes,  the  apex  beat  was  found  to  have  receded  half  an  inch  in  the  direction  of 
the  mesial  line,  and  nails  and  fingers,  which  had  been  snow-white  up  to  the  junction  of 
the  second  with  the  first  phalanx,  had  assumed  a  healthy  flesh  tint." 

This  healthy  reaction  of  the  skin  should  be  present  within  a  few  minutes 
after  the  bath.     Its  absence  indicates  that  the  treatment  has  been  too 

1  Put  up  by  R.  R.  Rogers  Chemical  Co.,  San  Francisco.  This  preparation  is  partic- 
ularly useful,  owing  to  the  excellent  grade  of  sodium  bisulphate  prepared  and  the  perma- 
nent and  convenient  form  in  which  it  is  put  up.  Moreover,  the  sodium  bisulphate  is  put  up 
in  lumps  the  size  of  a  hazel-nut,  which  allows  the  C02  to  be  generated  uniformly  through- 
out the  bath. 

2  Probably  the  pulse-pressure  had  actually  doubled. 


288  DISEASES  OF  THE  HEART  AND  AORTA. 

violent,  too  prolonged,  or  in  other  ways  unsatisfactory,  and  unless  this 
can  be  obviated  after  the  next  bath  or  two  the  treatment  should  be  dis- 
continued. 

After  the  bath  the  patient  should  be  made  to  lie  down  and  rest,  if  pos- 
sible to  sleep,  for  at  least  an  hour  before  leaving  the  building  or  doing  any- 
thing else,  and  upon  this  rest  as  much  as  anything  else  depends  the  success 
of  the  treatment. 

MUD   AND    PEAT   BATHS. 

A  number  of  observers  favor  the  use  of  mud  (Schlammbader)  and  peat 
baths  (Soolbader),  especially  those  containing  carbon  dioxide,  in  cases  of 
heart  disease.  Their  effects  are,  in  the  main,  similar  to  those  of  the  Nauheim 
baths,  but,  owing  to  the  after-cleaning,  the  procedure  is  somewhat  more 
severe  and  the  latter  is  to  be  preferred.  Boehr  is  particularly  careful  to  warn 
against  their  use  in  patients  with  anginal  symptoms. 

ELECTRIC   BATHS. 

Electric  baths,  in  which  the  patient  is  immersed  in  water  through  which 
an  electrical  current  is  passing,  are  also  used  extensively  in  the  treatment  of 
cardiac  disease. 

Either  alternating  or  sinusoidal  currents  are  employed,  using  large  copper 
or  zinc  electrodes.  The  current  should  be  strong  enough  to  produce  well- 
marked  prickly  sensations  upon  the  skin,  but  not  to  cause  suffering  to  the 
patient.  Sinusoidal  currents  are,  as  a  rule,  more  soothing  than  simple  alter- 
nating currents  and  therefore  have  a  somewhat  wider  application. 

In  the  main,  the  effects  of  electric  baths  are  similar  to  the  carbon  diox- 
ide baths,  the  chief  effects  being  the  vigorous  counterirritation  of  the  skin, 
dilatation  of  the  superficial  blood-vessels,  and  reflex  stimulation  of  the 
heart  through  the  prickly  cutaneous  sensation.  It  cannot,  however,  be 
stated  with  certainty  that  their  actions  are  the  same  in  every  particular, 
especially  since  Sir  William  Ewart  and  others  have  suggested  that  the  action 
of  the  Nauheim  baths  is  due  largely  to  the  excess  of  carbon  dioxide  escaping 
into  the  air  and  inhaled  by  the  patient,  a  factor  which  is  of  course  lacking 
in  the  electric  baths. 

On  the  other  hand,  the  electric  currents  produce  a  certain  amount  of 
stimulation  of  the  muscles  with  a  corresponding  dilatation  of  their  blood- 
vessels and  thus,  as  Budingen  and  Geissler  have  claimed,  exert  an  effect 
similar  to  mild  gymnastics. 

Accurate  comparisons  of  the  effects  of  electrical  and  carbon  dioxide  baths 
in  large  series  of  cases  are,  unfortunately,  lacking,  and  the  effects  depend  so 
largely  upon  the  watchfulness  and  discretion  of  the  individual  administrator 
that  it  is  difficult  to  draw  conclusions. 

As  Budingen  and  Geissler  have  stated,  the  indications,  contraindications, 
and  precautions  are  about  the  same  as  for  the  Nauheim  baths.  Rumpf 
reports  beneficial  results  in  cases  of  cardiac  overstrain,  arteriosclerosis,  and 
especially  in  the  hearts  of  acute  alcoholism;  but,  though  this  author  has  met 
with  no  ill  effects  in  cases  of  coronary  sclerosis,  most  observers  will  agree 
with  Budingen  that  this  treatment  is  contraindicated  in  such  cases. 


GYMNASTICS  AND  HYDROTHERAPY.  289 


CONSIDERATIONS   REGARDING   THE   ADVISABILITY   OF   BATH   AND   SPA 

TREATMENTS. 

In  spite  of  the  undoubted  excellent  results  which  are  obtained  by  hydro- 
therapeutic  measures,  it  must  always  be  borne  in  mind  that  the  class  of  cases 
in  which  these  effects  can  be  expected  is  a  limited  one.  From  the  earliest 
days  of  medicine  to  the  present  there  has  prevailed  a  tendency  to  look  upon 
the  mineral  spring  with  a  certain  superstitious  awe  as  some  miracle  of  nature, 
some  gift  of  the  gods  possessed  of  mysterious  powers,  rather  than  as  a  definite 
therapeutic  measure  exerting  definite  physiological  effects.  Accordingly,  as 
has  been  stated  above,  there  has  resulted  an  indiscriminate  flocking  to  the 
various  spas,  and  particularly  to  Nauheim,  of  all  classes  of  patients  in  all 
stages  of  disease;  and  many  patients  who  could  barely  survive  the  effort  of 
travel  have  hurried  off  to  the  spa  as  a  last  resort,  hoping,  with  the  fervor  of  a 
pilgrim  to  Lourdes,  to  obtain  a  cure  which  under  such  conditions  would  be 
indeed  miraculous.  To  expect  all  but  the  most  conscientious  of  the  spa 
physicians  to  refuse  or  delay  bath  treatment  to  a  patient  who  has  made  such 
a  pilgrimage  to  obtain  it  would  be  expecting  a  great  deal  of  human  nature. 
These  are,  of  course,  the  cases  which  result  badly  and  reflect  discredit  upon 
the  places  which  they  frequent  and  upon  spa  treatments  in  general. 

The  taking  of  all  forms  of  bath,  whether  hot  or  cold,  carbonated  or  non- 
carbonated,  whether  clear  or  muddy  or  charged  with  electricity,  constitutes 
more  or  less  of  an  effort  to  the  patient.  They  are,  therefore,  of  benefit  chiefly 
to  those  patients  who  are  capable  of  obtaining  benefit  from  graded  efforts, 
and  are  often  harmful  to  those  to  whom  such  efforts  are  injurious.  The 
patient  with  severe  angina  pectoris,  coronary  sclerosis,  badly  broken  com- 
pensation, anasarca  or  severe  dyspnoea  when  at  rest  is  not  the  one  for  whom 
the  bath  treatment  is  desirable,  unless  perhaps  under  exceptional  circum- 
stances. For  these  cases  the  bath  treatment  is  not  a  mode  of  treatment, 
but  an  after-treatment;  and  whether  one  agree  entirely  with  Mackenzie, 
that  their  effects  are  no  different  from  those  of  a  vacation  spent  elsewhere,  or 
whether  one  accepts  the  results  of  the  careful  studies  upon  blood-pressure 
mentioned  in  the  foregoing  chapter,  it  is  perhaps  a  safe  rule  not  to  recom- 
mend patients  to  a  treatment  at  a  spa  until  they  are  almost  in  a  fit  condition 
to  take  a  vacation  elsewhere. 

It  is  in  the  cases  between  the  grade  of  actual  cardiac  failure  and  complete 
return  to  vigor,  those  suffering  from  lassitude,  undue  fatigue  and  slight  dila- 
tation on  exertion,  that  the  good  effects  of  bath  and  spa  treatment  are  most 
pronounced.  Exactly  how  much  of  this  is  due  to  the  rest  and  change  of  scene, 
how  much  to  the  physiological  effects  upon  the  circulation,  and  how  much  to 
the  stimulating  effects  of  suggestion  from  the  surroundings  and  the  optimis- 
tic enthusiasm  of  fellow  patients  is  extremely  difficult  to  gauge;  and  on  the 
other  hand  it  must  be  borne  in  mind  that  recent  observations  have  shown 
the  presence  of  radio-active  substances  in  the  waters  of  just  those  springs  to 
which  popular  tradition  and  clinical  experience  had  ascribed  the  greatest 
medicinal  powers.  Radium  and  the  radio-active  substances  are  unquestion- 
ably possessed  of  tremendous  physiological  activity,  giving  rise  to  tissue 
changes  which  are  often  late  and  remote,  effects  difficult  to  study  with  accu- 
racy even  in  experiment. 

19 


290  DISEASES  OF  THE  HEART  AND  AORTA. 

In  cases  of  persistent  high  blood-pressure  of  arteriosclerotic  or  nephritic 
origin,  the  effect  of  baths  in  dilating  the  vessels  of  the  cutaneous  circulation 
is  often  of  benefit;  but  here,  again,  the  stage  of  the  disease  and  the  degree  of 
cardiac  compensation  is  of  more  importance  than  the  exact  nature  of  the 
condition.  What  is  beneficial  to  the  man  who  suffers  from  occasional  head- 
aches, insomnia  or  nervousness  but  who  remains  free  from  oedema  may 
prove  distinctly  harmful  to  the  same  individual  when,  a  few  years  later,  he  has 
passed  into  the  stages  of  dyspnoea  and  anasarca,  in  which  every  minimal 
effort  must  be  undertaken  with  caution.  Even  in  the  early  stages  of  high 
blood-pressure,  however,  too  great  caution  cannot  be  urged  in  the  prescribing 
of  heavily  carbonated  baths  or  baths  at  high  temperatures,  and  these  should 
when  ordered  be  carried  out  for  some  time  under  the  personal  supervision  of 
a  physician,  lest  some  momentary  weakening  effect  carry  the  heart  past  the 
limits  of  its  tonicity  and  a  dangerous  or  even  fatal  dilation  set  in. 

As  regards  the  use  of  home  modifications  of  the  various  baths  versus  a 
sojourn  at  a  spa,  each  case  must  be  considered  on  its  own  merits.  After 
carefully  weighing  the  question  of  whether  in  the  individaul  case  hydrother- 
apy is  advisable  at  all,  the  physician  should  balance  the  expense  and  efforts 
of  the  trip  against  the  beneficial  effects  of  the  stimulating  surroundings  at  a 
spa,  which  he  cannot  fail  to  realize  are  lacking  in  home  treatment.  In  this 
regard  the  home  conditions  and  the  mental  attitude  of  the  patient  himself 
toward  his  surroundings  play  quite  as  important  a  r61e  as  the  mere  physio- 
logical effects. 

BIBLIOGRAPHY. 

Gymnastics  and  Hydrotherapy. 

Herz,  M.:  Lehrbuch  der  Heilgymnastik,  Berl.  and  Vienna,  1903. 

Schott,  Aug.:  Zur  Therapie  der  chronischen  Herzkrankheiten,  Berl.  klin.  Wchnschr.,  1885. 
Thome,  W.  B. :  The  Schott  Methods  in  the  Treatment  of  Chronic  Diseases  of  the  Heart. 
Biidingen :  Ruhekuren  fur  Herzkranken  im  Verbindung  mit  passiven  Bewegungen,  Deutsches 

Arch.  f.  klin.  Med.,  Leipz.,  1911,  cii,  54. 
Nebel:  Bewegungskuren  mittelst  schwedischer  Heilgymnastik  und  Massage  mit  besonderer 

Beriicksichtigung  der  mechanischen  Behandlung  des  Dr.  G.  Zander,  Wiesbaden,  1889, 
Oertel:  Ueber  Terrainkurorte,  Leipz.,  1886.     Ueber  die  chronischen  Herzmuskelerkrank- 

ungen  und  ihre  Behandlung,  Verhandl.  d.  Kong.  f.  inn.  Med.,   Wiesb.,  1888,   v,  13. 

Allgemeine  Therapie  der  Kreislaufstorungen,  1891,  4th  ed. 
Beneke,  F.  W. :  Ueber  Nauheim's  Soolthermen,  Marburg,  1859;  Weitere  Mittheilungen 

ueber  die  Wirkung  der  Soolthermen  Nauheims,  Marburg,  1861;  Nauheim's  Soolther- 
men gegen  Gelenkrheumatismus  mit  oder  ohne  Herzaffection.,  Berl.  klin.  Wchnschr., 

1870,  269. 
Schott,  A.:  Die  Wirkung  der  Bader  auf  das  Herz,  ibid.,  1880,  xvii,  357,  372. 
Erlanger  and  Hooker,  1.  c,  page  54. 
Strasburger,  J.:  Ueber  Blutdruck,   Gefasstonus  und  Herzarbeit  bei  Wasserbadern  ver- 

schieder  Temperatur  und  bei  Solbadern,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  lxxxii, 

459. 
Satterthwaite :  Nauheim  Methods  in  Chronic  Heart  Disease  with  American  Adaptations, 

Internat.  Clin.,  Phila.,  1903,  13  ser.,  i,  52. 
Biidingen,  Th.,  and  Geissler,  G.:  Die  Einwirkung  der  Wechselstrombader  auf  das  Herz, 

Munchen.  med.  Wchnschr.,  1904,  li,  789. 
Rumpf :  Ueber  die  Einwirkung  oscillirender  Strome  bei  Herzkrankheiten. 
Biidingen,   Th.:  Grundzuge  der  Anstaltsbehandlung  nervoser  und  organisch  bedingter 

Herzstorungen,  Therap.  Monatsh.,  Berl.,  1907,  xxi,  467. 


VII. 

HYPERTROPHY   AND    ATROPHY. 

HYPERTROPHY. 

To  enable  the  heart  to  recover  from  an  overstrain  and  the  consequent 
dilatation,  to  maintain  the  circulation  in  the  presence  of  a  valvular  lesion 
or  dilatation,  or  to  reestablish  compensation  once  broken,  it  must  put  forth 
an  increase  in  force.  The  stimulus  for  this  seems  to  lie  in  the  increase  in. 
residual  blood  in  the  ventricle,  which  acts  as  an  increase  in  load  upon  the 
heart  muscle,  and  thus  tends  to  increase  both  irritability  and  force  of  con- 
traction, as  shown  by  O.  Frank  (see  page  204),  and  particularly  to  bring 


HYPERTROPHIED 

7oO  Q. 

7         • 

NORMAL 
250  G.    8oz. 

ATROPHIED 
I50G.          5oz. 

^^^H   WP. 

W 

H  ^i 

It^m 

•;  >^H 

m$*s 

^■jKkVsi^p!'*  4$: 

Fig.  136. — Hypertrophic,  normal,  and  atrophic  hearts.     (From  specimens  in  the  Army  Medical  Museum, 

Washington,  D.  C.) 

about  an  increase  in  tonicity.  It  seems  probable  that  this  increase  in 
tonicity  is  of  primary  importance  as  a  predisposing  factor  to  hypertrophy, 
and  Barcroft  and  Dixon  have  shown  that  increased  tonicity  is  accompanied 
by  an  increased  C02  metabolism  in  the  heart. 


PATHOLOGICAL    ANATOMY. 

Changes  in  the  Fibres. — The  main  visible  change  which  the  heart  muscle  undergoes 
is  a  swelling  of  the  individual  fibres  (Tangl,  Goldenberg,  Dehio,  R.  M.  Pearce)  with  little 
if  any  multiplication  of  the  muscle-cells.  Goldenberg  finds  that  the  muscle-cells  in  the 
wall  of  the  hypertrophic  heart  have  a  diameter  of  17.65  /*,  in  the  normal  heart  12.85  /*, 
and  in  the  atrophic  heart  10.S4  p.  The  striation  of  the  fibres  also  becomes  less  distinct, 
and  vacuoles  appear  in  the  sarcoplasm,  changes  which  are  similar  to  what  is  observed  in 

291 


292 


DISEASES   OF   THE   HEART   AND    AORTA. 


a  striated  muscle  as  the  result  of  prolonged  contraction.  Ranke  has  shown  that  in  skeletal 
muscle  these  changes  are  due  to  imbibition  or  endosmosis  of  water,  which,  according  to 
the  beautiful  experiments  of  J.  Loeb  and  his  pupil,  Miss  Cooke,  is  brought  about  in  the 
following  way:  During  the  muscular  contraction  the  more  complex  molecules  break  down 
into  several  simpler  ones,  thereby  increasing  the  number  of  molecules  in  solution  in  the 
muscle  plasma,  the  osmotic  pressure  rises,  and  hence  brings  about  an  endosmosis  of  water 
into  the  fibres.1  Having  once  entered,  the  water  molecules  remain  and  the  muscle  swells. 
There  can  be  little  doubt  that  the  same  process  is  going  on  in  cardiac  muscle,  and  H.  A. 
Stewart  (Proc.  Soc.  Exper.  Biol,  and  Med.,  1911,  viii,  13)  has  found  that  the  water  content 
of  heart  muscle  of  animals  with  experimental  aortic  insufficiency  is  greater  than  normal. 

In  cardiac  hypertrophy  three  anatomical  changes  may  be  said  to  take 
place  simultaneously:  (1)  an  increase  in  size  of  the  individual  muscle- 
cells,  but  apparently  no  increase  in  their  number;  (2)  a  certain  amount  of 


Fig.  137. — Photomicrographs  of  atrophic  and  hypertrophic  heart  muscle.  A.  Atrophic  heart 
muscle,  showing  small  cells.  The  specimen  also  shows  some  oedema  and  slight  mononuclear  infiltration 
between  the  muscle  cells.     B.  Hypertrophic  heart  muscle  showing  large  cells  with  swollen  nuclei. 

degeneration  is  almost  always  present  in  some  of  the  muscle-cells;  (3)  a 
proliferation  of  the  strands  of  connective  tissue  between  the  bundles  of 
muscle-fibres  (interfascicular  myofibrosis,  see  page  313). 

Dehio  and  Pearce  have  shown  that  each  fibre  may  pass  through  the 
following  stages:  normal  -»  hypertrophy  ->  degeneration,  the  latter  stage 
being  associated  with  proliferation  of  interstitial  connective  tissue  (myo- 
fibrosis). Accordingly,  we  may  find  the  heart-cells  in  the  following  con- 
ditions : 

(1)  Normal  +  hypertrophied  (heart  somewhat  enlarged:  as  in  athletes,  also  in  Kiilbs's 
dogs). 

(2)  Hypertrophied  +  degenerated;  some  proliferation  of  connective  tissue  (heart 
much  enlarged — cor  bovinum;  still  strong). 

(3)  Degenerated.  Marked  proliferation  of  connective  tissue.  Marked  weakness  of 
the  heart.    Large  failing  heart.      Hypertrophy  +  dilatation  (digitalis  often  harmful). 


1  Fleischer  and  Leo  Loeb  have  advanced  the  same  explanation. 


HYPERTROPHY  AND  ATROPHY.  293 

Types  of  Hypertrophy. — Hypertrophy  was  supposed  by  Cohnheim  to 
assume  three  types: 

(1)  General  concentric  hypertrophy,  involving  all  the 
chambers  of  the  heart  about  equally. 

(2)  Local  concentric  hypertrophy,  involving  the  walls 
of  one  or  more  chambers  of  the  heart  which  is  subjected  to  extra  work. 
The  fibres  are  not  especially  elongated. 

(3)  Local  (excentric)  hypertrophy  with  elongation  of 
the  muscle-fibres,  as  in  aortic  insufficiency.  The  elongation  of  the  fibres  is 
somewhat  out  of  proportion  to  the  increase  in  size  of  the  heart. 

The  existence  of  these  three  types  of  hypertrophy  as  separate  entities 
was  already  disputed  by  Cruveilhier  in  1833.  It  is  probable  that  the  size 
of  the  cavities  as  found  at  autopsy  bears  no  constant  relation  to  that  pres- 
ent during  life.  Moreover,  the  ventricular  cavities  in  cases  of  chronic 
nephritis  are  often  quite  as  large  as  those  in  hearts  of  aortic  insufficiency, 
though  the  former  typifies  the  so-called  concentric,  the  latter  the  excentric 
hypertrophy. 

Occurrence  and  Sites  of  Hypertrophy. — The  relative  frequency  with 
which  these  factors  occur  in  cases  of  hypertrophy  is  shown  in  the  following 
statistics  compiled  by  W.  T.  Howard  from  autopsies  made  in  the  Patho- 
logical Department  of  the  Johns  Hopkins  Medical  School  upon  108  subjects 
showing  hypertrophy  of  the  heart. 

Cases.  Per  cent. 

Arteriosclerosis 65  59 

Nephritis 14  13.4 

Valvular  lesions  of  the  heart 13  12.4 

Adherent  pericardium 8  7.6 

Hard  work 4  3.8 

Tumors 2  1.9 

Aneurism  of  the  heart  wall 1  0 .  95 

Hsemic  plethora 1  0 .  95 

Total 108  100 

The  right  ventricle  showed  hypertrophy  in  70  cases  (66  per  cent.),  of 
which  there  were — 

Arteriosclerosis  (often  of  pulmonary  artery),  52;  adhesive  pericarditis,  6;  valvular 
lesions,  8;  chronic  nephritis,  3;  hydraemic  plethora,  1. 

Hypertrophy  of  the  auricles  (atria)  was  most  marked  in  mitral  stenosis 
and  adhesive  pericarditis. 

Strain,  Exercise,  and  Hypertrophy. — In  normal  individuals  the  weight 
of  the  heart  is  almost  proportional  to  the  weight,  not  of  the  entire  body, 
but  of  the  musculature  (W.  Miiller,  Hirsch),  being  relatively  low  in  fatty 
and  relatively  high  in  muscular  individuals.  The  absolute  weight  of  the 
heart  is  about  yy^  (.0059)  of  the  body  weight  in  men,  Tfj  (.00546)  in 
women.  The  same  general  principle  applies  in  animals,  the  most  active 
animals  having  the  largest  hearts,  especially  race-horses,  hares,  etc.,  as 
compared  to  less  active  members  of  the  same  species. 

When,  however,  the  heart  is  subjected  to  abnormal  strain,  especially 
as  the  result  of  valvular  lesion,  it  hypertrophies  and  increases  in  size  to 
dimensions  which  are  often  enormous.     It  is  not  very  uncommon  to  find 


294  DISEASES   OF   THE   HEART   AND    AORTA. 

hearts  of  twice  or  even  three  times  the  normal  size  (500  to  800  Gm.,  17  tc? 
26  oz.),  and  in  the  Army  Medical  Museum  in  Washington  there  is  a  speci- 
men of  one  weighing  1000  Gm.  (33  oz.).  Another  heart  of  1400  Gm.  (46^ 
oz.)  has  been  reported.  Such  a  heart  is  usually  designated  as  a  beefy 
heart  or  cor  bovinum,  indicating  the  animal  to  which  its  size  would  be 
proportioned. 

Work  Hypertrophy. — Whether  a  true  hypertrophy  occurs  in  a  per- 
fectly healthy  heart  has  been  much  disputed,  many  writers  taking  the 
stand  with  Romberg  that,  "  though  the  possibility  of  a  '  work  hypertrophy ' 
cannot  be  denied,  more  proofs  of  its  existence  are  necessary." 


Fig.  138. — Heart  (A )  of  normal  dog  and   (B)  of  dog  which  has  run  for  three  months  on  a  tread-mill. 
(After  Kulbs,  Arch.  f.  exper.  Path.  u.  Pharmacol.,  lv.) 

Recently,  however,  absolute  proof  of  a  work  hypertrophy  without  myocardial  degen- 
eration has  been  brought  by  the  beautiful  experiments  of  Kiilbs.  This  observer  took  two 
dogs  of  the  same  litter  and  of  equal  size,  kept  them  in  neighboring  cages  upon  the  same 
diet,  but  compelled  one  of  them  to  run  upon  a  tread-mill  daily  for  three  to  six  months, 
while  the  other  was  kept  quiet  and  used  as  a  control.  At  the  end  of  this  time  both  dogs 
were  killed  in  the  same  manner. 

First  set.  Second  set. 

Work  dog.        Control.        Work  dog.       Control. 

Total  weight 15,200         15,000         19,200         20,400 

Musculature 5,696  5,342  6,489  6,776 

Heart 152  99  172  113 

Kulbs's  results  have  been  confirmed  by  Grober  and  by  Joseph. 

The  increase  in  size  of  the  heart  was  not  accompanied  by  any  change  in  the  skeletal 
musculature,  nor  were  any  pathological  changes  present  in  the  heart  or  arteries.  The 
muscle  here  simply  underwent  an  increase  in  size,  the  purest  form  of  hypertrophy.  Kulbs's 
dogs  were  simply  in  training  to  run  on  a  tread-mill.  The  process  was  exactly  the  same  as 
the  "training"  of  an  athlete,  and,  clinically,  it  is  often  found  that  athletes  have  mildly 
hypertrophied  hearts.  Schieffer  has  demonstrated  with  the  orthodiagraph  that  the  size 
of  the  heart  is  increased  in  persons  whose  occupations  require  hard  work  and  decreased  in 
those  with  sedentary  callings.  He  has  also  shown  that  the  hearts  of  the  young  men  doing 
military  service  in  the  German  Army  increase  in  size  somewhat  during  their  period  of 
service.  However,  these  men  often  indulge  in  excess  of  alcohol  or  tobacco,  so  that  before 
they  die  enough  myocardial  change  has  set  in  to  justify  the  scepticism  of  men  like  Krehl 
(I.e.)  and  Romberg  (I.e.).  Nevertheless,  though  a  true  "work  hypertrophy"  must  be 
admitted,  in  these  experiments  it  is  noticeable  that  the  increase  in  weight  of  the  heart 


HYPERTROPHY  AND  ATROPHY.  295 

amounted  to  only  52  per  cent,  as  compared  with  changes  of  100  to  300  per  cent,  often 
observed  in  man.  It  is  doubtful  whether  a  corresponding  degree  of  hypertrophy  would 
be  noticeable  clinically. 

ETIOLOGICAL    FACTORS. 

Hypertrophy  in  Chronic  Nephritis. — The  most  remarkable  and  most 
important  of  all  these  forms  of  hypertrophy  is  that  taking  place  in  chronic 
nephritis.  This  was  first  noticed  by  Richard  Bright  in  his  classical  descrip- 
tion of  dropsy  in  nephritis. 

In  1853,  Wilkes  thought  that  the  lesions  of  the  kidneys  and  arteries  were  part  of  the 
same  morbid  condition;  while  Gull  and  Sutton  assumed  that  the  general  arteriocapillary 
fibrosis  brought  about  an  increased  resistance  through  narrowing  of  the  arterial  bed,  and, 
as  a  result  of  this,  high  blood-pressure  and  hypertrophy  of  the  heart.  Senator  ascribed  the 
hypertrophy  to  a  "dyscrasic"  property  of  the  blood  in  nephritis,  stimulating  the  heart 
to  contractions  of  abnormal  force.  Passler  and  Heineke  have  recently  subjected  the 
matter  to  critical  experiment.  They  found  that  if  they  cut  out  pieces  of  kidney  from  a 
dog  bit  by  bit  until  renal  substance  equal  to  1£  kidneys  had  been  removed,  the  heart  then 
began  to  hypertrophy  and  the  blood-pressure  to  rise.  If  considerably  more  tissue  was 
removed,  the  animal  became  cachectic,  the  blood-pressure  remained  low,  and  the  heart 
did  not  hypertrophy.  They  ascribed  these  cardiac  changes,  as  George  Johnson  had  done, 
to  the  presence  in  the  blood  of  some  substance  having  a  digitalis-like  action,  being  either 
retained  in  the  circulation  in  abnormally  large  quantities  as  the  result  of  disturbed  excre- 
tion, or  being  a  true  internal  secretion  from  the  diseased  kidney.1 

Numerous  other  theories  of  cardiac  hypertrophy  in  renal  disease  have  been  advanced. 
Chief  among  these  is  the  theory  of  J.  Cohnheim  and  Traube  that  the  sclerosis  of  renal 
vessels  narrowed  the  arterial  bed  in  the  kidney,  thereby  introducing  an  increased  resistance 
into  the  general  circulation,  and  that  these  changes  in  the  renal  vessels  were  enough  to 
raise  the  general  blood-pressure.  It  would  appear  in  the  light  of  more  modern  research 
that  this  cutting  off  of  the  blood  stream  is  in  itself  insufficient.  Jores  (Deutsches  Arch.  f. 
klin.  Med.)  claims  to  find  hypertrophy  only  in  patients  with  red  granular  kidneys  (glom- 
erular sclerosis)  and  not  in  those  with  small  white  kidneys  (tubular  nephritis)  (see  page 
45).  There  is  a  true  hypertrophy  and  not  a  mere  growth  of  connective  tissue  as  suggested 
by  Buhl,  Huchard,  and  Albrecht. 

Hypertrophy  from  Overdrinking. — Closely  allied  to  this  condition  is  the 
tremendous  heart  hypertrophy  which  is  universally  found  to  result  from 
drinking  large  quantities  of  beer,  and,  since  it  does  not  accompany  excess 
in  any  other  form  of  alcohol  to  the  same  extent,  it  is  thought  to  be  due  to 
the  large  quantity  of  fluid  ingested.  That  increase  in  the  fluid  in  the  blood 
at  once  results,  not  so  much  in  a  rise  in  arterial  blood-pressure  as  in  rise  in 
venous  blood-pressure,  dilatation  of  the  heart,  and  increases  in  the  systolic 
output,  even  to  the  point  of  doubling  or  trebling  it,  can  easily  be  shown 
with  Henderson's  cardiometer,  and  this  no  doubt  illustrates  the  mechanism 
by  which  the  change  is  brought  about. 

Hypertrophy  and  Arteriosclerosis. — The  relation  of  hypertrophy  of  the 
heart  to  arteriosclerosis  independent  of  any  renal  changes  is  also  of  funda- 
mental importance.  The  coincidence  of  the  two  conditions  in  the  same 
individual  has  long  been  noted,  and  both  have  been  brought  about  experi- 
mentally by  administration  of  certain  poisons,  notably  adrenalin  (Josue, 
Erb,  Pearce,  et  al.). 

1  Tigerstedt  and  Bergmann  (Skand.  Arch,  f .  Physiol.,  Leipz.,  1S98,  viii,  224)  found  that 
injection  of  renal  extract  actually  raised  the  blood-pressure,  owing  to  the  presence  of  a 
substance  which  they  named  "renin." 


296  DISEASES   OF   THE   HEART   AND   AORTA. 

Cardiac  and  Adrenal  Hypertrophy. — A  new  light  has  been  thrown  upon 
the  subject  by  the  studies  of  Vaquez  and  Aubertin  (1905),  Aubertin  and 
Clinet,  Wiesel,  and  Gaillard. 

Aubertin  was  able  to  produce  cardiac  hypertrophy  in  rabbits  by  various  means, 
and  found  in  every  case  a  simultaneous  hyperplasia  of  the  medullary 
substance  in  the  adrenals.  A  similar  finding  had  been  made  by  Vaquez  and 
Aubertin  in  cases  of  chronic  nephritis  associated  with  hypertrophy  of  the  left  ventricle, 
which  was  confirmed  by  Wiesel  in  1907.  In  December,  1907,  Aubertin  and  Clunet  made 
a  study  of  120  unselected  autopsy  cases.  Of  these  18  showed  very  definite  hypertrophy 
of  the  medulla  of  the  adrenals,  and  16  of  these  18  showed  marked  hypertrophy  of  the 
heart.  On  the  other  hand,  but  10  of  these  hypertrophied  hearts  were  associated  with  renal 
disease:  the  others  occurred  in  conjunction  with  valvular  lesions,  congenital  defect  in  the 
septum  ventriculorum,  aortic  sclerosis,  etc.  Aubertin,  however,  states  very  definitely  that 
besides  these  groups  they  encountered  cases  of  cardiac  hypertrophy  without  the  existence 
of  adrenal  hyperplasia,  so  that  this  association  is  not  invariable;  and  they  conclude  that 
it  is  at  present  impossible  to  decide  whether  the  cardiac  hypertrophy  occurs  as  a  result  of 
oversecretion  of  adrenalin,  or  whether  the  hyperplasia  of  the  adrenals  occurs  as  a  result 
of  slight  venous  stasis  in  those  organs  while  the  hypertrophy  is  going  on.  Arteriosclerosis 
was  the  rule  but  not  invariably  in  these  cases  with  adrenal  hypertrophy. 

It  must  be  noted  that  the  action  of  adrenalin  is  just  that  which  might  be  expected 
to  bring  about  hypertrophy  of  the  heart,  for  it  causes,  (1)  a  general  vasoconstriction; 
(2)  a  marked  increase  in  the  tonicity  of  the  heart;  (3)  an  increase  in  the  force  of  the  beat 
and  in  the  systolic  output. 

However,  the  results  of  Cohn,  under  Aschoff  s  direction,  are  less  favor- 
able to  this  theory.  In  12  cases  of  hypertrophy  of  the  left  ventricle  with 
chronic  nephritis,  he  found  hypertrophy  of  the  adrenal  cortex  in  only  3 
(25  per  cent.),  while  in  23  cases  of  chronic  nephritis  without  hypertrophy 
of  the  heart  he  found  hypertrophy  of  the  adrenal  cortex  in  8  (34  per  cent.). 
These  findings  tend  to  throw  considerable  doubt  upon  the  theory  of  Vaquez 
and  Wiesel. 

Hypertrophy  and  Abdominal  Arteriosclerosis. — Hasenfeld  has  found 
that  no  hypertrophy  sets  in  unless  arteriosclerosis  is 
present  in  the  aorta  above  the  level  of  the  superior 
mesenteric  artery.  Practically  all  the  substances  which  are  known 
to  bring  on  arteriosclerosis  are  vasoconstrictors,  and  beginning  arteriosclero- 
sis in  man  seems  usually  to  be  accompanied  by  vasoconstriction.  It  is 
readily  conceivable  that  any  sclerotic  obstruction  below  the  mesenteric 
would  be  easily  compensated  for  by  dilatation  of  the  abdominal  vessels, 
and,  consequently,  would  bring  about  no  increased  resistance  to  blood  flow, 
while  at  the  higher  level  the  presence  of  sclerosis  is  more  or  less  equivalent 
to  clamping  the  abdominal  aorta.1 

DIAGNOSIS. 

It  would  appear  at  first  sight  to  be  extremely  easy  to  determine  clini- 
cally whether  in  a  given  case  hypertrophy  is  present  or  not,  and  the  older 
clinicians  laid  down  very  definite  rules  for  its  detection,  most  of  which  were 
fallacious.  In  general,  we  may  agree  with  Gibson  that  the  most  important 
signs  of  hypertrophy  of  the  left  ventricle  are  increase  in  cardiac  dulness  to 
the  left,  with  a  more  or  less  steady,  forceful,  and  "heaving"  impulse,  and  a 

1  An  excellent  discussion  of  the  theoretical  and  experimental  side  of  the  question  is 
given  by  R.  M.  Pearce. 


HYPERTROPHY  AND  ATROPHY. 


297 


booming  first  sound  of  low  pitch,  and  an  accentuated  second  sound  at  apex 
and  aortic  area.  These  signs  are  dependent  largely  upon  the  contact  of  the 
heart  with  the  chest  wall;  and  if,  as  is  often  the  case  in  an  emphysematous 
individual,  the  lung  intervenes  between  the  left  border  of  the  heart  and  the 
chest  wall,  all  the  signs  may  be  diminished  beyond  recognition.  The  diag- 
nosis may,  however,  often  be  made  from  the  history  in  spite  of  the  clinical 
findings.  Thus,  if  an  aortic  or 
mitral  insufficiency  has  persisted 
for  some  time  and  the  heart  is 
in  a  condition  of  moderate  vigor 
with  a  normal  pulse-rate,  it  may 
be  assumed  that  hypertrophy  of 
the  heart  has  had  to  take  place 
in  order  to  maintain  the  circula- 
tion, in  spite  of  distant  heart 
sounds  and  absence  of  the  apex 
beat.  Prolonged  high  blood- 
pressure  is  usually  associated 
with  some  degree  of  hypertrophy 
of  the  left  heart,  but  not  invari- 
ably. In  differentiating  from 
dilatation  it  may  be  stated  that, 
except  under  unusual  conditions 
brought  on  by  stimulation  of  the 
vagus,  the  factors  bringing  on 
dilatation  quicken  the  pulse- 
rate,  and  an  enlarged  but  slowly 
beating  heart  is  almost  always 
hypertrophied.  The  electrocar- 
diograms are,  however,  character- 
istic.1 In  hypertrophy  of  the  right 
ventricle  the  R  wave  is  normal  or 
inverted  in  the  first  derivation 
(Dl)  and  large  in  D2  and  D3 
(page  298).  In  hypertrophy  of 
the  left  it  is  inverted  in  D2  and 
D3  (Plate  XVI,   F). 

Hypertrophy  of  the  Left  Ven= 
tricle. — Palpation  of  the  apex  impulse,  which  many  writers,  even  as  late  as 
Romberg,  consider  a  most  important  sign  of  hypertrophy  of  the  left  ventricle, 
need  not  be  decisive,  since,  as  Katzenstein  has  shown,  the  weakest  hearts 
may  often  beat  the  most  violently,  especially  when  beating  rapidly;  the 
strongest,  on  the  other  hand,  may  be  separated  from  the  chest  wall  by  a 
layer  of  lung.     Dulness  is,  however,  increased  to  the  left. 

Hypertrophy  of  the  Right  Ventricle. — The  hypertrophy  of  the  right 
ventricle  is  not  so  easy  to  diagnose.  Its  presence  may  be  inferred  when 
the  area  of  cardiac  dulness  is  enlarged  and  a  systolic  retraction  is 

XT.  Lewis  (Heart,  1913 — 1914,  iv,  36)  has  shown  that  hearts  examined  by  Miller's 
method  gave  results  exactly  coinciding  with  the  electrocardiographic  diagnosis. 


Fig.  139. — Areas  of  pulsation  and  retraction  hyper- 
trophy of  the  right  and  left  ventricles.  —',  retraction; 
<-n,  pulsation.  The  light  line  indicates  the  area  of  the 
cardiac  dulness.  A.  Hypertrophy  of  the  left  ventricle. 
B.  Hypertrophy  of  the  right  ventricle. 


298  DISEASES  OF  THE  HEART  AND  AORTA. 


PLATE  XVI. 


PI 


;•    -            1 

R 

"j 

. 

_ML^ 

B 


k^         Makm./^s/a 


c 

R 


"E        T 


\  w'w/V  ¥^v\  ^aw\:  W/WV  „/***  «/^        Si  ^^ 


^y%Jl,||#fM>i^^ 


Electrocardiograms  showing  hypertrophy  of  the  ventricles.  A,  B,  C,  Tracings  from  a  case  of  hyper- 
trophy of  the  right  ventricle  by  the  first,  second  and  third  leads  (Dl,  D2,  D3)  respectively,  showing  inver- 
sion of  the  R,  wave  in  the  first  lead,  and  an  abnormally  high  R  wave  in  the  second  and  third. 


HYPERTROPHY  AND  ATROPHY.  299 

PLATE  XVI. 
D 


;/^^i(A^, 


%s 


E 


R 


**"<?  ^^^^ 


-Arj 


»fe*S£ 


F 


■— w, '  w  m^fi^immmm 


Tracings  from  a  patient  with  hypertrophy  of  the  left  ventricle  by  the  first,  second  and  third  leads  (Dl, 
D2,  D3)  respectively,  showing  inversion  of  the  R  wave  and  T  wave  in  the  third  lead  (F) . 


300  DISEASES   OF  THE   HEART   AND    AORTA. 

noted  at  the  point  of  maximal  impulse  and  over  the  interspaces  between 
it  and  the  sternum  as  well  as  in  the  epigastrium.  The  heart  need  not  be 
enlarged  toward  the  right,  since  the  right  ventricle  rarely  passes  the  sternal 
margin.  Indeed  it  rather  tends  to  lift  the  apex  and  shift  it  to  the  left.  The 
area  of  cardiac  flatness  is  increased  to  the  right,  reaching 
to  the  sternal  margin.  An  increased  area  of  dulness  to  the  right  of  the  ster- 
num is  due  to  the  right  auricle.  The  second  pulmonic  sound  is  intensified 
and  ringing,  but  this  may  also  be  the  case  in  any  condition  in  which  there 
is  some  obstruction  to  the  pulmonary  circulation  or  some  insufficiency  of 
the  left  heart. 

Hypertrophy  of  the  auricles  cannot  be  diagnosed  from 
objective  signs  except  in  mitral  stenosis,  in  which  an  hypertrophied  auricle 
gives  rise  to  a  loud  presystolic  murmur.  This  is  not  present  when  the  auri- 
cle is  weak.  Hypertrophy  of  the  right  auricle  is  sometimes  shown  by  a 
high  presystolic  wave  upon  the  jugular  venous  pulse-curve  and  very  rarely 
by  a  presystolic  wave  upon  the  liver  pulse  (Mackenzie) ;  but,  as  a  rule,  it 
shows  no  signs. 

Prognosis. — A  certain  amount  of  hypertrophy  is  necessary  whenever 
a  valvular  lesion  or  any  other  abnormal  factor  tending  to  increase  the 
work  of  maintaining  the  circulation  is  present.  Hence  failure  of  the  heart 
to  hypertrophy  under  these  conditions  would  be  regarded  as  an  unfavor- 
able condition,  and  would  probably  soon  be  associated  with  cachexia.  On 
the  other  hand,  an  extreme  degree  of  hypertrophy  is  evidence  that  the 
heart  is  doing  its  maximal  work,  that  the  fibres  ere  long  will  begin  to 
degenerate,  and  the  heart  must  be  spared  as  much  as  possible. 

Hypertrophy  in  itself  does  not  demand  treatment,  but  diminution  of 
the  causal  factor  as  far  as  is  possible  is  advisable.  If  this  be  nephritis  or 
arteriosclerosis,  a  quiet  life  and  diet  poor  in  salt  and  purin  bodies  should 
be  resorted  to,  with  occasional  courses  of  potassium  iodide.  If  a  valvular 
lesion  be  present  and  the  hypertrophy  is  slight,  little  attention  need  be 
paid  to  it  until  the  patient  reaches  the  latter  half  of  the  fourth  decade, 
when  he  should  begin  to  spare  his  heart  and  arteries  as  much  as  possible, 
should  abstain  from  alcohol,  coffee,  and  tobacco,  and  should  in  every  way 
avoid  those  influences  leading  to  the  production  of  high  blood-pressure  and 
arteriosclerosis. 

Reserve  Force  of  the  Hypertrophied  Heart. — One  of  the  most  impor- 
tant questions  that  arise  in  connection  with  hypertrophied  hearts  is 
whether  or  not  a  hypertrophied  heart  possesses  as  much  reserve  force  as  a 
normal  one.  This  question  is  variously  answered  in  the  text-books,  most 
of  them  agreeing  with  Krehl  et  al.  that  the  reserve  force  is  lessened;  while 
the  experimental  work,  especially  that  of  Romberg ""and  Hasenf eld,  indi- 
cates that  the  strength  of  the  hypertrophied  heart  muscle  itself  is  actually 
increased.  However,  a  great  deal  depends  upon  the  stage  of  hypertrophy 
in  which  the  individual  heart  happens  to  be.  Thus  a  heart  in  the  first 
stage,  with  fibres  normal  and  hypertrophied,  would  show  an  increased 
strength  (as  in  athletes'  hearts,  or  in  hearts  of  early  hypertrophy  after 
valvular,Jesion  as  compared  to  the  same  hearts  at  the  very  onset  of  the 
lesion) ;  while  a  heart  in  the  second  stage,  with  fibres  partly  hypertrophic, 
partly   atrophic,    would   in    most   cases    show    a    marked    diminution    in 


HYPERTROPHY  AND  ATROPHY. 


301 


strength  and  still  greater  loss  in  reserve  force,  and  an  increased  effort  would 
hasten  the  degeneration. 

Another  and  really  main  factor  in  the  apparent  weakness  of  the  hyper- 
trophied  heart  is  that  in  practically  all  hearts  the  hypertrophy  is  brought 
on  by  some  valvular  lesion  or  by  some  persistent  increase  in  peripheral 
resistance;  so  that  such  hearts  are  continually  wasting  much  of  their  energy 
in  overcoming  these  pathological  conditions,  besides  bestowing  the  usual 
amount  of  it  upon  the  maintenance  of  the  circulation.  In  bodily  exertion 
or  other  conditions  calling  upon  the  reserve  force,  not  only  the  actual 
circulation  must  be  increased,  but  the  abnormal  factor 
inducing  wasting  of  energy,  the  valvular  lesion,  etc.,  « 

becomes  more  severe  as  well,  and  hence  the  extra  call  fe         5  ' 

upon  the  diseased  heart  is  double  the  extra  call  upon  the 
normal  and  requires  double  the  reserve  force  to  meet  it. 
Otherwise  the  reserve  force,  though  actually  more,  may 
be  apparently  less  than  in  the  normal  heart,  as  shown 
diagrammatically  in  Fig.  140.  For  practical  purposes, 
however,  it  may  be  regarded  as  indisputable  that,  in 
every  case  where  a  cardiac  lesion  is  present,  the  hyper- 
trophied  heart  has  less  available  reserve  force  than 
normally,  and  in  some  cases  (stage  3)  less  than  if  it 
had  not  hypertrophied  at  all. 


1 


li 

DISEASED 
HEART 


ATROPHY. 


Fig.  140. — Diagram 
showing  power  of  nor- 
mal and  hypertrophied 
(athlete's)  heart  at  rest 
and  during  exercise,  also 
that  of  a  diseased  heart. 
The  length  of  the  arrow 
indicates  the  reserve 
force.  The  unshaded 
portion  indicates  the 
cardiac  energy  ex- 
pended, but  wastedt 
owing  to  the  lesion. 


Atrophy  of  the  heart  is  more  or  less  the  reverse 
process  of  hypertrophy.  Whenever  the  body  diminishes 
in  weight  from  cachexia,  infectious  disease,  or  starva- 
tion, the  heart  muscle  diminishes  with  it,  and  according 
to  Hirsch  in  about  the  same  ratio.  The  epicardial  fat, 
on  the  other  hand,  is  but  little  diminished.  When  the 
atrophy  is  the  result  of  starvation  it  may  be  of  very 
high  degree,  but  the  size  and  condition  of  the  heart  may  return  to  normal 
when  an  adequate  diet  is  resumed  (Schieffer). 

As  in  the  case  of  hypertrophy,  there  seems  to  be  little  change  in  the 
number  of  the  muscle-cells,  but  the  latter  diminish  in  size  (10.84  fx  instead 
of  12.85  /«,  Goldenberg),  and  the  removal  of  substance  is  marked  by  the 
deposition  of  brown  granules  of  hsematoidin  in  fusiform  arrangement  about 
the  nucleus.  These  granules  are  formed  when  part  of  the  muscle-cell  pro- 
teid  is  broken  down  during  the  atrophy,  the  hsematoidin  portion  being 
left.  Macroscopically  they  impart  a  tobacco-brown  color  to  the  heart,  so 
that  the  condition  is  often  designated  as  "brown  atrophy  of  the  heart." 

To  a  certain  extent  a  diminution  in  size  of  any  chamber  of  the  heart 
may  occur  if  its  work  is  lessened  by  obstruction  to  the  blood  flowing  into 
it;  as,  for  example,  the  left  ventricle  in  pure  uncomplicated  mitral  stenosis. 
The  atrophy  is  rarely  so  marked  here  as  in  starvation,  phthisis,  or  cachexia, 
and  is  indeed  the  exception  rather  than  the  rule  in  mitral  stenosis,  for  other 
factors,  tachycardia,  irregularity,  or  mitral  insufficiency,  usually  contrib- 
ute to  keep  the  left  ventricle  doing  an  at  least  normal  amount  of  work. 


302  DISEASES   OF   THE   HEART   AND    AORTA. 

Like  hypertrophy,  cachexial  atrophy  of  the  fibres  may  lead  on  to  growth 
of  interstitial  connective  tissue  and  fibrous  myocarditis,  but  true  brown 
atrophy  is  not  so  common  a  forerunner  of  myocarditis  as  is  hypertrophy 
of  the  heart.  Functionally,  the  force  of  the  heart  is  impaired  about  propor- 
tionally to  its  diminution  in  weight.  The  blood-pressure  is  usually  low 
and  the  muscle  easily  fatigued.  Overstrain  readily  occurs  in  such  hearts; 
and  sudden  death  is  not  uncommon. 

BIBLIOGRAPHY. 

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Thorel,  Ch.:  Pathologie  der  Kreislauforgane,  Lubarsch-Ostertag's  Ergebnisse  der  Patho- 

logie,  Wiesb.,  1903,  ix,  Abth.  I,  559. 
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viii,  400. 
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Berl.,  xxi,  321  and  521. 
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kol.,  Leipz.,  1906,  lv,  288. 
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Med.,  Leipz.,  1907,  xci,  502. 
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J.  Exper.  Med.,  N.  York  and  Lancaster,  190S,  x,  521. 
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klin.  Med.,  Leipz.,  1908,  xcii,  383;  also,  Ueber  den  Einfluss  des  Militardienstes  auf  die 

Herzgrosse,  ibid.,  1908,  xcii,  392. 
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HYPERTROPHY  AND  ATROPHY.  303 

Senator,  H.:  Ueber  die  Herzhypertrophie  bei  Nierenkranken,  Deutsch.  med.  Wchnschr., 

Leipz.  u.  Wien,  1903.     Die  Erkrankungen  der  Niere,  Nothnagel's  Handb.  d.  speziellen 

Pathol,  u.  Th.,  Wien. 
Passler,  H.-  Ueber  Ursache  und  Beutung  der  Herzaffektion  Nierenkranker,  Volkmann's 

Sammlung  klin.  Vortrage,  Leipz.,  1906,  No.  408. 
Johnson,  G.:  Lectures  on  Bright's  Disease  with  Especial  Reference  to  Pathology,  Diag- 
nosis, and  Treatment,  Lond.,  1873. 
Cohnheim,  J.:  Lectures  on  General  Pathology,  New  Sydenham  Society. 
Traube,  L.:  Gesammelte  Beitrage  zur  Pathologie  und  Physiologie,  Berl.,  1871-1878. 
Buhl:  Mitth.  a.  d.  pathol.  Inst.  Miinchen,  1878,  38. 
Huchard,  H.:  Maladies  du  Cceur,  Paris,  1899-1905. 
Albrecht,  E.:  Der  Herzmuskel,  Berl.,  1903. 
Josue  O.:  Hypertrophic  cardiaque  causee  per  l'adrenaline,  Compt.  rend.  Soc.  de  Biol., 

Par.,  1907,  lxiii,  285. 
Erb,  W.:  Experimentelle  und  histologische  Studien  iiber  Arterienerkrankung  nach  Adre- 

nalininjektionen,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1905,  liii,  173. 
Vaquez:  Hypertension  arterielle,  Bull.  soc.  med.  d.  hop.  de  Paris,  Feb.  5,  1904. 
Vaquez   and   Aubertin:  Sur  l'hyperplasie   surrenale   des   nephrites   hypertensives,   ibid., 

1905,  xxii,  705. 
Wiesel:  Renale  Herzhypertrophie  und  chromaffines  System,  Wien.  med.  Wchnschr.,  1907, 

lvii,  673. 
Schur,  H.,  and  Wiesel,  J.:    Beitrage  zur  Physiologie  und  Pathologie  des  chromaffinen 

Gewebes,  Wien.  klin.  Wchnschr.,  1907,  xx,  1202.     Also,  Ueber  eine  der  Adrenalin- 

wirkung  analoge  Wirkung  des  Blutserums  von  Nephritikern  auf  das  Froschauge,  Wien. 

klin.  Wchnschr.,  1901,  xx,  699. 
Gaillard.     Quoted  from  Aubertin. 
Hasenfeld,  A.:  Ueber  die  Entwicklung  einer  Herzhypertrophie  bei  der  Pyocyaneusendo- 

carditis  und  der  dadurch  verursachten  Allgemeininfection,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,   1899,  lxiv,  763. 
Hasenfeld  und  Romberg:  Ueber  die  Reservekraft  des  hypertrophischen  Herzmuskels, 

u.  s.  w.,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  1897,  xxxix,  333. 
Katzenstein,  J.:  Dilatation  und  Hypertrophic  des  Herzens,  Muenchen,  1903. 
Aschoff  and  Cohn:  Bemerkungen  zu  der  Schur- Wieselschen  Lehre  von  der  Hypertrophic 

des  Nebernierenmarkes  bei  chronischen  Erkrankungen  der  Nieren  und  des  Gefass- 

apparatus,  Verhandl.  d.  deutsch.  path.  Gesellsch.,  Jena,  1908,  xii.  131 


VIII. 

FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 

Fat  may  be  deposited  in  the  heart  in  two  ways:  (1)  In  solid  masses 
of  adipose  tissue,  especially  in  the  pericardium  in  fat  individuals,  particu- 
larly in  those  addicted  to  alcohol,  and  very  often  associated  with  coronary 
sclerosis.   This  condition  is  designated  as  fatty  infiltration  or  obese 


Fig.  141. — Distribution  of  fat  in  and  about  the  heart.    A,  normal;  B,  deposit  in  an  obese  heart;  C,  deposit 

in  a  fatty  degenerated  heart. 

heart  (Mastfettherz,  Kisch).  (2)  In  fine  droplets  occurring  diffusely 
within  the  heart  muscle-cells,  especially  in  anaemia,  infectious  diseases,  in 
persons  poisoned  by  phosphorus,  arsenic,  and  numerous  other  substances, 
and  in  association  with  other  changes  in  the  myocardium.  This  condition 
is  called    fatty    degeneration. 

FATTY   INFILTRATION   OR    OBESITY    OF    THE   HEART. 
DEPOSITION    OF    THE    FAT. 

Harvey,  the  discoverer  of  the  circulation,  describes  the  hearts  of  certain 
fat  persons  as  covered  with  a  layer  of  fat  so  extensive  as  almost  to  obscure 
the  heart  muscle  from  view,  and  this  condition  is  one  of  not  very  infrequent 
occurrence.  In  normal  hearts  there  is  a  considerable  amount  of  fat  (30 
to  60  Gm.,  1  to  2  ounces)  collected  just  beneath  the  endothelial  layer  of  the 
pericardium,  along  the  auriculoventricular  and  interventricular  grooves 
(coronary  and  longitudinal  sulci),  at  the  base  of  the  aorta,  and  scattered 
elsewhere  over  the  heart.  As  the  individual  lays  on  more  body  fat,  more 
fat  is  deposited  in  the  pericardium,  at  first  only  at  the  usual  sites  along  the 
sulci;  but  later  it  spreads  over  and  into  the  myocardium,  penetrating  into 
it  between  the  larger  strands  of  muscle,  and  finally  settling  beneath  the 
endocardium,  especially  about  the  bases  of  the  papillary  muscles. 

The  weight  of  adipose  tissue  may  actually  exceed  the  weight  of  cardiac  muscle 
(W.  Miiller,  Hirsch,  Kisch),  as  shown  by  the  following  figures  determined  by  W.  Miiller 
(who  dissects  off  the  fat  and  weighs  the  heart  muscle). 
304 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 


305 


Total  weight 
of  heart. 


Heart 
muscle. 


Fat  removable  by 
dissection. 


Per  cent, 
of  fat. 


253.6 
363.5 
327.6 
494.3 


240.7 
326.2 
181.3 
228.3 


12.9 
37.3 

146.3 

266 


5.1 

10.3 
45.6 
53.5 


Normal  male  (thin). 
Cardiac  hypertrophy. 

Eg*} fatty  heart. 


Nature  of  the  Fatty  Deposit. — Under  these  circumstances  the  fat  is  deposited  in 
exactly  the  same  manner  as  elsewhere  in  the  body.  The  pathological  character  con- 
sists not  in  the  process  but  in  the  amount  of  the  deposit.  The  adipose  tissue  in  this 
region  does  not  differ  macroscopically  or  microscopically  from  the  fat.  elsewhere.  Neither 
does  it  differ  chemically.  It  is  ordinary  "  translocation  fat"  (Rosenfeld,  Leick  and 
A 


Fig.  142. — Photomicrographs  of  fat  deposits  in  the  heart.  A.  Heart  muscle  of  an  obese  indi- 
vidual, showing  fat  cells.  B.  Heart  muscle  of  a  patient  who  died  of  pneumonia,  showing  fat  droplets 
within  the  cells  (fatty  degeneration).     (Photomicrograph  by  Dr.  Chas.  S.  Bond.) 

Winckler),  derived  directly  from  the  food  ;  for  Leick  and  Winckler  have  shown  that  if 
dogs  be  overfed  with  mutton  tallow,  the  fat  deposited  in  the  pericardium  has  an  iodine 
absorption  coefficient  approaching  more  nearly  to  what  is  in  the  sheep  than  to  that  of  the 
dog.  The  pericardial  fat  differs  from  the  fat  elsewhere  in  but  one  important  respect,  and 
one  which  is  especially  to  be  borne  in  mind  in  treating  the  condition,  namely,  that  it  is 
relatively  poor  in  lipase,  the  enzyme  which  forms  and  splits  fat,  and  h e n ce  is 
relatively  stable.  According  to  Loevenhart  it  would  appear  that  lipase  is  present 
in  the  cells  in  considerable  amounts  at  the  time  the  fat  is  deposited,  but  is  then  gradually 
destroyed;  so  that  if  subsequently  the  fat  of  the  body  is  reduced  from  inanition  or  other 
cause,  there  is  no  more  enzyme  remaining  in  the  pericardium  to  split  up  what  is  stored 
there  and  to  return  it  to  the  general  circulation.  Accordingly,  it  is  found  that  in  starva- 
tion the  pericardial  and  perirenal  fat  remain  after  all  the  rest  has 
disappeared  from  the  body  (Loevenhart,  Schieffer).  This  matter  will  be  re- 
ferred to  again  in  connection  with  treatment. 
20 


306 


DISEASES    OF   THE    HEART    AND    AORTA. 


CARDIAC    CONDITIONS    ASSOCIATED    WITH    OBESITY. 

There  are  three  definite  conditions  which,  though  in  no  way  part  of 
the  general  process  of  obesity,  are  often  associated  with  it;  and  it  is 
these,  rather  than  the  obesity  itself,  which  give  rise  to 
the    symptom    complex    referred  to    as  "fatty  heart,"  or,  as 

Romberg  more  properly  designates 
it,  "cardiac  insufficiency  of  fat  per- 
sons" (Die  Herzmuskelinsufncienz 
der  Fettleibingen) .  These  are  (1) 
atrophy  of  the  heart  muscle,  and 
(2)  s  c  1  e  r  o  s  i  s  of  the  coronary  arte- 
ries,  (3)   a  high  diaphragm. 

1.  Atrophy  and  Cardiosclerosis. 
— It  is  especially  worthy  of  notice 
that  the  increase  in  size  and  weight 
of  the  heart  may  conceal  an  actual 
atrophy  of  the  heart  muscle  (Hirsch) 
(see  table  above)  and  a  correspond- 
ing weakness  of  the  heart.  Accord- 
ing to  most  writers,  this  lies  mainly 
in  the  left  ventricle,  but  Hirsch  has 
shown  that  not  only  does  the  fatty 
infiltration  penetrate  chiefly 
the  wall  of  the  right  ventricle,  but 
that  the  symptoms  most  common 
among  fat  persons  are  those  due  to 
primary  failure  of  the  right 
side  of  the  heart.  A  general  cardio- 
sclerosis (see  page  325)  is  often  asso- 
ciated with  the  deposit  of  fat.  It  is  a 
self-evident  fact  that  such  enormous 
deposits  of  fat  increase  the  work 
done  by  the  heart',  first  by  increas- 
ing the  weight  to  be  moved  at  each 
systole,  and  secondly  by  increasing 
the  total  bed  of  the  blood  stream. 
It  might  be  supposed  that  this  would 
in  itself  bring  about  hypertrophy,  but  hypertrophy  is  rarely  demonstrable. 
The  tendency  to  obesity  usually  occurs  either  in  persons  whose  lives  are 
sedentary  and  whose  skeletal  and  cardiac  muscles  are  therefore  under- 
developed, or  else  in  those  addicted  to  excesses  of  alcohol  or  overeating,, 
factors  which  in  themselves  bring  on  myocardial  changes  and  hypertrophy. 

2.  Coronary  Sclerosis. — The  pathological  changes  and  symptoms  due 
to  sclerosis  of  the  coronary  arteries  do  not  differ  from  those  arising  without 
the  presence  of  abnormal  fat  deposits  and  will  be  discussed  in  a  separate 
chapter  (page  378). 

3.  High  Diaphragm. — V.  Frey  and  Krehl  have  shown  in  animals  that 
pushing  up  the  diaphragm,  and  thus  displacing  the  heart,  greatly  inter- 


f£  I 

^n^                      '  xb 

k| 

\ 

Fig.  143. — An  excessive  deposit  of  epicardia 
fat.  (From  a  specimen  in  the  Army  Medical  Mu 
seum,  Washington,  D.  C.) 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  307 

feres  with  the  work  of  the  latter.  Myers  and  Schott  found  that  soldiers 
whose  diaphragms  are  pushed  up  by  tight  belts  about  the  abdomen  exhibit 
symptoms  of  cardiac  overstrain  much  more  readily  than  do  normal  indi- 
viduals. Myers  found  acute  dilatations  most  common  in  the  British 
regiments  in  which  cuirasses  and  tight  belts  were  worn. 

Wenckebach  has  called  attention  to  the  fact  that  a  large  amount 
of  intra-abdominal  fat  pushes  up  the  diaphragm  and  thus  pushes  the 
heart  into  a  more  transverse  position  (apex  often  in  the  fourth  interspace), 
thereby  hampering  its  action.  This  factor  must  be  reckoned  with  in  the 
genesis  of  the  cardiac  weakness  of  fat  persons. 

ETIOLOGY. 

Clinically,  the  cardiac  manifestations  in  fat  persons  are  very  variable. 
They  occur  most  frequently  in  association  with  (1)  general  obesity,  either 
hereditary  or  arising  primarily  from  over-eating;  (2)  in  childhood;  (3)  after 
castration  or  menopause;  (4)  overindulgence  in  alcohol,  especially  malt 
liquors,  with  or  without  the  presence  of  gout;  (5)  diabetes  mellitus  with 
obesity  (lipogenous  diabetes) ;  (6)  they  are  most  frequent  and  most  intense 
after  the  age  of  fifty. 

PHYSICAL    SIGNS. 

Upon  physical  examination  the  most  striking  features  are  the  general 
obesity;  the  relative  weakness  of  the  skeletal  muscles;  the  groups  of  dilated 
venules,  especially  the  "Bardolphian"  "butterfly"  area  of  dilated  venules 
about  nose  and  cheeks,  as  well  as  similar  areas  along  the  attachment  of 
the  diaphragm  and  elsewhere.  According  to  Hirsch,  dilatation  of  the 
superficial  veins  in  the  subcutaneous  fat  is  a  premonitory  sign  of  cardiac 
weakening;  but  this  is  certainly  not  the  case  always.  Often  there  is  no 
visible  apex  impulse;  the  relative  cardiac  dulness  is  increased  to  both  left 
and  right,  owing  to  the  transverse  position;  the  cardiac  flatness  is  dimin- 
ished. The  heart  sounds  usually  have  a  distant  character  and  may  be  free 
from  murmurs.  Occasionally  there  may  be  slight  cedema  of  the  feet  and  a 
small  amount  of  albumin  in  the  urine.  In  advanced  cases  of  cardiac  insuf- 
ficiency the  patient  may  become  much  thinner  (owing  to  diminished  absorp- 
tion of  fat  from  the  intestine,  see  page  but  the  pericardial  fat  may 
remain  undiminished. 

TREATMENT. 

The  treatment  of  cardiac  weakness  of  fat  persons  depends  entirely  upon 
the  stage  at  which  the  patient  is  seen.  If  cedema  and  persistent  dyspnoea  or 
palpitation  upon  slight  exertion  are  already  present,  the  case  must  be  treated 
exactly  like  one  of  cardiac  overstrain  or  heart  failure  from  any  other  cause 
manifesting  similar  symptoms,  except  that,  owing  to  the  frequent  atrophy 
and  infiltration  of  the  heart  muscle,  drugs  of  the  digitalis  group  are  often 
of  little  use  and  may  even  be  harmful.  The  patient  should  be  put  upon  rest, 
restricted  diet,  with  liquids  restricted  to  1000  c.c,  purged  freely,  and 
bled  if  symptoms  of  failure  of  the  right  heart  set  in.  Amyl  nitrite,  nitro- 
glycerin, and  erythrol  tetranitrate  may  be  used  to  relieve  attacks  of  dysp- 
noea, and  massage,  passive  movements,  and  finally  resisted  movements,  and 
cold  water  or  Nauheim  baths  when  the  patient  is  able  to  get  out  of  bed. 


308 


DISEASES   OF  THE   HEART   AND    AORTA. 


When,  as  is  usually  the  case,  the  patient  is  seen  before  the  stage  of 
actual  heart  failure  has  set  in  and  is  suffering  only  from  what  may  be  con- 
sidered as  the  premonitory  symptoms  of  cardiac  affection, — palpitation 
and  shortness  of  breath  on  exertion,  weakness,  and  giddiness, — the  treat- 
ment should  then  be  directed  toward  the  obesity  rather  than  toward  the 
heart.  A  main  indication  is  then  gradually  to  restrict  the  diet  to  a  heat 
equivalent  of  about  1200  to  1700  calories,  of  which  500  calories  (about  120 
Gm.,  4  oz.)  should  be  proteid  (v.  Noorden). 

(1)  Restricted  Diet. — Numerous  restricted  diets  have  been  laid  down, 
especially  by  Banting,  Oertel,  Hirschfeld,  Kisch,  and  Ebstein.  The  restric- 
tion should  not  take  place  suddenly,  for  fear  of  weakening  the  patient,  but 
should  take  place  in  several  stages,  reducing  500  calories  each  week  until 
the  lower  limit  is  reached.1 

(2)  Liquids  should  be  restricted  to  less  than  1000  c.c.  (1  quart)  per 
day;  this  also  should  be  done  gradually.2 

Sample  Diet. — V.  Noorden  gives  the  following  outline  diet,  which  is  very  satisfactory 
as  a  basis  capable  of  modification: 


Prot. 


8  A.M. 


10  A.M. 

12  m. 


1  P.M. 


3  P.M. 

4  P.M. 
6  P.M. 
8  P.M. 


Breakfast — 

80  Gm.  cold  lean  meat 

\  white  roll  (25  Gm.) 

1  egg 

1  cup  lean  bouillon 

{  1  small  plate  clear  soup 

j  150  Gm.  (5  oz.)  lean  meat  or  fish 

\  100  Gm.  potatoes 

I  Peas,  beans,  cauliflower,  asparagus 

t  100  Gm.  fresh  fruit 

Black  coffee 

200  Gm.  fresh  fruit 

250  c.c  (1  glass)  skim-milk 

Supper — 

125  Gm.  cold  lean  meat  with  pickles 

Red  beets,  radishes,  etc 

30  Gm.  graham  bread 

2-3  teaspoonfuls  boiled  fruit  (no  sugar) . . . 

Total 


30.5 
1.8 
6.5 

0.8 
57.3 
1.9 
3.0 
0.5 

6 
6.8 

36 
2 

2.0 
0.5 


1556       28.6 


Fat. 


1.4 
0.2 
6.1 

0.8 
2.0 

2.8 

10 


2.0 
3 
0.3 


Carb. 


14 


180 
15 

8 

16 
12 


5 
12 


112 


Cal 


205 

85 

7 


583 

0 

90 

97 


299 
10S7 


1  100  Gm.  (3  oz.)  raw  meat  (proteid  20  per  cent.,  fat  1.7  per  cent.)  =  100  cal.  100  Gm. 
(3  oz.)  cooked  lean  meat  (proteid  37  per  cent.,  fat  2.5  per  cent.)  =  175  cal.  (about  25  per 
cent,  higher  in  well-done  roasted  meats).  100  Gm.  (3  oz.)  cooked  meat  of  stall-fed  animals 
(no  visible  fat)  (proteid  36  per  cent.,  fat  6  per  cent.)  =  200  cal.  1  egg  (6.5  Gm.  proteid 4- 
6.2  Gm.  fat)  =85  cal.  Cheese  (proteid  28  per  cent.,  fat  30  per  cent.,  carbohydrate  2  per 
cent.)  =400  cal.  Milk  (proteid  3.4  per  cent.,  fat  3.0  per  cent.,  sugar  4.5  per  cent.)  =  60  cal. 
per  100  c.c.  (20  cal.  per  ounce).  Potatoes  100  Gm.  (3  oz.)=80  cal.  Bread  (proteid  7-9 
per  cent.,  carbohydrate  35  to  80  per  cent.,  the  latter  in  zwieback  and  dry  breads)  100  Gm.  = 
200-350  cal.     Sugar  100  Gm.  =  400  cal.     Butter  100  Gm.  =  930  cal. 

2  Oertel  and  Schweninger  thought  that  drinking  water  is  a  factor  producing  fat. 
Straub  and  others  have  shown  that  this  is  by  no  means  the  case.  The  only  influence  of 
the  water  lies  in  the  fact  that  when  a  meal  is  taken  dry  the  appetite  is  less  than  when  water 
is  taken,  and  consequently  less  is  eaten.  However,  considerable  amounts  of  fluid  increase 
the  volume  of  blood  and  the  work  of  the  heart,  and  hence  the  limitation  of  fluid  saves 
the  heart  in  this  way. 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART. 


309 


(3)  Increased  Exercise. — Increase  exercise  gradually  as  much  as  pos- 
sible, especially  by  walking,  either  on  the  level  or  on  gentle  gradual  ascents, 
interrupted  by  frequent  rests  before  either  weariness  or  shortness  of  breath 
sets  in.1  In  this  way  the  energy  used  by  the  body,  and  hence  also  the  fat 
burned  up,  can  be  materially  increased. 


Weight  of  patient 

Rate  2.7  miles  per  hour. . . 
Rate  3.4  miles  per  hour.  .  . 


Per 

mile. 

150  lbs. 
60  cal. 
75  cal. 

200  lbs. 

85  cal. 

100  cal. 

Walking  on  Level. 


Per  hour. 


150  lbs. 
170  cal.  (18  Gm.  fat) 
230  cal.  (30  Gm.  fat) 


200  lbs. 
225  cal.  (25  Gm.  fat) 
310  cal.  (40  Gm.  fat) 


In  walking  up  grade  the  energy  used  up  is  equal  to  elevation  X  weight  of  patient 
plus  the  energy  expended  in  traversing  the  distance;  but  this  is  theoretically  equalled 
by  the  energy  saved  in  the  subsequent  descent,  and,  on  the  other  hand,  both  are 
increased  by  bringing  into  play  a  different  group  of  muscles;  these  factors  can  scarcely 
even  be  approximately  estimated  in  the  individual  case.  However,  Zuntz  gives  the  fol- 
lowing empirical  figures:  a  man,  150  lbs.,  climbing  3  kilometres  (1.8  miles)  in  one  hour 
upon  a  10  per  cent,  grade  uses  up  about  28  Gm.  (almost  1  ounce)  of  fat. 

(4)  Resisted  movements  (Schott)  carried  out  under  the  supervision  of 
an  attendant;  or  contraction  of   antagonistic  muscles  (Herz)  (see  page  280). 

(5)  Nauheim  baths  (see  page  286)  or  daily  cold  baths  as  cold  as  can 
be  borne  by  the  patient  without  shock. 

(6)  Drug  Treatment.  —  Strychnine  may  be  administered  to  increase 
muscular  tone,  provided  this  does  not  also  increase  the  appetite  too  much. 

Thyroid  extract  and  other  "antifat"  medication  should  be 
scrupulously  avoided.  Metabolism  experiments  have  shown  that  the  admin- 
istration of  thyroid  substance,  though  increasing  the  oxidative  processes,  causes  a  split- 
ting of  proteid  to  a  greater  degree  than  of  fat,  and  hence  defeats  its  own  end,  namely, 
that  of  burning  up  the  fat  without  affecting  the  muscle.  It  also  brings  about  palpita- 
tion, tachycardia,  and  other  distressing  symptoms,  and  tends  to  increase  rather  than  to 
diminish  the  cardiac  features,  even  though  it  maybe  diminishing  the  obesity  itself . 

In  the  obesity  of  the  menopause,  tablets  of  ovarian  extract  are 
used  to  increase  oxidation,  as  this  effect  has  been  demonstrated  in  animals, 
but  clinically  the  results  from  its  use  are  rather  uncertain. 

FATTY  DEGENERATION. 


PATHOLOGY. 

Pathological  Anatomy. — In  the  condition  known  as  "fatty  degenera- 
tion" the  fat  is  deposited  not  by  an  increase  of  adipose  tissue  but  in  the 
form  of  fine  droplets  within  the  heart  muscle-cells  (Figs.  141  and  142). 

In  some  cases  these  droplets  can  be  seen  to  almost  fill  the  entire  cell, 
in  others  they  appear  as  a  few  diffusely  scattered  droplets  in  the  sarcoplasm. 

1  It  must  be  borne  in  mind  that  sclerosis  of  the  coronary  arteries  is  a  frequent  con- 
comitant of  heart  weakness  in  fat  people,  and  hence  sudden  overexertion  or  severe  exer- 
cises are  to  be  avoided,  at  least  until  the  physician  has  thoroughly  acquainted  himself  with 
the  patient's  condition  and  endurance. 


.310  DISEASES    OF   THE   HEART    AND    AORTA. 

Not  all  the  cells  are  invaded  by  the  fat,  but  with  the  naked  eye  yellow  areas 
of  fatty  degeneration  may  be  seen  mingled  with  normal  areas  of  red-brown 
color,  which  appear  normal  in  structure  under  the  microscope. 

As  regards  distribution,  Ribbert  recognizes  three  types:  (1)  diffuse  general 
fatty  degeneration,  in  which  all  the  cells  are  loaded  with  fat;  (2)  mottled  de- 
generation, occurring  in  the  areas  which  lie  midway  between  or  at  points 
most  distant  from  the  larger  arteries;  occurring  especially  in  anaemic  individuals 
and  in  persons  whose  blood-pressure  is  very  low,  so  that  the  cells  which  are  most  distant 
from  the  arteries  suffer  from  ischaemia;  (3)  mottled  periarterial  fatty  de- 
generation produced  by  the  action  of  poisonous  substances  in  the  circulating  blood,  such 
as  phosphorus,  arsenic,  bacterial  poisons,  etc.,  in  which  those  cells  suffer  most  which  are 
brought  most  closely  into  contact  with  the  poison,  i.e.,  the  cells  lying  in  the  vicinity  of  the 
larger  arteries,  while  the  areas  remote  from  these  vessels  are  normal  or  involved  to  a  lesser 
degree. 

Nature  of  Fatty  Degeneration.  —  The  fatty  degeneration  may  go  on 
in  hearts  otherwise  healthy  in  connection  with  infectious  diseases,  or  in 
chronic  myocarditis  and  in  valvular  heart  diseases.  The  exact  nature  of 
the  process  is  not  clear.  Virchow  termed  it  a  "degeneration,"  but  this 
term,  although  in  very  general  use,  does  not  seem  to  designate  accurately 
the  process.  It  appears  to  be  a  disturbance  of  cellular  metabolism  rather 
than  a  degeneration  of  cell  protoplasm,  and  it  has  been  suggested  that 
perhaps  this  is  due  to  some  interference  with  the  oxidizing  enzymes  such 
that  the  fat  cannot  be  oxidized,  just  as  the  sugar  fails  to  be  oxidized  in 
diabetes.     But  this  suggestion  is  not  founded  upon  any  experimental  data. 

It  is  therefore  most  important  from  the  stand-points  of  both  pathology 
and  prognosis  to  learn  where  this  fat  comes  from  and  how  it  is  formed. 
Virchow  was  the  first  to  teach  that  there  was  a  true  fatty  degeneration,  that 
is  that  the  fat  was  formed  from  non-fatty  (probably  proteid)  substances 
of  the  sarcoplasm.  It  must  be  borne  in  mind  that  the  fat  might  be  present 
in  combination  as  it  is  in  lecithin  without  being  visible,  but  that  it  may 
become  visible  when  it  is  split  off  from  the  lecithin  molecules  and  deposited 
as  highly  refractive  droplets  of  true  fat. 

However,  the  analyses  of  numerous  observers  (Bottcher,  Krehl,  Rosenfeld)  show  a 
definite  increase  in  the  fat  present  in  the  heart  muscle  in  fatty  degeneration.  Indeed, 
according  to  Rosenfeld,  the  muscle  shows  "  fatty  degeneration  "  whenever  it  contains  more 
than  15-17  per  cent,  of  fat  within  the  muscle-cells  (in  marked  fatty  degeneration  usually 
20-21  per  cent.).  As  he  put  it,  ''there  is  no  true  fatty  degeneration,  b  ut 
the  cell  becomes  poor  in  proteid  and  fat  enters  it."  That  this  fat  is 
not  derived  from  the  breaking  down  of  cell  substance,  but  is  derived  either  from 
the  fat  of  the  food  or  from  that  transferred  from  the  subcutaneous  tissue  else- 
where in  the  body,  has  been  shown  in  many  ways.  In  the  first  place,  Krehl  demonstrated 
that  the  lecithin  content  of  the  heart  muscle  was  practically  constant  and  quite  indepen- 
dent of  the  degree  of  fatty  degeneration,  and  hence  that  the  fat  was  not  derived  from  this 
source.  Secondly,  Rosenfeld  showed  that  in  a  heart  whose  left  ventricle  appeared  normal, 
but  whose  right  ventricle  was  very  yellow  in  appearance  (and  showed  fatty  degeneration 
on  section),  the  nature  of  the  fat  was  identical  in  both.  Thirdly,  it  was  shown  also  by  Rosen- 
feld that  if  dogs  were  starved  until  their  subcutaneous  fat  had  disappeared  and  were  then 
poisoned  with  phosphorus,  the  fatty  degeneration  did  not  then  appear  as  it  did  in  well- 
fed  dogs.  This  fact  was  further  demonstrated  by  Leick  and  Winckler,  who  poisoned  their 
dogs  with  phosphorus  and  then  fed  them  on  mutton  tallow  (iodine  absorption  coefficient 
38.2),  and  obtained  a  deposit  within  the  heart  muscle  not  of  dog  fat  (I.  A.  C.  58.6)  but  of 
mutton  tallow.  This  seems  to  prove  that  the  "fatty  degeneration"  of  heart  muscle  is 
simply  a  deposit  of  fat  within  the  muscle-cell,  just  as  it  occurs  within  the  connective-tissue 
cell  under  normal  circumstances.     The  deposition  of  this  fat  is  not  associated  with  any 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  311 

change  in  the  lipase  of  the  heart  muscle  nor  of  the  liver,  in  spite  of  the  apparent  increase 
in  fat  metabolism.  The  author  also  found  that  the  amount  of  lipase  in  the  lean  areas  of 
a  human  liver  mottled  with  fatty  degeneration  was  the  same  as  in  the  neighboring  yellow 
areas.  It  would  appear,  therefore,  that,  chemically,  the  primary  change  being  absent,  fatty 
degeneration  lies  not  in  the  heart  but  elsewhere  in  the  body.  This  is  further  borne  out  by 
the  fact  that  in  animals  poisoned  with  phosphorus,  oil  of  pulegon,  etc.,  the  total  amount 
of  fat  in  the  body  is  diminished,  while  that  in  the  heart  and  liver  is  increased.  The  latter 
organs  seem  merely  to  deposit  the  fat  thrown  into  the  general  circulation. 

ETIOLOGY. 

Fatty  degeneration  in  the  human  heart  occurs  most  commonly  in 
association  with  alcoholism,  either  acute  or  chronic,  primary  and  secondary 
anaemias,  after  hemorrhages,  in  association  with  myocarditis,  valvular 
and  other  cardiac  lesions,  in  most  infectious  diseases,  in  miners,  smelters, 
and  many  metal  workers,  as  well  as  in  numerous  other  industries  where 
poisonous  substances  are  employed.  In  a  number  of  cases  of  death 
from  chloroform  anesthesia  fatty  degeneration  has  been  found  and  is 
usually  ascribed  to  the  action  of  the  chloroform,  but  Rosenfeld  believes 
that  in  these  cases  the  fatty  degeneration  is  always  present  before  the 
chloroform  was  given,  and  that  this  fact  accounts  for  the  death  of  the 
patient. 

Not  infrequently,  as  in  cases  of  phosphorus  poisoning  and  of  infectious 
diseases,  the  same  agent  which  brings  about  the  fatty  degeneration  also 
gives  rise  to  diminished  tone  of  the  vasomotor  centre.  Failure  of  the  cir- 
culation may  result  from  the  latter  factor,  but  this  need  scarcely  be  ascribed 
to  the  fatty  change  in  the  heart. 

STRENGTH  OF  HEART  WITH  FATTY  DEGENERATION. 

These  results  of  chemical  investigation  also  find  their  parallel  in  the 
effects  upon  muscle.  Welch,  in  1888,  was  able  to  show  that  the  hearts  of 
rabbits  rendered  fatty  by  prolonged  exposure  to  high  temperatures  were 
quite  normal  as  regards  preservation  of  blood-pressure,  reactions  to  vagus 
stimulation,  etc.;  while  Hasenfeld  and  Fenyvessy  ten  years  later  showed 
that  animals  poisoned  with  phosphorus  withstood  the  strain  from  clamping 
the  abdominal  aorta  quite  as  well  as  did  normal  animals.  On  the  other 
hand,  de  la  Camp  compelled  his  phosphorus  dogs  to  run  a  tread-mill  until 
fatigue  set  in,  and  found  with  the  X-ray  that  their  hearts  had  dilated, 
whereas  those  of  normal  dogs  did  not  dilate  under  these  circumstances. 
The  tonicity  of  the  cardiac  muscle  was  diminished. 
De  la  Camp's  experiments  have  not  been  repeated  as  yet,  but  they  seem 
to  have  been  very  carefully  carried  out.  It  seems  certain  that,  as  Kraus 
claims,  there  is  a  considerable  difference  between  the  endurance  of  normal 
hearts  and  of  those  with  fatty  degeneration. 

Moreover,  patients  with  fatty  degeneration  of  the  heart  are  very  sen- 
sitive to  digitalis  and  are  frequently  injured  by  it.  Sudden  death  from 
overdose  of  digitalis  or  from  acute  cardiac  overstrain  is  more  common  in 
patients  with  fatty  degeneration  of  the  heart  than  in  almost  any  other 
condition.  The  relative  frequency  with  which  fatty  degeneration  is  asso- 
ciated with  spontaneous  rupture  of  the  heart  is  also  evidence  of  weakness 
of  the  walls. 


312  DISEASES   OF   THE   HEART   AND    AORTA. 


SYMPTOMS    AND    SIGNS.    ' 

The  most  characteristic  symptoms  associated  with  the  condition  are 
those  of  general  debility  and  feebleness,  more  or  less  languor  and  somno- 
lence, as  a  rule  without  marked  cardiorespiratory  symptoms  except  short- 
ness of  breath  on  exertion.  The  pulse  is  usually  small,  rather  collapsing, 
and  feeble;  the  blood-pressure  is  below  normal,  except  when  complicated 
by  chronic  myocarditis  or  valvular  lesion  (maximal  pressure  90  to  115 
mm.  Hg) ;  the  pulse-rate  is  increased.  On  physical  examination  the  heart 
may  be  either  normal  or  dilated,  the  sounds  either  feeble  and  distant  or 
short  and  sharp;  the  apex  impulse  may  or  may  not  be  well  marked.  The 
liver  and  spleen  are  often  enlarged  as  part  of  the  general  malady  of  which 
the  cardiac  condition  also  forms  a  part.  There  is  sometimes  oedema  of  the 
feet  and  ankles.  However,  it  must  be  frankly  admitted  that  none  of  these 
is  either  constant  or  characteristic;  and  the  diagnosis  may  have  to  be 
made  from  inference  only. 

DIAGNOSIS. 

The  diagnosis  of  fatty  degeneration  may  often  be  made  with  more  or 
less  probability  from  a  knowledge  of  the  etiological  factors,  but  not  from 
any  of  the  physical  signs,  so  that,  as  Krehl  puts  it,  the  re  are  no  clin- 
ical signs  for  the  diagnosis  of  fatty  degeneration  of 
the   heart. 

TREATMENT. 

When  the  condition  is  recognized,  or  rather  suspected,  the  treatment 
consists  of  absolute  rest  in  bed  for  at  least  two  weeks  after  the  acute  dis- 
turbance has  passed  off  and  until  slowed  respiration  and  increased  tolerance 
to  mild  but  gradually  increasing  arm  exercises  show  that  the  heart  muscle 
has  regained  its  normal  condition.  Whether  it  is  possible  to  overcome  the 
fatty  degeneration  of  a  chronically  diseased  heart  is  questionable,  but  in 
that,  as  in  other  conditions,  treatment  must  be  guided  by  the  general 
response  of  the  patient,  and  over-exertion  must  constantly  be  shunned. 

It  must  be  borne  in  mind  that  hearts  which  are  in  a  state  of  fatty 
degeneration  are  particularly  sensitive  to  digitalis;  so  that,  when  this  con- 
dition is  suspected,  digitalis  should  be  either  avoided  or  given  in  smaller 
doses  than  usual. 

PROGNOSIS. 

Spontaneous  recovery  is  the  rule  if  too  great  a  burden  is  not  imposed 
on  the  heart;  but  in  spite  of  the  results  of  animal  experiments,  especially 
those  of  Welch  and  Hasenfeld  and  Fenyvessy,  attention  must  be  called 
to  the  fact  that  sudden  death  is  far  from  a  rare  occurrence  in  hearts  with 
fatty  degeneration.  It  occurs  most  frequently  after  or  during  exertion. 
One  can  scarcely  avoid  the  suspicion  that  perhaps  the  condition  which 
brings  about  the  change  in  the  fat  metabolism  is  also  one  which  limits  the 
total  metabolism  of  the  heart  muscle-cells  and  consequently  their  contrac- 
tility; so  that  after  a  certain  limit  is  passed  they  suddenly  cease  their  func- 
tion, just  as  is  the  case  in  the  cellular  asphyxia  of  intermittent  claudica- 


FATTY  DEPOSITS  IN  AND  ABOUT  THE  HEART.  313 

tion  and  coronary  sclerosis  (see  page  380,  Fig.  166),  or  in  toxic  myocarditis 
from  diphtheria.  Spontaneous  rupture  of  the  heart  is  par- 
ticularly common  in  cases  of  fatty  degeneration.  The  latter  was  present 
in  77  per  cent,  of  the  cases  collected  by  Hamilton. 

BIBLIOGRAPHY. 

Heart  of  Obesity. 

Kisch,  H.:  Zur  Lehre  vom  Mastfettherzen,  Muenchen.  med.  Wchnschr.,  1902,  Hi,  546. 
Mtiller,  W.:  Die  Massenverhaltnisse  des  menschlichen  Herzens,  Hamb.  u.  Leipz.,  1883. 
Hirsch,   K.:  Ueber  den  gegenwartigen  Stand  der  Lehre  vom  sogenannten  Fettherzen, 

Muenchen.  med.  Wchnschr.,  1901,  xlviii,  1867. 
Leick  and  Winckler:  Herkunft  des  Fettes  bei  Fettmetamorphose  des  Herzfleisches,  Arch. 

f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1902,  xlviii,  163. 
Loevenhart,  A.  S.:  On  the  Relation  of  Lipase  to  Fat  Metabolism— Lipogenesis,  Am.  J. 

Physiol.,  Bost.,  1902,  vi,  331. 
Schieffer:  Ueber   den   Einfluss   des   Ernahrungszustandes   auf  die    Herzgrosse,  Deutsch. 

Arch.  f.  klin.  Med.,  Leipz.,  1908,  xcii,  54. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
V.  Noorden,  K.:  Die  Fettsucht,  Nothnagel's  Spec.  Pathol,  u.  Therap.,  Vienna,  1900,  vol. 

vii,  1st  half. 
Banting,  W.:  Letter  on  Corpulence;  address  to  the  public,  1863,  1864,  1865,  1868. 
Oertel:    Kritisch-physiologische    Besprechung   der   Ebstein'schen    Behandlung  der  Fett- 

leibigkeit,  Leipz.,  1885.     Obesity,  Twentieth  Century  Practice  of  Med.,  N.  Y.,  1895. 
Hirschfeld:  Die  Behandlung  der  Fettleibigkeit,  Ztschr.  f.  klin.  Med.,  Berl.,  1893,  xxii,  142. 
Kisch:  Das  Mastfettherz,  Prag,  1894.     Zur  Insumcienz  des  Mastfettherzens,  Therap.  d. 

Gegenwart,  1899,  xl,  296. 
Ebstein,  W.:  Die  Fettliebigkeit  und  ihre  Behandlung,  Wiesbaden. 

Fatty  Degeneration  of  the  Heart. 

Ribbert,  H.:  Beitrage  zur  pathologischen  Anatomie  des  Herzens,  Arch.  f.  path.  Anat.  etc., 

Berl.,  1897,  cxlvii,  193. 
Krehl,  L.:  Ueber  fettige  Degeneration  des  Herzens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1893,  li,  1,  416. 
Rosenfeld,  G.:  Der  Prozess  der  Verfettung,  Berl.  klin.  Wchnschr.,  Berl.,  1904,  xli,  587. 

Ueber  Herzverfettung  beim  Menschen.,  Zentralbl.  f.  innere  Med.,  Leipz.,  1901,  xxii,  145. 
Leick  and  Winckler:  Herkunft  des  Fettes  bei  Fellmetamorphose  des  Herzfleisches,  Arch. 

f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1902,  xlviii,  163. 
Rubow:  Ueber  die  Lecithingehalt  des  Herzens  und  der  Nieren  unter  normalen  Verhalt- 

nissen,  Hungerzustande  und  bei  der  Fettigen  Degeneration,  Arch.  f.  exper.  Path.  u. 

Pharmakol,  Leipz.,  1904-5,  Hi,  173. 
Welch,  W.  H.:  Cartwright  Lectures  on  the  Nature  of  Fever,  Medical  News,  N.  Y.,  1888. 
Hasenfeld,  A.,  and  Fenyvessy,  B.:  Ueber  die  leistungsfahigkeit  des  fettig  entarteten  Her- 
zens, Berl.  klin.  Wchnschr.,  1899,  xxxvi,  80,  125,  150. 
De  la  Camp,  O.:  Quoted  on  page  201. 
Kraus,  F.:  Die  klinische  Bedeutung  der  fettigen  Degeneration  des  Herzmuskels  schwer 

anaemischer  Individuen,  Berl.  klin.  Wchnschr.,  1905,  xlii,  p.  44A. 


IX. 

AFFECTIONS  OF  THE  MYOCARDIUM. 

A  certain  amount  of  degeneration  in  the  fibres  of  the  heart  muscle 
occurs  during  the  course  of  every  acute  febrile  disease  or  intoxication.  As 
has  been  seen  in  previous  chapters,  the  heart  under  these  conditions  exhibits 
signs  of  overstrain,  and  the  diagnosis  of  myocarditis,  therefore,  depends 
upon  the  degree  rather  than  the  mere  existence  of  cardiac  weakness. 
However,  in  certain  cases  the  signs  of  cardiac  weakness  overshadow  those 
of  the  original  disease  and  it  is  in  these  that  acute  myocarditis  is  usually 
recognized.  The  chronic  changes,  however,  which  follow  long  after  the 
original  disease  has  subsided,  present  a  less  complicated  picture  and  there- 
fore are  more  easily  recognized. 

PATHOLOGICAL    ANATOMY. 

The  lesions  of  acute  and  chronic  myocarditis  are  merely  different 
stages  in  a  process  which  is  more  or  less  continuous.  The  lesions  of  chronic 
myocarditis  are  always  preceded  by  the  acute  lesions,  but  the  degeneration 
may  not  be  so  severe  at  any  of  the  earlier  periods  as  to  give  rise  to  symp- 
toms of  cardiac  weakness. 

In  the  first  stage  of  acute  myocarditis  there  is  injury  and  degeneration 
of  the  muscle-fibres,  with  cedema  about  them,  and  infiltration  of  polymorpho- 
nuclear or  mononuclear  cells  into  the  cedematous  spaces  between  the  fibres. 

Degenerative  Changes.  — The  degenerative  changes  which  take 
place  in  the  heart  muscle  are:  (1)  parenchymatous  degeneration, 
(2)  fatty  degeneration,  (3)  hyaline  and  amyloid  degenera- 
tion, (4)  calcareous  degeneration,  and  (5)  fragmentation. 

Parenchymatous  degeneration  of  the  heart  muscle  was  first 
described  by  Virchow  and  Boettcher.  The  muscle-fibres  swell,  lose  their 
striation,  and  the  plasma  contains  numerous  granules  of  an  albuminous 
material,  probably  altered  muscle  proteid  (myosin).  They  retain  their 
contractile  power  to  a  certain  extent,  but  its  force  at  this  stage  is  somewhat 
impaired,  and  the  cell  may  subsequently  return  to  normal  without  under- 
going complete  necrosis.  In  the  more  severely  injured  cells  the  nucleus 
is  destroyed,  the  sarcoplasm  becomes  filled  with  vacuoles,  takes  on  a  basic 
stain,  and  is  gradually  absorbed,  leaving  only  the  sarcolemma.  Often,  but 
not  always,  parenchymatous  and  fatty  degeneration  go  on  in  the  same 
fibre,  the  fat  being  deposited  as  the  proteicl  is  removed. 

In  some  cases  fibres  undergo  hyaline  or  waxy  degeneration 
(Zenker)  and  present  an  absolutely  homogeneous  appearance,  taking  up  the 
acid  stains  (protoplasmic)  with  great  avidity.  In  rarer  cases  there  is  a 
calcareous  degeneration  with  deposit  of  calcium  salts  in  the  muscle- 
cells.  These  cells  then  take  up  the  basic  (or  nuclear)  stains  (description  of 
314 


AFFECTIONS   OF   THE   MYOCARDIUM. 


315 


a  case  and  discussion  of  the  literature  is  to  be  found  in  the  article  of  E.  K. 
Cullen).  The  degeneration  is  never  uniformly  distributed  throughout  the 
cells,  not  all  the  cells  being  affected  at  once  or  in  the  same  degree. 

Occasionally  the  heart  muscle-cells  show  peculiar  splits  extending  transversely  across 
the  whole  or  part  of  the  cell.  This  condition  is  known  as  "fragmentation."  The 
fibres  may  show  no  other  signs  of  degeneration,  the  transverse  striations  may  be  clear,  and 
the  longitudinal  striae  may  be  distinct  up  to  the  line  of  the  fracture.  Fragmentation  has 
been  found  after  death  from  a  tremendous  variety  of  causes,  even  in  individuals  dying  from 
accident.  It  does  not  seem,  therefore,  to  be  a  sign  of  specific  degeneration.  Dietrich's 
attempts  to  prove  it  an  artefact,  and  either  to  exclude  it  when  once  present  or  to  bring  on 
fragmentation  by  allowing  the  heart  to  pass  through  various 'stages  of  decomposition,  have 
been  unsuccessful,  and  Buhlig  in  a  very  careful  research  seems  to  have  shown  that  it 
is  an  artefact  which  is  produced  when  the  microtome  knife  cuts  at  right  angles  to  the 
muscle-fibres.  This  observation  still  requires  confirmation.  Otherwise  the  consensus  of 
opinion  seems  to  be  that  fragmentation  is  the  result  of  some  change  in  the  muscle-fibres 
occurring  during  the  death  agony,  and  that  it  is  not  to  be  regarded  as  a  degeneration. 

As  illustrating  the  frequency  of  the  several  types  of  myocardial  degeneration  Romberg 
finds  the  following  frequency  in  29  cases: 

Typhoid  fever — 11  cases:  Parenchymatous  (albuminous)  degeneration,  moderate  or 
intense  10:   fatty,  present  6,  absent  5;  hyaline  or  waxy  (slight)  2,  absent  9. 

Scarlet  fever — 10  cases:  Albuminous  degeneration,  present  8,  absent  1,  not  noted  1; 
fatty,  intense  1,  moderate  1,  absent  8;  hyaline  or  waxy,  moderate  3,  absent  7. 

Diphtheria — 8  cases:  Albuminous,  intense  1,  moderate  4,  absent  3;  fatty,  intense  5, 
absent  3;  hyaline  or  waxy,  present  2,  absent  6. 


Fig.  144. — Infiltration   along   the   course  of  the  blood-vessels  in  subacute  myocarditis.     Blood-vessels 
injected.     A.  Low  power.     B.  Same,  higher  power.      (Photomicrograph  by  Dr.  C.  S.  Bond.) 

Distribution  of  Myocardial  Changes.— In  man,  according  to  Krehl,1 
acute  myocardial  lesions  are  particularly  common  in  the 
papillary   muscles   of    the    left    ventricle    and    in    the    mus- 

1  Examination  of  Specimens. — In  cases  in  which  the  state  of  the  myocardium  is 
of  importance,  the  microscopic  structure  of  the  heart  muscle  should  always  be  examined 
by  the  method  of  Krehl.  Krehl  cuts  the  heart  into  cubical  blocks  1  cm.  in  size,  numbering 
them  in  order  so  that  the  exact  location  of  each  block  can  be  accurately  determined.  These 
blocks  are  fixed  in  Midler's  solution  and  a  section  or  two  from  each  is  examined.  In  this 
way  a  very  thorough  idea  of  the  extended  distribution  of  lesions  may  be  gained,  and  a  study 
of  a  very  few  hearts  thus  reveals  more  accurate  knowledge  than  can  otherwise  be  gained 
from  a  large  number  of  organs  examined  less  thoroughly. 


316 


DISEASES  OF  THE  HEART  AND  AORTA. 


culature  about  the  left  auriculoventricular  ring,  lying  within 
the  lymph  spaces  about  the  small  arteries,  which  they  sur- 
round in  sleeve,  cuff,  or  signet-ring  distribution.  The  oedema 
produced  during  experimental  cardiac  overstrain  (Roy  and  Adami)  and  the 
myocardial  lesions  produced  with  adrenalin  (Josue,  Loeb  and  Fleisher,  Pearce) 
and  adrenalin  and  spartein  (Loeb  and  Fleisher),  all  have  this  same  distribution. 
Loeb  and  Fleisher  have  shown  that  two  deleterious  agents,  such  as  adren- 
alin and  spartein  or  caffein,  given  together  produce  myocarditic  lesions  in  a 
much  greater  number  of  cases  than  either  of  them  acting  alone,  and  this  rule 
is  probably  true  for  all  diseases  and  intoxications.     They  found  oedema  of  the 

connective  tissue  appearing  within  two  days,  fol- 
lowed by  perivascular  infiltration  several  days 
later  and  then  by  fibrosis  in  a  few  weeks.  The 
muscle-fibres  were  at  first  swollen  and  vacuo- 
lated, and  later  either  remained  enlarged  (hy- 
pertrophied)  or  underwent  atrophic  changes. 

Abscess.  —  The  form  which  the  foci  as- 
sume depends  chiefly  upon  the  nature  and 
properties  of  the  infective  agent.  If  the 
virulence  of  the  germ  is  great,  abscesses  may 
be  produced  in  the  heart  muscle  (suppurative 
myocarditis)  as  elsewhere  in  the  body.  These 
abscesses  are  usually  produced  by  small  septic 
thrombi  which  plug  the  minute  branches  of 
the  arteries.  Under  the  influence  of  the  fibrin 
ferment  secreted  by  the  bacteria,  the  vessel 
soon  becomes  completely  filled  with  a  throm- 
bus, an  area  of  ischsemia  results  in  the  heart 
muscle,  which  quickly  becomes  infected  and 
breaks  down  to  form  an  abscess.  These  ab- 
scesses vary  in  size  from  a  submiliary  nodule 
to  a  cavity  separating  the  muscle  layers  in  the 
entire  interventricular  septum.  They  are 
usually  produced  by  the  pyogenic  cocci  in 
septicaemia  or  following  trauma  to  the  heart  (see  page  629).  The  outcome 
is  usually  fatal.  Occasionally  there  is  rupture  of  the  ventricle  through 
the  necrotic  portions  of  the  wall. 

"Rheumatic"  Foci. — In  the  less  virulent  infections,  such  as  rheuma- 
tism, typhoid  fever,  influenza,  the  foci  do  not  undergo  suppuration,  but 
the  lymph  spaces  around  the  arteries  and  capillaries  are  filled  with  cellular 
infiltration,  polymorphonuclear  in  most  of  the  acute  infectious  diseases, 
while  mononuclear  cells  predominate  in  myocarditis  from  typhoid  fever 
and  subacute  rheumatism. 

Since  rheumatic  fever  is  perhaps  the  most  common  cause  of  myocar- 
ditis, the  lesions  which  it  produces  are  of  particular  interest.  Romberg, 
Aschoff,  Geipel,  and  Coombs  have  called  attention  to  the  presence  of  small 
submiliary  foci  0.1-0.2  mm.  in  diameter,  which  occur  with  great  frequency 
in  rheumatic  patients,  especially  in  the  musculature  about  the  mitral  ring. 
Each  focus  consists  of  a  hyaline  centre  formed  by  agglutinative  thrombosis 
within  a  capillary.    About  this  there  is  a  zone  of  giant  cells  each  containing 


Fig.  145. — Septic  myocarditis  with 
multiple  abscesses  in  the  heart  wall. 
The  arrows  point  to  the  abscesses. 


AFFECTIONS   OF   THE   MYOCARDIUM. 


317 


2-4  nuclei,  and  these  in  turn  are  surrounded  by  a  wider  zone  of  mononuclear 
cells  interspersed  with  eosinophiles.  The  writers  mentioned  regard  these 
foci  as  pathognomonic  of  rheumatism,  although  they  may  bear  only  the 
general  features  of  a  subacute  inflammation  about  an  area  of  hyaline  throm- 
bosis. Indeed  the  most  typical  specimen  of  these  found  in  the  Johns 
Hopkins  Pathological  Museum  was  seen  in  a  case  of  non-rheumatic  myocar- 
ditis. On  the  other  hand,  Freund  has  reported  a  case  of  acute  rheumatic 
myocarditis  in  which  the  infiltration  was  mainly  polymorphonuclear. 

Bracht  and  Wachter  have  recently  produced  arthritis,  endocarditis,  and  myocarditis 
with  lymphocytic  infiltrations  in  animals  by  injection  of  cultures  of  diplococci  obtained 
from  two  cases  of  acute  articular  rheumatism.  These  infiltrations  contrast  sharply  with 
the  polymorphonuclear  infiltrations  usually  produced  by  pyogenic  streptococci. 


Fig.  146. — Photomicrograph  showing  an  abscess  in  the  heart  muscle.  A.  Low  power.  B.  Same,  higher  power. 

Subsidence  of  Lesions. — The  changes  which  occur  in  the  myocardium 
when  the  patient  recovers  from  the  acute  infection  or  intoxication,  which 
is  the  causal  factor,  vary  both  with  duration  and  intensity  of  the  disease 
and  the  rapidity  and  completeness  of  the  recovery.  If  the  causal  factor 
completely  disappears  and  its  sojourn  in  the  body  has  been  a  short  one,  no 
permanent  changes  may  have  taken  place.  The  oedema  of  the  fibres  disap- 
pears, the  cellular  exudate  may  be  absorbed  in  toto,  and  the  myocardium 
may  resume  its  normal  appearance.  If  areas  of  fibres  have  been  destroyed 
their  place  may  be  taken  by  scar  tissue.  But  if  the  duration  of  the  process 
has  been  so  long  that  connective  tissue  has  begun  to  be  formed  in  the 
exudate,  the  traces  are  no  longer  obliterated  and  a  chronic  myocarditis 
has  set  in. 


PATHOLOGICAL    PHYSIOLOGY. 

As  has  been  seen  in  previous  chapters,  hearts  whose  muscle 
is  injured  become  dilated  upon  comparatively  slight 
exertion,  while  healthy  hearts  resist  dilatation  in  spite  of  tremendous 


318  DISEASES  OF  THE  HEART  AND  AORTA. 

exertion.  Moritz  and  Dietlen,  whose  X-ray  studies  have  demonstrated 
that  the  normal  heart  becomes  smaller  in  severe  exercise,  have  shown  that, 
on  the  contrary,  the  heart  whose  muscle  is  diseased  undergoes  tremendous 
dilatation.  Fleisher  and  Loeb  found  that  cedema  of  the  lungs  from  NaCl 
infusion  sets  in  much  more  readily  in  myocarditic  than  in  normal  rabbits. 
The  blood-pressure  is  usually  low  in  acute  myocarditis,  but  this  is  due  to. the 
fact  that  the  toxic  substances  which  injure  the  heart  muscle  also  depress  the 
vasomotor  centre.  The  low  blood-pressure  is  due  to  the  latter  influence  and 
not  to  the  weakness  of  the  heart. 

These  facts  were  brought  out  by  very  interesting  studies  of  the  physiology  of  the 
heart  muscle  after  injections  of  diphtheria  toxin  which  were  made  by  Roily  and  later  by 
v.  Stejskal.  Roily  used  a  dose  of  toxin  which  just  killed  his  rabbits  in  twenty-four  hours, 
and  then  began  his  experiments  about  twenty-two  hours  after  the  injection.  He  found 
that  at  this  time  the  blood- pressure  and  pulse-rate  of  the  animal 
were  still  quite  normal,  and  that  the  heart  was  still  able  to  respond  well  to 
increased  work  thrown  upon  it  by  compressing  the  abdominal  aorta,  etc.,  and  that  the  blood- 
pressure  increased  considerably.  About  half  an  hour  before  death,  however,  the  blood- 
pressure  began  to  fall,  owing  to  loss  of  vasomotor  tone,  as  had  been  shown  by  Romberg. 
Even  at  this  time  the  heart  was  still  strong  enough  to  respond  by  a  second  rise  of  blood- 
pressure  upon  clamping  the  abdominal  aorta.  Very  soon  after  this,  however,  within  a 
few  minutes,  the  rate  became  irregular  and  the  heart  weak- 
ened completely.  V.  Stejskal's  results  were  similar.  The  action  of  the  diphtheria 
toxin  had  not  been  immediate,  but  it  had  required  several  hours  to  combine  with  the  heart 
muscle,  after  which  its  weakness  was  manifest. 

The  conclusion  reached  by  Roily  and  v.  Stejskal  is  that  the  heart 
remains  competent  in  spite  of  muscular  weakness  until 
a  certain  degree  of  strain  is  imposed  upon  it,  when  it 
suddenly  crosses  the  threshold  that  leads  to  failure,  dilatation,  and  even 
death.  The  threshold  of  cardiac  overstrain  in  the  healthy  heart  is  at  a 
much  higher  level. 

Arrhythmia  in  Acute  Myocarditis. — Irregularity  of  the  pulse  cannot  be 
brought  about  by  injuring  the  myocardium  by  injection  of  alcohol,  iodine, 
or  even  KCN,  but  often  occurs  in  man  as  a  result  of  myocardial  lesions, 
especially  after  exercise  and  overstrain.  Gerhardt,  Muller,  and  Schonberg 
have  called  attention  to  the  association  of  irregularity  with  structural 
changes  in  the  right  auricle  and  fibrillation.  In  mitral  disease  it  is  probable 
that  irregularity  arises  in  the  left  auricle  rather  than  in  the  right,  since  the 
latter  is  then  not  the  seat  of  pathological  conditions.1 

Bradycardia  is  met  with  in  the  late  forms  of  diphtheric,  influenzal, 
and  pneumonic  myocarditis  and  occasionally  during  the  febrile  stage.  It 
is  often  vagal  in  origin,  but  is  sometimes  due  to  depressed  conductivity 
of  the  auriculoventricular  bundle,  the  ventricle  responding  only  to  alter- 
nate contractions  of  the  auricle  (2  :  1  rhythm) .  It  is  probable  that  under 
these  conditions  toxic  myocardial  changes  have  taken  place  in  the  bun- 
dle (Mackenzie).  It  is  not  unlikely  that  some  of  the  sudden  deaths 
during  convalescence  from  diphtheria  may  be  due  to  this  cause  (Dunn, 
see  page  578). 

1  More  fully  discussed  in  chapter  on  Mitral  Stenosis. 


AFFECTIONS   OF  THE   MYOCARDIUM.  319 


SIGNS    AND    SYMPTOMS. 

The  most  characteristic  sign  of  myocardial  weak- 
ness is  dilatation  of  the  heart  (see  page  202).  The  heart 
is  usually,  but  by  no  means  always,  rapid,  the  sounds  may  be  clear  but  are^ 
usually  short  and  sharp;  they  may  be  embryocardiac  in  rapid  hearts;  a 
gallop  rhythm,  especially  of  the  presystolic  type,  may  be  present, 
or  the  sounds  may  be  definitely  split  (reduplicated).  It  is  also  very  com- 
mon to  hear  soft  systolic  murmurs  over  the  apex  or  the  tri- 
cuspid area,  due  to  functional  insufficiencies  at  the  auriculoventricular 
orifices  (see  page  422),  or  to  hear  the  "accidental"  systolic  murmur  in 
the  pulmonary  area.  The  second  pulmonic  sound  is  usually  ac- 
centuated  from  stasis  in  the  pulmonary  vessels. 

Clinically,  uncomplicated  myocarditis  is  met  with  in  the  course  of  the 
febrile  diseases  and  the  intoxications,  especially  alcohol- 
ism, phosphorus  poisoning,  and  ptomaine  poisoning.  It  is  present 
also  in  a  certain  degree  in  almost  every  case  of  acute  endocarditis  or  peri- 
carditis, where  it  is  but  part  of  the  general  "carditis." 

Its  manifestations  are  simply  those  of  acute  heart  failure  or  of  cardiac 
overstrain  occurring  while  at  rest  or  upon  very  slight  exertion.  The  symp- 
toms are,  therefore,  sometimes  those  of  broken  pulmonary 
compensation  (failure  of  the  left  ventricle,  page  207),  sometimes 
those  of  broken  systemic  compensation  (failure  of  the 
right  ventricle) ,  according  as  the  left  ventricle  or  the  right  is  the  one  most 
affected.  In  many  cases  there  are  attacks  of  precordial  pain 
amounting  almost  to  angina  pectoris,  coming  on  when  the  heart  is  acutely 
dilated  after  excitement  or  exertion. 

ACUTE    MYOCARDITIS    IN    RHEUMATIC    FEVER. 

Although  weakening  of  the  heart  is  one  of  the  most  important  factors 
in  general  asthenia  that  accompanies  or  follows  tonsillitis  or  rheumatic 
fever,  it  does  not  often  kill  the  patient  and  hence  is  not  often  a  striking  fea- 
ture at  the  autopsy  table. 

The  following  history  illustrates  the  course  in  fatal  cases,  showing  (1) 
the  gradual  insidious  onset,  (2)  shortness  of  breath,  extreme  weakness, 
and  finally  ascending  oedema,  (3)  dilatation  of  the  heart,  with  oedema  and 
degenerative  changes  in  the  heart  muscle,  without  either  hypertrophy, 
fibrous  changes,  or  valvular  lesion. 

Case  of  Acute  Rheumatic  Myocarditis. 

Annie  Jones,  female,  colored,  48,  admitted  July  5,  1904,  complaining  of  "  rheu- 
matism,'' of  which  she  has  had  attacks  for  many  years,  especially  marked  during  the 
last  two  years.  The  knees  and  shoulders  have  been  the  joints  most  frequently 
affected.  She  has  had  no  other  infectious  diseases  and  the  previous  history  is  otherwise 
negative.  No  shortness  of  breath  nor  palpitation.  During  past  four  weeks  has  been  com- 
pelled to  sleep  upright  in  a  Morris  chair,  and  has  had  incontinence  of  faeces. 

Physical  Examination. — Patient  is  a  very  stout  colored  woman,  lying  quietly 
on  her  back  in  bed.     Pupils  equal  and  react  to  light  and  accommodation.    Chest  clear. 

Heart . — Impulse  is  not  visible.  Relative  cardiac  dulness  extends  13 
cm.   to  left  of  midline  in  fourth  interspace,  30  cm.  to  the  right.    First  sound  at  apes 


320 


DISEASES   OF   THE   HEART   AND    AORTA. 


is  very  loud  and  not  perfectly  clear,  though  there  is  no  definite  murmur.  Second  sound 
resembles  the  first  in  quality  but  is  clear.  Pulse  regular,  of  good  volume,  rather  high 
tension,  100  per  minute.    Vessel  wall  somewhat  thickened. 

Abdomen  is  extremely  large  and  swollen;  there  is  dulness  in  dependent  portion. 
Liver  is  not  enlarged.  Legs  are  extremely  swollen  and  indurated;  do  not  even  pit  on 
pressure.  Knee-  and  ankle-joints  much  swollen  and  stiff.  A  round  perforating  ulcer  is 
present  at  left  heel.    No  disturbance  of  sensation  anywhere. 

Temperature  99°;  red  blood-corpuscles  4,046,000;  haemoglobin  55  per  cent.;  leuco- 
cytes 3800. 

Ordered  rest  in  bed;  soft  diet;  diuretin  1  Gm.  (gr.  xv)  q.  4  h.;  ulcer  of  foot  to  be 
irrigated  with  sol.  potass,  permang.  1:20000  b.  d.  On  July  7,  ordered  tinctura  dig- 
italis 1  c.c.  (ttlxv)  q.  4  h.,  ad  dos.  viii;  this  was  then  repeated  and  continued  throughout 
the  course  of  disease.  Spts.  glycerylis  nitrat.  gtt.  ii,  q.  4  h.,  alternating  with  sod.  nitrit. 
0.3  Gm.  (gr.  v)  q.  4  h.;  morphin.  sulph.  0.00S  Gm.  (£  gr.)  p.r.n. 

July  12.  Heart's  action  irregular;  first  sound  reduplicated  over  tricuspid  area;  no 
murmurs.  July  15.  There  is  a  large  perforating  ulcer  just  below  coccyx.  This  was  irri- 
gated with  potass,  permanganate  1  :  20000  and  packed  with  iodoform  gauze.  July  16. 
Temperature  106°;  percussion  note  impaired  at  left  base  behind,  where  breath  sounds  are 
absent.  A  few  rales  have  previously  been  heard  in  this  area.  Ordered  strychnine  sulph. 
0.003  Gm.  (jV  gr.)  and  digitalin  0.003  Gm.  (tV  gr.)  hypo.  q.  4  h.  At  7.30  p.m.,  respiration 
shallow  with  expiratory  grunt.    At  11.00  became  unconscious,  and  died  at  12.45. 

Autopsy  showed  about  1  litre  of  fluid  in  peritoneal  cavity;  congestion  of  lower  lobe 
of  lungs. 

Heart . — Several  opaque  white  patches  over  epicardium,  one  with  a  diameter  of 
3  cm.  Coronary  arteries  soft  and  smooth.  Heart  muscle  soft,  flabby, 
and  of  yellowish -brown  color,  studded  with  numerous  small 
opaque   white   areas.     The  muscle  bundles  are  widely  separated  nuclei.    Under  the 

microscope  the  muscle-fibres  are  seen  to  be 
swollen;  little  new  growth  of  interstitial  connective 
tissue.  Heart  weighs  250  Gm.  Slight  sclerosis  about 
base  of  aorta,  none  elsewhere.  Kidneys  normal  in  size, 
pale  and  cloudy.    Liver  shows  some  fatty  degeneration. 

DIPHTHERIC    AND    INFLUENZAL    MYOCARDITIS. 

Acute  myocarditis  is  the  chief  cause  of  death 
in  diphtheria  and  influenza.  In  these  conditions 
it  may  manifest  itself  either,  (1)  as  an  early  form 
during  the  course  of  the  fever,  or  (2)  as  a  late  form 
which  becomes  manifest  after  the  temperature 
has  fallen.  The  cases  of  diphtheric  myocarditis 
have  been  most  carefully  studied  by  Hibbard 
in  800  cases  with  119  deaths  (15  per  cent.)  at 
the  Boston  City  Hospital.  In  spite  of  the  high 
average  mortality,  the  mortality  was  less  than 
5  per  cent,  in  those  cases  in  which  the  pulse- 
rate  was  below  130  per  minute,  increasing  as  the  pulse-rate  increased 
above  that  figure.  Death  was  especially  frequent  in  those  cases  in  which 
a  gallop  rhythm  was  noted.  Bradycardia  (under  60  per  minute)  was  not 
a  severe  sign  in  adults  (14  cases  without  a  death;  only  2  with  cardiac 
symptoms),  whereas  in  cases  under  7  years  it  was  a  very  grave  sign 
(6  cases,  5  deaths).  In  all  Hibbard's  fatal  cases  there  were  both  acute 
myocardial  change  and  degeneration  of  the  fibres  of  the  vagus. 

Sudden  death  is  not  uncommon  in  cases  of  diphtheric  myocar- 
ditis; in  Dunn's  case,  from  the  onset,  heart-block  (Adams-Stokes  syndrome) 


Fig.  147. — Orthodiagraphic  out- 
lines of  the  heart  of  a  child  during 
the  course  of  a  severe  diphtheria. 
(After  Dietlen,  Miinchen  med. 
Wchnschr.,  1905,  Hi.)  +  +  +  ++, 
outline  on  fifth  day  (MR.  =  3.0 
cm.,  ML.  =  6.0  cm.,  L.  =  9.1  cm.); 

,  outline   on    seventh  day 

(MR.  =  3.5  cm.,  ML.  =  8.1  cm.,  L. 

=  12.4    cm.);     ,    outline    on 

twenty-sixth  day  (MR.  =  2.0  cm., 
ML.  =  6.5  cm.,  L.  =  9.3  cm.). 


AFFECTIONS   OF  THE   MYOCARDIUM.  321 

was  the  result  of  myocardial  change  in  the  vicinity  of  the  auriculoventricular 
bundle.  The  slow  pulse  also  is  often  due  to  partial  heart-block,  2  :  1 
rhythm,  though  this  may  be  due  to  overstimulation  of  the  vagus  as  well 
as  to  injury  of  the  bundle. 

Just  as  diphtheria  affects  the  myocardium  in  the  very  young,  influenza 
affects  it  in  the  aged.  Indeed  myocarditis  constitutes  one  of  the  gravest 
effects  of  this  disease,  and  is  especially  to  be  feared  after  the  sixth  decade. 

The  following  case  serves  as  an  example : 

Case  of  Influenzal,  Myocarditis. 

Patient,  aged  75,  of  sedentary  habits,  rather  stout,  but  free  from  all  cardiac  symp- 
toms. Pulse  had  always  been  of  good  volume  and  regular.  Had  a  severe  attack  of 
influenza  in  March,  1903,  confining  her  to  bed  for  a  month.  No  special  car- 
diac features.  After  a  short  convalescence  she  was  again  able  to  be  up  and  about.  A  few 
days  later,  just  after  retiring,  she  had  a  severe  attack  of  cardiac  asthma, 
breathlessness,  orthopnoea,  and  slight  precordial  pain.  No  true 
angina.  Moderate  degree  of  cyanosis.  Pulse  small,  rapid,  irregular.  Cardiac  dulness 
slightly  enlarged.  Soft  systolic  murmur  heard  over  the  entire  heart.  The  attack  lasted 
half  an  hour,  symptoms  being  much  relieved  by  inhalations  of  amyl  nitrite. 

Patient  was  given  complete  rest  in  bed  for  a  few  days,  with  fluidextract  of  digitalis 
ff\,v  (0.3  c.c.)  three  times  a  day  and  soft  diet,  and  was  then  kept  at  rest  in  a  large  arm-chair. 
Gradual  convalescence.  Soon  became  free  from  symptoms,  but  pulse  remained  70  and 
irregular  and  she  was  compelled  to  refrain  from  every  effort  except  one  daily  trip  up  and 
down  stairs,  during  which  she  rested  at  each  step  long  enough  to  count  twenty.  In  June 
and  July,  1904,  she  had  several  similar  attacks,  and  though  she  improved  somewhat  her 
pulse  remained  permanently  irregular.  Died  suddenly  a  year  and  a  half  later,  death  fol- 
lowing six  weeks  after  a  severe  cellulitis  of  the  leg. 

Case  of  Subacute  Alcoholic  Myocarditis. 

B.  C.  S.,  reporter,  married,  aged  36,  admitted  to  the  service  of  Prof.  J.  O.  Hirsch- 
felder,  City  and  County  Hospital  of  San  Francisco,  January  23,  1905,  complaining  of 
shortness  of  breath  and  swelling  of  feet.  Father  and  brother  are  subject  to  rheumatism, 
and  patient  himself  had  swelling  of  joints  four  years  ago,  about  the  time  of  a  gonorrhoea! 
infection.  He  had  measles,  whooping-cough,  and  scarlet  fever  as  a  child,  and  typhoid 
fever  seven  years  ago.  Denies  syphilis.  Married,  but  has  had  no  children.  Uses  tobacco 
in  moderation,  but  drinks  whiskey  in  excess,  as  a  probable  result  of  which  he  has  fallen 
from  the  best  to  the  lowest  strata  of  society. 

Present  Illness. — Four  weeks  ago  while  in  the  midst  of  a  series  of  debauches  he 
noticed  that  his  shoes  became  tight,  and  in  a  few  days  his  legs  became  so  swollen 
that  he  could  not  put  on  his  drawers.  He  had  pain  in  the  legs  on  walking,  owing  to  the 
oedema.  He  also,  felt  very  weak  and  became  exhausted  easily.  Has  had  shortness 
of  breath  on  exertion. 

Physical  Examination. — Well-nourished  man  of  good  color.  Tongue  and  uvula 
deviate  slightly  to  the  right.  General  glandular  enlargement.  Epitrochlears  palpable. 
Chest  negative  except  for  a  few  moist  rales  over  right  axilla  and  base. 

Heart . — Cardiac  impulse  not  visible.  Relative  cardiac  dulness  extends  to  12.5 
cm.  from  midline  in  fifth  interspace  (3  cm.  outside  mammillary  line),  4  cm.  to 
right  of  midline  and  above  to  the  third  rib.  Sounds  are  very  rapid,  the  first  sound  every- 
where replaced  by  a  systolic  murmur  which  is  loudest  at  the  apex;  not  transmitted  to  the 
axilla;  pulmonic  second  accentuated.  Pulse  108,  regular  in  force  and  rhythm,  low  tension, 
fairly  good  volume.    Radial  artery  not  palpable. 

Liver  just  palpable.  No  scar  on  genitalia.  Lower  extremities  are  covered 
with  pediculi  and  raw  scratch  marks.  Marked  oedema  of  both  legs.  Urine  nega- 
tive, sp.  gr.  1028. 

Ordered  liquid  diet;  fluidextract  digitalis  0.3  c.c.  ("lv)  q.  4  h.;  spir.  glycerylis  nitratis 
1  gtt.  q.  4  h.;  sol.  magnes.  sulphat.  sat.  30  c.c.  (oi);  ung.  zinci  oxid.  to  legs. 
21 


322  DISEASES   OF   THE   HEART    AND    AORTA. 

Jan.  30.  Pulse  slow  and  somewhat  irregular,  venous  tracing  show- 
ing that  some  of  the  auricular  impulses  did  not  reach  the  ventricle  (2  :  1  heart-block). 
Given  atropine  0.0015  Gm.  (|  gr.)  at  12.45  p.m.  At  2.00  p.m.,  max.  pr.  135,  min.  75- 
80.  Pulse-pressure  60 X  pulse-rate  60  =  3600.  Pulse- rate  absolutely  regular,  as 
shown  in  the  brachial  artery  tracing  taken  at  1.45  p.m.  Digitalis  was  now 
discontinued. 

Feb.  2.  (Edema  gone.  Soft  systolic  murmur  still  present  at  apex.  Pulse-rate  72,  abso- 
lutely regular,  responding  to  all  impulses  from  the  auricle.    It  never  again  became  irregular. 

Feb.  11.  Feels  quite  strong.  Up  and  about.  Heart  has  been  regular  and  all  mur- 
murs gone. 

March  2.  Has  had  slight  swelling  of  feet.  Was  again  put  to  bed.  The  swelling 
disappeared  within  24  hours. 

In  a  few  days  the  patient  was  again  up  and  about,  and  in  a  week  or  ten  days  later  was 
allowed  to  continue  his  work  in  the  pantry.  Was  discharged  apparently  cured  about 
May  15. 

DIAGNOSIS. 

As  has  been  seen,  the  diagnosis  of  acute  myocarditis  in  many  cases  is 
made  more  by  inference  than  by  definite  signs.  The  presence  of  symptoms 
of  cardiac  weakness  in  an  infectious  disease,  out  of  proportion  to  the 
severity  of  the  latter  or  to  the  apparent  severity  of  the  endocardial  lesion, 
is  presumptive  evidence  of  severe  myocardial  involvement.  The  symptom- 
complex  of  restlessness  or  marked  dulness,  constriction  over  the  chest,  and 
precordial  pain,  vomiting,  cyanosis,  and  increase  in  the  area  of  cardiac 
dulness,  during  or  after  an  attack  of  an  infectious  disease  or  of  delirium 
tremens,  is  practically  pathognomonic.  The  presence  of  a  systolic  murmur 
at  the  apex  and  over  the  body  of  the  heart,  which  may  even  be  transmitted 
to  the  axilla  but  which  disappears  during  convalescence,  added  to  the  other 
symptoms  above  mentioned,  would  indicate  myocarditis  rather  than  endo- 
carditis. It  must  be  borne  in  mind,  moreover,  that  the  presence  of  true 
endocarditis  or  pericarditis  is  evidence  in  favor  rather  than  against  the 
presence  of  an  additional  myocarditis,  and  that  in  the  acute  form  the  symp- 
toms are  quite  as  liable  to  be  due  to  the  insufficiency  of  the  muscle  as  to 
the  valves.  On  the  other  hand,  just  as  a  most  acute  nephritis  may  be  pres- 
ent without  the  presence  of  albumin  or  casts  in  the  urine,  so  acute  myo- 
cardial changes  may  be  present  without  definite  signs  of  cardiac  weakness 
other  than  a  tendency  to  fatigue.  In  view  of  the  observations  of  de  la 
Camp,  Moritz,  Dietlen,  and  Hornung,  myocardial  changes  may  be  diag- 
nosed in  cases  in  which  the  heart  undergoes  transitory  dilatation  (with 
or  without  transitory  valvular  insufficiencies)  upon  comparatively  slight 
exertion.  The  cardiac  area  under  such  conditions  must  be  most  carefully 
outlined,  if  possible  with  the  orthodiagraph.  In  the  absence  of  the  latter 
careful  percussion  may  often  suffice.  The  changes  must  be  1  cm.  or  more 
before  they  should  be  considered  as  definite. 

TREATMENT. 

The  management  of  a  case  of  acute  myocarditis  differs  essentially  from 
that  of  the  chronic  form,  owing  to  the  fact  that  in  the  former  the  changes 
in  the  muscle  may  be  of  a  temporary  character,  while  in  the  latter  the 
changes  are  permanent.  Accordingly,  in  the  acute  form  the  aim 
is    to    allow   the    muscle   to   return   to   its   normal   state, 


AFFECTIONS   OF   THE   MYOCARDIUM.  323 

while  in  the  chronic  form  this  cannot  be  hoped  for, 
and  the  treatment  is  directed  toward  obtaining  the  best  functional  result 
possible  in  the  changed  muscle  that  is  left.  The  one  aims  at  bringing 
about  subsidence,  the  other  at  inducing  hypertrophy. 

Accordingly,  even  in  the  mildest  form  of  acute  myocarditis  rest  is  all- 
important — c  omplete  rest  in  bed  until  the  degenerative 
changes  in  the  muscle  have  subsided.  This  is  especially 
important,  since  cardiac  overstrain  sets  in  very  easily  in  such  hearts,  and 
it  is  probable  that  this,  in  even  the  slightest  degree,  increases  the  injury 
to  the  muscle-fibres  as  well  as  the  extent  of  the  interstitial  cedema  and 
infiltration.  The  patient  should  be  kept  in  bed  at  least  two  weeks  after 
any  indications  of  myocardial  weakness  have  subsided,  and  if  possible 
until  the  pulse-rate  has  again  become  slow.  An  easily  digestible  diet  equiva- 
lent to  about  1000-1500  calories  should  be  enforced  (see  page  235),  frequent 
feeding  of  small  quantities  being  resorted  to  in  the  place  of  three  compara- 
tively large  meals. 

An  ice-bag  should  frequently  be  applied  to  the  precordium,  since  it 
tends  to  slow  the  heart-rate.  Some  writers,  especially  Caton,  strongly 
favor  the  application  of  small  blisters  to  the  precordium  and  the  administra- 
tion of  small  doses  (0.3  Gm.  or  5  gr.)  of  potassium  iodide,  but  it  is  extremely 
doubtful  whether  this  has  any  effect  upon  the  course  of  the  disease. 

If  anaemia  arises,  iron  should  be  ordered  in  some  form,  usually  as 
Blaud's  pills, — ferri  carbonas  saccharatus  (0.25  Gm.,  4  gr.), — or  Vallet's 
mass  (same  as  Blaud's  pills  with  honey  instead  of  sugar  but  more  perma- 
nent), or  elixirferri,  quininseet  strychninse  phosphatum  (4  c.c,  1  fluidrachm). 
If  constipation  or  other  digestive  disturbances  result,  hsematin  or  some 
other  "  organic "  iron  preparation,  that  is,  where  the  iron  is  combined  with 
proteid.  The  patient's  bowels  should  be  kept  freely  moving  without  effort, 
best  by  means  of  Rochelle  salts,  sodium  phosphate,  Epsom  salts,  or  Seicllitz 
powders.  The  effervescent  citrate  of  magnesia  usually  causes  greater 
abdominal  distention  than  is  desirable,  owing  to  the  upward  displacement 
of  the  diaphragm. 

Hypersensibility  to  Digitalis.  —  The  usefulness  of  digitalis  in  acute 
myocarditis  is  a  debatable  question.  Digitalis  acts  as  a  spur  to  the  heart 
and  raises  the  strength  of  the  contraction  until  it  enables  the  fibres  to  draw 
on  their  reserve  force  at  each  contraction,  but  it  does  not  raise  the  limit 
strength.  When  that  limit  is  already  approached  it  spurs  them  too  far, 
and  drives  them  to  overstrain  and  even  to  death. 

Whether,  in  any  individual  case,  digitalis  will  do  good  or  harm  will 
depend,  therefore,  upon  the  degree  to  which  degenerative  changes  have 
progressed  and  the  amount  of  reserve  force  that  is  left.  Thus,  in  the  case 
of  B.  C.  S.,  the  myocardial  degeneration  was  slight  and  the  beneficial  action 
of  digitalis  was  marked.  With  A.  J.,  however,  the  case  was  different. 
Degeneration  had  reached  too  advanced  a  stage  and  the  drug  was  useless, 
perhaps  even  harmful. 

Even  the  heart  of  B.  C.  S.,  however,  manifested  the  abnormal  suscepti- 
bility of  such  hearts  to  digitalis,  since  it  produced  partial  block  and  extra- 
systoles  with  doses  which  barely  sufficed  to  slow  the  heart  of  the  average 
patient. 


324 


DISEASES   OF   THE   HEART   AND    AORTA. 


Moreover,  in  acute  myocarditis  the  heart  is  hypersensitive  to  digitalis. 
For  example,  in  the  case  of  B.  C.  S.,  a  normal  dose  produced  an  abnormally 
intense  reaction  with  signs  of  the  first  stage  of  digitalis  poisoning — partial 
heart-block  and  extrasystoles.  Fortunately  in  this  case  the  good  effects 
outweighed  the  bad,  but  it  belonged  to  the  group  of  cases  which  prove  con- 
clusively that  in  acute  myocarditis  digitalis  should  always  be  given  in 
smaller  doses  than  would  be  used  for  a  heart  with  a  valvular  lesion  which 
showed  the  same  degree  of  heart  failure. 

Strychnine. — As  regards  strychnine,  both  its  beneficial  and  its  harmful 
effects  are  less  marked  than  those  of  digitalis.  It  is  therefore  less  liable  to 
overstep  the  limit  of  tolerance.  In  ordinary  doses  it  tends  to  increase  the 
cardiac  tonicity,  as  well  as  to  stimulate  the  cardiac  nerves,  the  respiratory 
and  vasomotor  centres,  so  that  it  becomes  a  valuable  drug  in  such  conditions. 

CHRONIC   MYOCARDITIS. 


PATHOLOGICAL    ANATOMY. 

Pathologically  the  chronic  inflammatory  changes  in  the  myocardium 
may  be  divided  into  three  groups: 

1.  Cicatricial  patches  or  scars  arising  from  the  healing  of  isolated  areas  of  inflam- 
mation (abscess  or  focal  infiltrations)  or  from  the  organization  of  areas  of  infarction. 

2.  Thickening  of  the  septa  that  separate  the  muscle  strands  (interfascicular  myo- 
fibrosis, Dehio)  occurring  when  the  heart  muscle  hypertrophies. 

3.  Diffuse  degeneration  of   the  muscle-fibres  with  invasion  of  the  fibre  bundles  by 
strands  of   connective  tissue   (cardiosclerosis,   Huchard;    interstitial   myofibrosis,   Dehio). 


Fig.  148. — Specimen  showing  a  cardiac  aneurism 
covered  with  pericardial  adhesions. 


Fig.  149.  —  Chronic  myocarditis   (cardiosclerosis). 


Cardiac  Cicatrices. — The  areas  of  cardiac  cicatrices  are  quite  common 
in  coronary  sclerosis,  in  which  they  represent  the  site  of  healed  infarcts 
in  the  area  supplied  by  the  affected  artery.  The  fibrous  tissue  composing 
the  scar,  relatively  poor  in  elastic  fibres,  is  weaker  than  the  rest  of  the 
heart  wall,  presenting  the  condition  termed  by  Ziegler  myomalacia  cordis, 
and  it  may  bulge  out  to  form  an  aneurism  of  the  heart  (Fig.  148). 


AFFECTIONS   OF   THE   MYOCARDIUM. 


325 


Spontaneous  rupture  occurs  in  such  areas,  and  death  occurs  from  hemor- 
rhage into  the  pericardium,  though,  according  to  Hamilton,  this  is  not  as 
frequent  a  cause  of  spontaneous  rupture  as  is  fatty  degeneration. 

On  the  other  hand,  the  smaller  areas  of  cicatrization  may  represent 
complete  obliteration. 

Interfascicular  Connective-tissue  Proliferation.  —  Interfascicular  myo- 
fibrosis or  hyperplasia  of  the  septa  between  the  bundles  is  to  be  regarded 
as  a  concomitant  of  cardiac  hypertrophy,  and  represents  a  strengthening 
rather  than  a  weakening  of  the  heart. 


Fig.  150. —  Specimens  showing  chronic  myocarditis.  (Photomicrographs  by  Dr.  Chas.  S.  Bond.) 
A.  Intrafascicular  myofibrosis,  penetrating  into  the  bundles  of  muscle-fibres.  Hypertrophy  of  some  fibres; 
atrophy  of  others.  B.  Coarse  strands  of  connective  tissue  penetrating  between  the  bundles  of  muscle- 
fibres  (interfascicular  myofibrosis). 

Cardiosclerosis. — The  most  important  form  of  lesion  in  chronic  myo- 
carditis is  the  interstitial  myofibrosis  or  cardiosclerosis.  This 
form  is  met  with  in  senile  hearts  and  in  most  cases  of  chronic  heart  failure. 
According  to  Dehio,  it  occurs  only  in  those  hearts  which  have  been  sub- 
jected to  long-continued  dilatation,  frequently  in  hearts  in  which  hyper- 
trophy has  preceded  the  dilatation.  The  heart  muscle  is  cedematous. 
The  fibres  are  found  in  all  stages  of  change — normal  fibres,  large  healthy 
hypertrophic  fibres,  large  vacuolated  degenerating  fibres,  and  small  ones 
in  the  various  stages  of  atrophy — in  a  single  microscopic  field.  Many  of 
them  are  undergoing  fatty  degeneration.  In  response  to  the  well-known 
biological  law  that  wherever  the  parenchyma  of  an  organ  is  gradually 
destroyed  hyperplasia  of  the  interstitial  tissue  takes  its  place  (Weigert, 
Dehio),  fine  strands  of  connective  tissue  are  seen  everywhere  winding 
their  way  between  the  muscle-fibres  and  gradually  taking  their  places. 


RELATION  OF  SITE  OF  MYOCARDIAL  LESION  AND  DISTURBANCE  OF  FUNCTION. 

Lesions  in  the  Ventricles.  — Attempts  have  been  made  by  numerous 
investigators  to  demonstrate  a  definite  connection  between  the  exact  site 
of  the  myocardial  lesions  and  the  disturbance  of  function  met  with. 
Krehl,  who  under  Ludwig's  inspiration  was  the  pioneer  in  this  field,  inau- 


326 


DISEASES   OF   THE   HEART   AND    AORTA. 


gurated  the  method  of  studying  sections  "from  every  part  of  the  heart,  and 
found  that  the  papillary  muscles  and  the  musculature  about  the  mitral 
ring  were  affected  with  great  frequency;  but  he  was  unable  to  establish  more 
definite  relations.  Albrecht's  attempt  to  do  this  for  the  various  muscle 
layers  discovered  by  Krehl  and  J.  B.  MacCallum  has 
called  forth  a  vigorous  contradiction  from  Aschoff 
and  Tawara,  who  have  made  a  most  careful  study 
of  150  pathological  hearts  by  Krehl's  method. 

On  the  other  hand,  His,  Erlanger,  Stengel, 
Schmoll,  and  a  host  of  others  have  demonstrated  that 
lesions  in  the  auriculoventricular  bundle  give  rise  to 
heart-block,  while  Aschoff,  Tawara,  Saigo,  Barker, 
and  Hirschfelder  have  shown  that  lesions  affecting 
one  branch  of  this  bundle  do  not  affect  the  contrac- 
tion of  either  ventricle.  Very  recently,  however,  H.  E. 
Hering  has  revived  interest  in  these  questions  by 
showing  upon  the  excised  heart  that  if  the  strand  of 
Purkinje  fibres  (conduction  system)  to  one  papillary 
muscle  is  cut  or  injured,  that  papillary  ceases  to  con- 
tract, although  the  rest  of  the  heart  continues  to  do  so. 
Lesions  in  the  Auricles. —  Studies  of  lesions  in 
the  auricles,  though  fewer,  have  been  still  more 
remunerative.  Dehio  and  his  pupil,  Radasewsky, 
demonstrated  that  in  chronically  dilated  hearts  the 
myocardial  changes  in  the  auricles  were  much  more 
marked  than  those  in  the  ventricles;  and  Schonberg, 
under  D.  Gerhardt's  direction,  has  shown  that  per- 
manent arrhythmia  with  auricular  paralysis  is  asso- 
ciated with  infiltrations  of  the  intervenous  area  which  correspond  to  the 
embryonic  sinus,  the  spot  at  which,  the  cardiac  impulse  probably  originates. 


Fig.  151. — Hypertrophy 
of  some  muscle  bundles  in 
the  auricle  with  atrophy 
(transparency)  of  other 
areas.  (From  a  specimen 
in  the  Army  Medical  Mu- 
seum, Washington,  D.  C.) 


PATHOLOGICAL    PHYSIOLOGY. 

The  chief  physiological  features  of  chronic  myocarditis  are : 

(1)  Chronic  weakness  of  the  heart,  with  tendency  to  undergo  dilatation  and  overstrain. 

(2)  Frequency  of  extrasystolic  or  absolute  irregularities. 

Compensation  in  Myocarditis. — The  course  and  characteristics  of  myo- 
cardial weakness  have  been  fully  discussed  under  the  pathological  physiol- 
ogy of  cardiac  overstrain  (page  190).  Indeed,  the  persistence  of  a  primary 
overstrain  with  the  concomitant  cedema  of  the  heart  muscle  may  be  an 
important  factor  in  instituting  chronic  myocardial  changes  or  in  rendering 
the  heart  especially  susceptible  to  alcohol,  toxins,  tobacco,  or  other  influ- 
ences that  would  otherwise  not  affect  it.1  The  changes  in  the  myocardium, 
the  lowered  tonicity,  the  persistent  cedema,  the  reduction  in  the  number  of 
efficiently  contracting  muscle-fibres,  all  tend  to  lower  the  threshold  of  exertion 
at  which  overstrain  is  ushered  in.  Whether  the  overstrain  manifests  itself  as 
a  broken  pulmonary  or  a  broken  systemic  compensation,  or  as  both  together, 

1  R.  H.  Babcock  (J.  Am.  M.  Ass.,  1909,  Hi,  1904)  has  found  that  chronic  cholecystitis 
predisposes  to  myocardial  insufficiency. 


AFFECTIONS  OF  THE  MYOCARDIUM. 


327 


depends  upon  the  relative  and  absolute  strength  of  the  two  ventricles  as  well 
as  the  nature  of  the  exertion. 

Blood=pressure. — The  occurrence  of  such  overstrain  is,  however,  quite 
consistent  with  the  maintenance  of  a  normal  or,  especially,  a  high  blood- 
pressure.  This  high  blood-pressure,  strange  to  say,  is  in  itself  the  result  of  the 
chronic  cardiac  insufficiency  and  the  slowing  of  the  circulation.  With  the 
slowing  of  the  circulation  there  comes  asphyxia  of  the  medul- 
lary centres,  which  stimulates  them  and  brings  on  an  intense  vaso- 
constriction. The  vasoconstriction  narrows  the  arterial  bed  so  much  the 
arterial  pressure  must  be  raised  until  the  blood  flows  through  the  medullary 
centres  at  the  proper  rate.  The  weakened  heart  must  thus  rise  to  the  occa- 
sion and  sacrifice  itself  to  save  the  medullary  centres.  The  more  it  fails  the 
more  work  these  inexorable  centres  demand  from  it,  the  more  they  throttle 
the  arteries  in  their  struggle  to  get  blood  from  the  flagging  heart.  The  more 
the  arteries  are  throttled  the  greater  the  constriction,  the  smaller  the  arterial 
bed,  and  the  less  the  systolic  output  necessary  to  overfill  the  arteries,  the 
greater  the  force  necessary  to  drive  it.  The  heart  may  therefore  empty  itself 
incompletely  but  at  high  pressure  against  this  high  peripheral  resistance, 
while  the  increase  in  residual  blood  within  the  ventricles  leads  to  dilatation 
and  stasis.  This  condition  of  stasis  with  high  pressure,  both  resulting  from 
chronic  cardiac  weakness,  is  usually  termed  "high  pressure 
stasis"  (Hochdruckstauung) .    Its  factors  actually  constituted  vicious  circle : 

Cardiac  weakening 

I  I 

Increased  cardiac  effort  Slowed  circulation 

High  blood-pressure  through  medulla 

t  .1 

Vasoconstriction 


rVl""H~r  ' 


- 


Fig.  152. —  Curve  of  blood-pressure  in  a  case  of  chronic  myocarditis,  showing  the  high  blood-pressure  per- 
sisting until  shortly  before  death.     (High-pressure  stasis.) 


This  accounts  for  the  fact  that  under  such  circumstances  venesec- 
tion may  raise,  digitalis  may  lower  the  blood-pressure, 
and,  on  the  other  hand,  the  blood-pressure  may  rise  rather  than  fall  as  death 
approaches  (Fig.  152). 

Arrhythmia. — In  many  cases  of  chronic  myocarditis  the  heart  is  irregular 
in  both  force  and  rhythm,  especially  in  the  later  stages. 


328  DISEASES   OF   THE   HEART   AND    AORTA. 

The  chief  types  of  arrhythmia  observed  are : 

(1)  Extrasystoles    of    auricular    or    more    frequently    of    ventricular 

origin. 

(2)  Perpetual  absolute  arrhythmia. 

The  extrasystoles  seem  to  result  from  the  overloading  of  the 
chambers  in  which  they  arise;  the  perpetual  arrhythmia  both 
from  the  overloading  of  the  auricle  and  the  presence  of  chronic  myocardial 
changes  in  the  muscle  strands  of  the  intervenous  area  (embryonic  sinus 
reuniens).  (The  mechanism  and  significance  and  diagnosis  of  these  ar- 
rhythmias have  been  discussed  on  page  107).  This  irregularity  in  itself 
also  exerts  an  unfavorable  action  upon  the  circulation.  When  the  site  at 
which  the  impulse  arises  is  diseased,  it  may  be  impossible  for  this  area  to 
generate  cardiac  impulses  in  rapid  succession,  and  hence  the  pulse  and  the 
circulation  may  remain  slow  in  spite  of  the  needs  of  the  body  for  increased 
aeration. 

SYMPTOMS    AND    SIGNS. 

From  the  above  cited  cases  it  will  be  seen  that  the  symptoms  of  chronic 
myocarditis  are  usually  those  of  gradually  developing  cardiac  weakness, 
progressively  increasing  weakness  and  dyspnoea,  at  first  on  exertion,  later 
when  at  rest,  and  finally  reaching  the  stage  of  orthopncea.  Palpitation  is 
a  frequent  symptom;  sometimes  there  is  precordial  pain,  usually  behind 
the  sternum,  associated  with  sudden  dilatation  of  the  heart.  Swelling  of 
the  abdomen  and  often  pain  in  the  right  hypochondrium  are  associated 
with  the  stretching  of  the  capsule  of  the  liver  as  the  latter  enlarges. 
(Edema  ascending  from  the  feet  and  legs,  diminution  in  the  amount  of 
urine,  at  first  during  the  day,  with  frequent  and  increased  micturition  at 
night,  and  later  marked  diminution  in  total  urine  secretion  mark  the  later 
stages  of  broken  systemic  compensation. 

Physical  signs  are :  cyanosis;  dilatation  of  the  venules,  especially 
over  the  face;  general  engorgement  of  the  larger  veins,  often 
with  disappearance  of  the  "double"  venous  pulse,  and  either  total  absence 
of  the  pulsation  in  the  jugular  veins  or  appearance  of  a  "single"  venous 
pulse ;  often  irregularity  of  the  arterial  pulse,  usually  with  presence  of  marked 
arteriosclerosis;  increase  in  area  of  cardiac  dulness  to  right  or  felt;  occasion- 
ally a  catarrhal  jaundice  is  a  marked  sign  of  the  hepatic  engorgement. 

The  blood  count  often  shows  polycythemia  and  high  haemoglobin, 
without  change  in  leucocytes.  Blood-pressure  may  or  may  not  be  elevated; 
but  in  most  cases  it  is  not  decreased.  Pulse  tracings  from  the  radial  and 
carotid  arteries  and  jugular  veins  often  show  persistent  absolute  arrhyth- 
mia, with  paralysis  of  the  auricles,  with  absence  of  signs  of  organic  valvular 
lesion.  There  may  be  a  more  or  less  transitory  soft  systolic  murmur 
present  at  apex  due  to  functional  mitral  insufficiency,  but  this  is  rarely 
transmitted  to  the  axilla  and  often  passes  off  during  treatment.  The  same 
applies  to  the  systolic  murmur,  which  may  be  loudest  over  the  tricuspid 
area.  There  is  usually  absence  of  diastolic  murmurs  except  in  cases  in 
which  functional  pulmonary  or  aortic  insufficiencies  are  suspected. 

A  mild  bronchitis  with  rales  and  some  cedema  is  common,  espe- 
cially at  right  base.     Enlargement  of  the  liver,  with  either  systolic  impulse 


AFFECTIONS   OF  THE   MYOCARDIUM.  329 

(tricuspid  insufficiency)   or  systolic  retraction  (tumultuous  action  of  the 
right  ventricle),  occurs  in  the  later  stages. 

The  urinary  findings,  cardiac  symptoms,  and  clinical  course  in  such 
cases  may  be  very  similar  to  those  of  cases  which  are  primarily  renal  in  origin. 

Case  of  Chronic  Myocarditis. 

George  G.,  a  laborer,  aged  56,  was  admitted  to  Prof.  J.  O.  Hi rschf elder's  wards  of 
the  City  and  County  Hospital,  San  Francisco,  on  April  21,  1905,  complaining  of 
asthma.  His  father  had  died  of  dropsy.  The  patient  had  had  rheumatism  in  1887 
and  1895,  and  has  had  to  pass  water  during  the  night  for  some  years. 

Except  for  occasional  shortness  of  breath  he  was  well  until  two  weeks  before  admis- 
sion. He  has  had  shortness  of  breath  for  the  past  two  years;  weakness  and  oedema  of  the 
feet  for  the  past  two  weeks. 

Physical  Examination.  —  Patient  is  a  fairly  nourished  man  ;  face  flushed  and 
venules  dilated.  No  marked  respiratory  distress.  Head  is  of  peculiar  shape.  Pupils  equal 
and  react  to  light  and  accommodation.  No  jaundice.  Definite  congenital  external  stra- 
bismus of  right  eye.  Eyes  move  well  in  all  directions.  Tongue  coated.  Throat  clear; 
tonsils  not  enlarged;  no  tracheal  tug.  No  enlargement  of  lymph-glands.  Thorax 
barrel-shaped.  Vocal  fremitus  equal  except  below  level  of  tenth  dorsal  vertebra  on  right 
side,  where  it  is  increased.  Percussion  note  everywhere  clear  except  over  this  area,  where 
breath  sounds  are  distant  and  a  few  rales  are  heard.  A  few  moist  rales  are  also  heard  over 
the  apices.  Heart . — Diffuse  but  feeble  impulses  in  sixth  left  interspace  15 
cm.  from  midline,  from  which  point  cardiac  dulness  extends  above  to  the  upper 
border  of  the  third  rib  and  6  cm.  to  the  right  of  the  midline  in  the  fourth  interspace.  Heart 
sounds  feeble  and  accompanied  by  a  soft  systolic  murmur.  Neither  sound 
at  base  specially  accentuated.  Pulse  very  feeble,  rapid,  and  irregular.  There  is  no  auricu- 
lar wave  upon  the  tracing  of  the  venous  pulse,  and  the  arrhythmia  is  devoid  of  any 
regularity  in  sequence.    Radial  arteries  are  very  sclerotic.    No  oedema  of  feet  or  legs. 

Patient  has  some  cough,  raising  mucopurulent  sputum,  with  large  numbers  of  strepto- 
cocci but  no  influenza  or  tubercle  bacilli.  Urine  negative;  sp.  gr.  1010;  no  albumen, 
casts,  or  sugar. 

Ordered:  Soft  diet.  Pil.  cathart.  co.,  ii,  q.  n.;  sol.  magnesii  sulphatis  sat.,  30  c.c. 
(,fi)  q.  a.m.;  fluidextract  digitalis,  0.3  c.c.  (tt\,v)  q.  4  h.;  spir.  glycerylis  nitratis,  q.  \  h., 
commencing  with  1  gtt.  and  increasing  1  gtt.  at  each  third  dose  until  patient  feels  throb- 
bing of  the  head  or  flushing  of  face,  after  which  next  dose  is  to  be  omitted,  and  subsequent 
doses  of  1  gtt.  less  than  the  last  are  to  be  then  given.  Morphin.  sulph.,  0.008  Gm.  (|  gr.) 
p.  r.  n.  (for  extreme  dyspnoea). 

April  25,  7.00  p.m.  No  change  in  condition.  No  urgent  dyspnoea.  Haemoglobin 
110  per  cent.  (Dare).  Cyanosis  still  marked.  No  auricular  wave  in  venous  pulse.  Heart's 
action  still  weak  and  irregular. 

1100  c.c.  of  blood  were  then  removed  from  right  arm,  after  which 
haemoglobin  fell  to  65  per  cent.  The  right  border  of  cardiac  dulness  retreated 
1  cm.  toward  midline;  upper  border  receded  .5  cm.;  left  border  unchanged.  No  change 
in  cardiac  sounds  nor  in  pulse  tracing.  No  auricular  wave  in  venous  tracing.  Blood- 
pressure:  before  venesection,  7.00  p.m.,  maximal  107,  minimal 
87,  pulse-pressure  20,  pulse-rate  116,  pulse-pressure  X  pulse-rate  =  2320;  after  vene- 
section 8.30  p.m.,  maximal  112,  minimal  92,  pulse-pressure  20,  pulse- 
rate  112K  pulse-pressure  X  pulse-rate  =  2240  (see  chart,  page  242).  Cyanosis  has,  however, 
been  replaced  by  a  healthy  color,  and  patient  feels  decidedly  better.  The  improvement 
in  this  case  is  due  entirely  to  relief  of  the  over-distended  right  heart,  partly  by  diminution 
of  fluid,  partly  by  diminution  in  the  viscosity  of  the  blood  from  the  removal  of  so  many 
blood-corpuscles. 

The  patient  passed  a  comfortable  night  and  for  several  days  felt  somewhat  better. 
The  course  of  symptoms  and  their  relation,  medication,  and  blood-pressure  changes  are 
shown  in  the  chart  (Fig.  131).  He  was  bled  (350  c.c.)  again  on  May  14,  with 
considerable  benefit,  and  from  that  time  his  condition  steadily  improved. 


330 


DISEASES   OF   THE   HEART   AND    AORTA. 


PARALLELISM    BETWEEN    MANIFESTATIONS    OF    PRIMARY    MYOCARDITIS     AND 

PRIMARY    NEPHRITIS. 

The  cases  of  chronic  myocarditis  with  arteriosclerosis  and  secondary 
renal  involvement  often  very  closely  resemble  those  of  primary  renal 
involvement  with  secondary  myocarditis,  since  there  are  both  cardiac  and 
renal  failure  in  both  conditions. 

The  following  abstracts  show  the  close  parallelism  between  the  symptoms  and  signs 
of  two  such  cases  which  in  the  early  stages  were  almost  exactly  similar: 


Illness. 


Signs. 


Urine. 


Autopsy. . 


Chronic  myocarditis  (C.  B.).     (Diagnosis  on 
first  admission  "  chronic  nephritis  "  ). 


Shortness  of  breath,  palpitation,  cough, 
swelling  of  abdomen  and  legs.  Voids 
during  night. 

Pale  pasty  color.  Moist  rales  in  chest. 
Heart  dilated  to  left  (15  cm.);  rapid 
regular  pulse  120;  sclerotic  radials. 
Maximal  blood-pressure.  180  mm. 
Hg.  Later,  two  attacks  of  angina 
pectoris,  with  death  in  the  second. 


Varying  from  2000-3000  c.c.  per  day, 
with  sp.  gr.  1007,  trace  of  albumen 
and  a  few  hyaline  casts,  to  less  than 
1700  c.c,  with  sp.  gr.  1020,  large 
amount  of  albumen,  and  numerous 
hyaline  casts. 

Heart  hypertrophied  650  Gm.,  auri- 
cles dilated;  intense  cardiosclerosis, 
with  some  hypertrophy.  Both  coro- 
nary arteries  diseased,  left  descend- 
ing branch  almost  obliterated. 

Kidneys  large,  purple,  with  a  few 
depressed  scars  and  retention  cysts; 
cortex  thicker  than  normal;  no  in- 
crease in  interstitial  tissue;  no 
marked  nephritic  changes. 

Adrenals  — fatty  degeneration  of 
cortical  cells;    no  hypertrophy. 


Chronic  nephritis  (J.  B.). 


Shortness  of  breath,  orthopncea,  swell- 
ing of  legs. 


Pale  pasty  color.  Moist  rales  in  chest. 
Heart  dilated  to  left  (14  cm.)  and 
right  (5  cm.).  Pulse  rapid  and 
regular.  Maximal  blood-pressure 
200  mm.  Hg;  later  ranged  from 
130  to  170  mm.  Hg.  Fundi  oculo- 
rum  normal.  Later,  Cheyne-Stokes 
breathing.  Delirium;  headache;  dul- 


Urine  varied  from  400  c.c,  with  sp. 
gr.  1022,  2.5  Gm.  albumen  per  litre, 
and  numerous  hyaline  and  granular 
casts,  to  2500  c.c,  sp.  gr.  1007,  trace 
of  albumen,  and  few  casts. 


Heart  dilated  350  Gm.;  pale  pink 
walls,  with  slight  fibrosis.  Coronary 
arteries  sclerotic. 


Kidneys  small,  scarred,  cortex  thin; 
extensive  epithelial  degeneration 
with  corresponding  proliferation .  of 
connective  tissue.  Many  glomeruli 
have  undergone  fibrosis. 


It  may  be  almost  impossible  to  establish  differential  diagnosis  between 
two  such  cases  early  in  the  disease.  The  course  of  the  two  cases,  however, 
showed  clearly  the  divergence,  the  one  toward  the  type  of  coronary  sclerosis, 
dilated  heart,  precordial  pain,  paroxysmal  dyspnoea,  the  other  toward 
the  ursemic,  with  progressive  dulness,  oliguria.  Albuminuric  retinitis  did 
not  develop  in  the  case  cited,  or  the  diagnosis  might  have  been  simplified. 

Phenolsulphonphthalein  and  Catalase  Tests. — Geraghty  and  Rowntree 
(J.  Am.  M.  Ass.,  1911,  lvii,  811)  have  shown  that  in  many  cases  the  diagno- 


AFFECTIONS  OF  THE  MYOCARDIUM.  331 

sis  can  be  made  by  injecting  6  mg.  phenolsulphonphthalein  subcutaneously 
and  estimating  colorimetrically  the  amount  excreted  in  the  urine  in  two  hours. 
In  nephritis  this  may  be  reduced  to  a  mere  trace,  but  in  heart  disease  about 
50  per  cent,  is  excreted  in  all  but  the  most  severe  cases  of  broken  compensa- 
tion. In  these  it  may  fall  to  about  fifteen  per  cent.,  but  rises  rapidly  as  the 
patient  improves.  In  these  severe  cases  in  which  diagnosis  with  phenol- 
sulphonphthalein would  be  doubtful,  Winternitz  has  found  that  the  catalase 
of  the  blood  remains  normal  in  myocarditis,  but  is  reduced  in  nephritis. 

DIAGNOSIS. 

In  making  the  diagnosis  it  is  most  important  to  differentiate  chronic 
myocarditis  from  the  following  conditions:  (1)  organic  valvular  heart 
lesions,  (2)  obesity,  (3)  primary  cardiac  overstrain,  (4)  primary  chronic 
nephritis,  (5)  chronic  polycythemia  (erythremia)  with  enlarged  spleen,  (6) 
neurasthenia  and  psychasthenia,  (7)  chronic  nephritis. 

In  cases  of  chronic  myocarditis  it  may  be  extremely  difficult  to  exclude  an 
organic  valvular  disease.  This  is  especially  true  of  mitral  insufficiency,  for 
there  is  frequently  a  functional  mitral  insufficiency  present  with  systolic  murmur  and 
horizontal  dilatation  of  the  heart  to  the  left.  While  it  is  true  that  the  murmur  of  a  func- 
tional mitral  insufficiency  is  rarely  as  rough  as  those  of  organic  origin  may  become,  and  is 
as  a  rule  not  as  well  transmitted  into  the  axilla,  nevertheless  in  individual  cases  these 
differences  may  not  be  striking.  Much  more  striking  are  the  changes  in  the  character  of 
the  murmur  as  the  patient's  condition  improves.  In  organic  lesions  the  murmur  will 
become  louder  as  improvement  sets  in,  because  the  heart  has  become  stronger.  In 
functional  cases,  though  it  may  become  louder  at  first,  it  will  vary  greatly  in  character 
and  in  intensity,  especially  if  the  patient  is  made  to  exercise  slightly.  It  may  show  a  ten- 
dency to  disappear  altogether  during  recovery. 

The  presence  of  a  large,  slow,  heaving  apex  beat  with  slow  pulse  and  systolic  mur- 
mur as  well  as  a  large  slow  pulse  speaks  in  favor  of  organic  mitral  insufficiency  (marked 
hypertrophy  of  the  left  ventricle),  though  a  functional  papillary  insufficiency  might  per- 
sist from  localized  myocarditis  of  one  of  the  papillary  muscles  in  spite  of  the  hypertrophy. 

From  other  valvular  diseases  the  diagnosis  is  comparatively  easy.  In 
occasional  cases  the  beat  of  the  auricle  becomes  audible,  suggesting  the  presystolic  rumble 
of  mitral  stenosis  (Sewall);  and  occasionally  blowing  diastolic  murmurs  at  the  sternal 
margin  suggest  organic  aortic  or  pulmonic  insufficiency.  But  such  dilatations  of  the  aortic 
ring  and  conus  arteriosus  or  cardiopulmonary  murmurs  are  rather  rare  and  are  usually 
transitory. 

A  functional  tricuspid  insufficiency  results  so  constantly  from  weak- 
ening of  the  right;  ventricle  that  it  is  a  lesion  to  be  included  under  rather  than  excluded 
from  the  picture  of  chronic  myocarditis. 

Primary  cardiac  overstrain  may  be  excluded  through  the  history,  the 
trouble  in  the  latter  condition  coming  on  suddenly  in  a  previously  healthy  individual 
during  or  immediately  after  a  severe  strain,  while  in  chronic  myocarditis  there  is  usuallv 
a  more  gradual  onset  of  symptoms,  frequently  traceable  to  febrile  disease  or  intoxication. 

Obesity  is  diagnosed  from  the  general  appearance  of  the  patient,  concomitant 
chronic  myocarditis  being  excluded  when  the  trouble  seems  to  bear  a  relation  to  too  good 
health  rather  than  to  disease.    However,  myocardial  changes  may  be  very  hard  to  rule  out. 

The  differentiation  from  chronic  nephritis  has  been  discussed  above. 

Chronic  polycythaemia  (erythremia)  with  enlarged  spleen  may  present 
a  picture  very  similar  to  primary  chronic  myocarditis,  and  in  the  later  stages  a  consider- 
able grade  of  myocarditis  may  be  present.  The  size  and  hardness  of  the  spleen,  the  color, 
and  the  high  blood  count  are  the  features  upon  which  the  diagnosis  is  made. 

Neurasthenia,  cardiac  neuroses,  or  pseudocardiac  visceral  disease, 
must  be  carefully  excluded  (see  page  694).  In  the  former  the  weakness  when  self- 
conscious  and  the  strength  when  the  mind  is  distracted  are  totally  disproportionate; 
while  the  myocarditic  is  reminded  of  his  weakness  by  the  stern  hunger  for  air. 


332  DISEASES  OF  THE  HEART  AND  AORTA. 

Acareful  general  examination  should  always  be  made  to  exclude  cardiac  weakness  from 
enteroptosis  and  similar  disorders  that  may  reflexly  give  rise  to  a  true  cardiac  weakness. 

The  venous  pulse  helps  somewhat,  the  presence  of  a  visible  "single  venous 
pulse"  of  auricular  fibrillation  or  extrasystoles  suggesting  myocardial  change.  However, 
these  may  not  be  conclusive.  For  the  past  year  the  writer  has  had  under  observation  a 
young  athlete  with  permanently  irregular  pulse  and  auricular  fibrillation  and  symptoms  of 
slight  cardiac  weakness  on  exertion.  There  are,  however,  no  infectious  diseases  nor  indis- 
cretions to  account  for  the  production  of  a  myocarditis,  and,  though  the  writer  inclines 
toward  the  diagnosis  of  the  latter  condition,  it  seems  difficult  in  so  healthy  a  young  person 
to  exclude  a  neurotic  basis. 

TREATMENT. 

The  treatment  of  chronic  myocarditis  in  the  main  should  follow  the 
general  scheme  laid  down  in  detail  in  Chapters  IV,1  V,  and  VI:  rest  in  bed 
during  the  severer  stages  of  failure,  purgation,  light  diet,  digitalis  or 
strophanthus  in  severe  cases,  graduated  resistance  exercises  and  Nauheim 
baths  during  convalescence,  gradually  increasing  walks  and  moderate  exer- 
cise before  returning  to  every-day  life.  However,  certain  exceptions  must 
be  noted,  especially  in  the  severer  forms  of  myocarditis.  For  example,  digi- 
talis only  occasionally  corrects  an  irregularity  which  has  become 
relatively  permanent;  though  it  is  very  useful  in  curing  the  milder  forms  of 
irregularity,  such  as  a  continual  bigeminal  pulse  or  occasional  ventricular 
extrasystoles.  It  is  less,  indeed  rarely,  efficient  in  removing  the  irregularities 
arising  at  the  auricles.  On  the  other  hand,  in  dealing  with  the  advanced 
grades  of  permanent  arrhythmia  with  fibrillation  of  the  auricles,  where  there 
is  usually  advanced  myofibrosis  and  only  a  few  of  the  heart  muscle-cells 
have  survived  the  general  atrophy,  it  is  found  that  these  often  respond  well 
to  small  doses  (about  half  the  normal),  whereas  anormal  dose  may 
give  rise  to  symptoms  of  definite  digitalis  poi- 
soning and  often  hasten  death.  This  is  not  always  to  be  avoided  by  the 
apparently  mild  routine  of  administering  the  drug  in  "  courses,"  since  the 
initial  dose  may  be  too  large  for  the  individual  case.  Each  case  must  be 
considered  for  itself,  with  these  facts  constantly  borne  in  mind.  The  moder- 
ate-sized initial  dose  or  two  followed  by  prolonged  administration  of  very 
small  doses,  suggested  by  Frankel  (see  page  258),  seems  to  be  the  safest  and 
surest  method  in  these  cases,  in  order  to  prevent  cumulative  effects. 

The  recent  introduction  of  single  doses  of  strophanthin  intra- 
venously, which  does  not  increase  peripheral  resistance,  gives  promise 
of  great  results  in  the  future,  especially  in  this  group  of  cases,  although  its 
use  has  not  yet  become  general  enough  to  warrant  a  verdict. 

As  to  graduated  exercises,  these  are  useful  in  many  cases, 
but  are  distinctly  contraindicated  after  myofibrosis  has  set  in  and  dyspnoea 
persists  while  the  patient  is  at  rest.  Mere  arrhythmia,  even  with  paralysis 
of  the  atria,  does  not  contraindicate  their  use,  but  points  a  warning,  and 
in  many  cases  shows  that  the  practitioner  is  treading  on  dangerous  ground. 
This  applies  also  to  Nauheim  and  other  baths.  Coronary  sclerosis,  on  the 
other  hand,  stenocardia,  and  severe  pains  down  the  arms  furnish  distinct  con- 
traindications to  all  exercises  except  such  as  are  necessary.  Even  those  of 
Schott  must  be  carried  out  with  the  utmost  precaution,  and  the  bending  exer- 

1  W.  Ebstein  (Miinchen.  med.  Wchnschr.,  1911,  lviii,  615)  calls  attention  to  the  fact 
that  chronic  constipation  alone  may  bring  on  or  perpetuate  myocardial  insufficiency. 


AFFECTIONS  OF  THE  MYOCARDIUM.  333 

cises  may  well  be  eliminated.  The  walks,  etc.,  which  terminate  the  treatment 
must  be  taken  slowly  and  with  the  greatest  precaution  in  avoiding  fatigue. 

For  the  stenocardiac  attacks  and  paroxysmal  dyspnoea  the  greatest 
relief  is  given  by  a  pearl  or  two  ofamyl  nitrite  followed  by  nitro- 
glycerin and  sodium  nitrite.  Indeed,  these  drugs  furnish  a 
good  deal  of  relief  where  the  arteriosclerotic  element  is  prominent. 

When  the  blood-pressure  is  elevated  above  140  mm.  the  salt  in  the 
food  should  be  reduced  as  low  as  possible  (see  page  235). 

Venesection  may  be  of  the  greatest  value  in  tiding  over  periods 
of  acute  dilatation,  as  shown  in  the  case  of  G.  G.,  even  when,  as  in  that  case, 
it  produces  no  change  in  maximal  or  minimal  blood-pressure  or  pulse-rate. 
This  case  also  exemplifies  the  fact  that  the  venesection  may  often  be  of 
great  benefit  before  acute  signs  of  cardiac  overfilling  set  in,  and  then  it  is 
to  be  regarded  as  "  a  stitch  in  time,"  the  relief  of  the  over-distention  enabling 
the  heart  to  right  itself.  This  may  be  owing  to  the  fact  that  the  over- 
stretched fibres  are  allowed  to  gain  their  optimum  length,  or,  on  the  other 
hand,  to  the  removal  of  a  large  number  of  red  corpuscles  from  the  circulatory 
system,  thus  decreasing  the  viscosity.  It  is  easier  to  pass  than  to  seize  the 
moment  at  which  a  venesection  would  do  most  good. 

In  this  every  one  some  day  or  other  receives  his  lesson.  For  example,  the  writer 
had  a  patient  under  his  care  in  San  Francisco  who  one  night  had  a  moderate  degree  of 
dyspnoea  and  cyanosis,  though  scarcely  enough  to  cause  alarm,  and  immediate  venesec- 
tion was  considered.  The  right  heart  was  not  markedly  enlarged  and  none  of  the  objec- 
tive signs  seemed  urgent.  It  was  decided  to  do  the  venesection  the  next  day,  and  the 
patient  was  given  fifteen  milligrams  (a  quarter  grain)  of  morphine,  after  which  he  fell 
into  a  quiet  sleep  almost  immediately.  A  couple  of  hours  later  he  became  restless  and 
sank  gradually  within  an  hour.  We  had  let  the  right  moment  for  the  venesection  pass, 
and  had  masked  the  symptoms  by  the  morphine. 

Dangers  from  Morphine. — Another  danger  due  to  morphine  lies 
in  the  danger  of  habituation  (see  page  217),  and  the  further  danger  that 
in  order  to  get  it  the  patient  will  simulate  a  paroxysm  of  dyspnoea  and 
actually  make  himself  sick  or  even  endanger  his  life  by  the  effort  entailed 
in  doing  so.  Several  patients  whom  the  writer  has  gradually  broken  of 
their  morphine  habit  confessed  to  having  done  so,  even  though  they  knew 
at  the  time  that  the  simulation  of  dyspnoea  made  them  feel  worse. 

THROMBI    IN    THE    CARDIAC    CHAMBERS. 

When  the  circulation  is  slowed,  and  especially  when  one  of  the  cardiac 
chambers  empties  itself  insufficiently,  large  clots  are  liable  to  form  along 
its  wall  (mural  thrombi).  This  occurs  especially  in  those  portions  which 
are  away  from  the  axial  stream,  such  as  the  recesses  between  the  trabecule 
carnese  and  behind  the  papillary  muscles,  and  also  out  in  the  tip  of  the  auric- 
ular appendages. 

Thrombosis  within  the  left  auricle  occurs  quite  frequently  in  mitral  stenosis, 
especially  when  the  blood  stagnates  there  during  periods  of  overstrain.  These  thrombi 
if  fresh  sometimes  break  loose  to  form  emboli  (page  219).  Sometimes  the  clot  loosened 
from  the  auricular  appendix  is  so  large  that  it  cannot  pass  through  the  auriculoventricular 
orifice,  but  plugs  the  latter  entirely,  producing  sudden  death.  When  the  clot  remains 
adherent  to  the  wall  for  some  time,  more  or  less  organization  goes  on.    Thrombi  which 


334  DISEASES   OF   THE   HEART   AND    AORTA. 

adhere  to  the  wall  by  a  few  strands  of  newly  formed  connective  tissue  are  of  every-day 
occurrence,  and  constitute  the  classical  sign  for  differentiation  between  intra-vitam  and 
post-mortem  thrombi.  In  older  thrombi  the  organization  is  more  complete,  so  that  a 
thrombus  mass  may  adhere  to  the  cardiac  wall  by  a  pedicle  of  fibrous  tissue.  It  is  quite 
possible  that  in  some  cases  these  thrombi  vibrate  to  and  fro  and  cause  extrasystoles  by 
striking  against  the  walls  of  the  heart,  just  as  occurred  in  Cameron's  air-bubble  experi- 
ment (quoted  on  page  115).  In  several  cases  such  masses  have  been  known  to  act  as  a 
ball-valve   at  the  mitral  orifice,  giving  rise  to  signs  of  mitral  stenosis. 

The  symptoms  and  signs  given  by  such  thrombi  are,  however,  very  obscure.  The 
fact  that  they  usually  arise  during  the  course  of  a  cardiac  failure  adds  to  the  complexity 
of  the  clinical  picture,  and  the  diagnosis  can  rarely  be  made  until  embolism  sets  in. 
In  one  case  of  mitral  stenosis  recently  seen  by  the  writer,  in  which  the  whole  descending 
abdominal  aorta  was  suddenly  plugged  by  an  embolus  and  gangrene  of  both  lower  extremi- 
ties set  in,  the  diagnosis  of  a  clot  within  the  heart  was  warrantable.  Such  cases  are,  how- 
ever, rare,  and  the  diagnosis  is  then  made  after  the  harm  has  been  done. 

TUBERCULOSIS  OF  THE  HEART. 

In  spite  of  the  great  frequency  with  which  tuberculosis  affects  the  lungs,  pleura,  and 
pericardium,  independent  affection  of  the  myocardium,  endocardium,  and  valves  is  quite 
infrequent.1  Thus  Willigk  found  only  2  cases  of  tubercle  of  the  myocardium  in  1845 
autopsies  on  persons  with  tuberculosis.     Other  observers  confirm  this  view  of  its  rarity. 

Pathologically  the  lesions  in  tuberculosis  of  the  myocardium  resemble  those  of  tuber- 
cles elsewhere;  they  are  somewhat  more  common  in  acute  miliary  tuberculosis  than  in 
the  chronic  form,  but  in  the  latter  are  larger  in  size.  The  most  common  cardiac  lesion  of 
tuberculosis  is,  however,  neither  miliary  nor  large  solitary  tubercles,  but  a  fatty  degener- 
ation of  the  myocardium,  due  in  part  to  the  ansemia  and  in  part  to  the  toxins  secreted 
by  the  bacilli. 

The  effect  of  the  tuberculous  lesions  upon  the  circulation  is  usually  masked  by  the 
general  cardiac  weakness  due  to  the  intoxication  and  ansemia,  and,  as'  v.  Leyden  states, 
does  not  present  any  characteristic  features.  It  is  almost  impossible  to  diagnose  clinically, 
for  the  symptoms  and  signs  are  quite  independent  of  the  tubercle.  Often,  as  in  Pollak's 
case,  a  man  of  65  who  had  a  large  tubercle  in  the  wall  of  the  auricle,  there  are  no  signs  what- 
ever, even  of  cardiac  weakness.  V.  Tabora  and  Tilp  report  a  case  in  which  a  systolic  mur- 
mur was  heard  over  the  apex,  but  this,  of  course,  presents  nothing  characteristic  and  might 
well  have  been  due  to  the  accompanying  weakness  of  the  myocardium  or  papillary  muscles. 
Indeed,  as  Romberg  states,  tuberculosis  of  the  myocardium  interests  the  pathologist  rather 
than  the  clinician. 

SYPHILIS  OF  THE  MYOCARDIUM. 

Syphilitic  affection  of  the  heart  is  more  frequent  and  presents  a  somewhat  more 
definite  picture  than  tuberculosis.  The  most  common  form  in  which  syphilis  affects  the 
heart  is  the  sclerotic  lesion  of  the  aortic  valves  (see  page  451),  though 
in  this  case  the  pathological  process  originates  in  the  aorta  rather  than  in  the  myocardium. 

Grassmann  has  called  attention  to  the  frequency  with  which  signs  of  severe  cardiac 
weakness  occur  during  the  secondary  stage  of  syphilis,  accidental  or  functional 
systolic  murmurs  being  present  in  40  per  cent,  of  his  cases.  Dilatation,  especially  of  the 
right  heart,  was  common,  as  well  as  alterations  of  rhythm, — sometimes  arrhythmia, 
sometimes  bradycardia,  sometimes  tachycardia.  Precordial  pain  and  anginal 
attacks  were  frequent.  The  blood-pressure  was  usually  low,  as  was  also  the  haemoglobin. 
It  is  not  impossible  that  the  major  role  in  many  of  these  cardiac  manifestations  is  played 
by  the  anaemia  and  the  fever  rather  than  by  spirochaete  pallida  within  the  heart  muscle; 
but  the  presence  of  tertiary  myocardial  lesions  demonstrates  that  the  latter  play  an  im- 
portant part.  The  diagnosis  is  based  upon  the  above-mentioned  symptoms  arising 
during  the  secondary  stage.  Treatment  should,  of  course,  be  vigorous,  and  as  a  precau- 
tionary measure  the  patient  should  be'  kept  in  bed  until  all  cardiac  weakness  has  passed. 
If  the  symptoms  do  not  rapidly  subside,  a  few  doses  of  digitalis  or  strophanthus  may  be 

1  Tuberculous  endocarditis  is  discussed  on  page  402. 


AFFECTIONS   OF  THE   MYOCARDIUM.  335 

given.  Indeed,  a  few  small  doses  of  one  of  these  drugs  may  well  be  given  to  relieve  promptly 
the  dilatation  and  thus  to  forestall  the  danger  that  may  lurk  in  an  oedematous  heart  muscle 
(see  page  313). 

Cardiac  lesions  are  rather  common  in  congenital  syphilis,  though  this  is 
not  true  of  typical  gummata.  Thus  Mracek  found  myocardial  changes  (acute  myocarditis 
with  patches  of  perivascular  infiltration  of  mononuclear  cells)  present  in  24  Out  of  150 
autopsies  upon  syphilitic  foundlings,  but  gummata  in  only  4.  The  non-gummatous 
changes  are  well  describfcd  by  I.  Adler  as  infiltrations  of  mononuclear  cells  about  the 
blood-vessels,  accompanied  by  a  very  early  chronic  endarteritis  and  mesarteritis,  with 
frequent  hemorrhages  into  and  about  the  vessel  wall.  Warthin  (Am.  J.  M.  Sc,  1911, 
cxli,  398)  and  others  have  found  these  tissues  loaded  with  spirochaetse.  Clinically  hereditary 
lues  of  the  myocardium  probably  cooperates  with  the  other  syphilitic  lesions  in  bringing 
about  the  death  of  the  child,  but  the  importance  of  its  role  cannot  be  judged,  since  it  is 
rarely  if  ever  the  only  luetic  lesion  present. 

The  tertiary  myocardial  lesions  of  adults  are  fairly  common.  The  lesions 
in  60  cases  collected  by  Mracek  showed  the  following  distribution:  gummatous  myocar- 
ditis, 10;  fibrous  myocarditis,  9;  gummatous  and  fibrous,  8;  endocarditis,  2;  coronary 
arteries  alone,  3;  pericardium  alone,  1;  myocardium  and  pericardium,  15;  pericardium, 
myocardium,  and  endocardium,  1;  myocardium  and  coronary  arteries,  1;  all  parts  of  the 
heart,  6;  cardiac  ganglia,  4. 

Judging  by  the  number  of  cases  of  Adams-Stokes  syndrome  due  to 
lues  (see  page  566),  the  intraventricular  septum  seems  to  be  a  rather  frequent  site  for 
the  lesions.  Excepting  such  lesions  as  are  so  situated  that  they  give  rise  to  heart-block 
or  to  the  Adams-Stokes  syndrome,  the  syphilitic  lesions  of  the  myocardium  rarely  give 
distinct  manifestations.  A  general  myocardial  weakness,  shortness  of  breath,  dilatation 
with  or  without  exertion  in  persons  who  have  had  lues  (especially  with  other  visceral 
involvement)  is  suggestive  evidence  of  fibrous  luetic  myocarditis  with  or  without  gumma. 
The  latter  can  rarely  if  ever  be  diagnosed.  Huchard  and  Fiessinger  report  a  case  in  which 
dyspnoea  set  in  suddenly  15  days  before  death,  due  to  the  growth  of  a  gumma  involving 
the  tricuspid  valve,  but  even  in  such  a  case  the  data  are  too  uncertain  to  permit  a  definite 
clinical  diagnosis.  A  positive  Wassermann  reaction,  which  Collins  and 
Sachs  and  W.  Longcope  have  found  so  useful  in  the  diagnosis  of  luetic  aortic  insufficiency, 
is  of  less  value  in  the  diagnosis  of  luetic  myocarditis,  since  the  evidences  of  myocarditis 
are  in  themselves  less  definite.  However,  in  cases  of  chronic  myocardial  weakness  in  which 
lues  is  suspected,  the  presence  of  a  positive  Wassermann  reaction  renders  a  vigorous  ad- 
ministration of  mercurial  inunctions  or  hypodermic  injection  of  mercurial  salts,  as  well 
as  vigorous  doses  of  potassium  iodide,  highly  advisable.  Occasionally  excellent  results 
are  obtained  in  Adams-Stokes  disease,  but  syphilitic  myocardial  lesions  are  often  very 
stubborn.  Salvarsan  ("606")  has  shown  itself  to  be  so  dangerous  in  cardiovascular  disease 
that  large  doses  of  it  are  distinctly  contraindicated,  and  the  usefulness  of  doses  sufficiently 
small  to  be  free  from  danger  is  still  uncertain. 

TUMORS  OF  THE  HEART. 

Primary  tumors  of  the  heart  are  so  rare  that  in  3000  consecutive  autopsies  at  Niirn- 
burg  Thorel  did  not  encounter  a  single  one,  and  Hektoen,  who  reported  three  cases  in  1893, 
states  that  reports  of  only  110  cases  of  cardiac  tumors  were  to  be  found  in  the  Index  Cata- 
logue of  the  Surgeon-General's  Library,  and  most  of  these  were  secondary. 

Primary  Tumors. — Bertheson  was  able  to  collect  28  primary  tumors  of  the  following 
types:  sarcoma  9;  myxoma  7;  fibroma  6;  carcinoma  3;  lipoma  2;  cystoma  1.  Link 
(1909)  has  recently  collected  the  data  of  91  cases;  61  of  these  were  as  follows:  carcinoma 
7;  fibroma  7;  myoma  5;  lipoma  8;  sarcoma  13;  myxoma  18;  rhabdomyoma  1;  tera- 
toma 1;  papilloma  1.  In  addition  to  these  Knox  and  Schorer  and  Wolbach  have  collected 
12  cases  of  rhabdomyoma;  6  of  which  were  associated  with  other  malformations,  especially 
cerebral  sclerosis  and  hydrocephalus. 

Hektoen  calls  attention  to  the  fact  that  the  heart,  and  hence  also  its  primary  tumors, 
are  of  mesoblastic  origin;  which  accounts  for  the  relative  rarity  of  primary  car- 
cinomata  and  the  preponderance  of  sarcomata.  Thorel  believes  that  many  of  the  fibro- 
mata found  represent  merely  old  organized  thrombi  clinging  to  the  heart  wall,  and  believes 
that  many  of  the  (relatively  frequent)  myxomata  represent  merely  degenerating  forms  of 


336  DISEASES   OF  THE   HEART   AND    AORTA. 

such  thrombi.  The  lipomata  he  regards  merely  as  abnormally  large  pockets  of  epicardial 
or  intramural  fat  rather  than  as  true  tumors. 

As  regards  site,  Link  found  in  right  auricle  10;  left  auricle  24;  right  ventricle  14; 
left  ventricle  8;  valves  16;  interauricular  septum  2. 

Metastatic  Involvement  of  the  Heart.-— Secondary  neoplasms  affecting  the  heart  are 
somewhat  more  common,  and  scarcely  any  pathologist  of  experience  has  failed  to  meet 
with  them,  especially  in  cases  with  multiple  metastasis.  Of  the  metastatic  neoplasms 
carcinomata  are  the  most  frequent.  Thorel  encountered  6  instances  in  his  3000  autopsies, 
the  primary  sites  being  uterus  2,  rectum  1,  gall-bladder  1,  kidney  1,  lung  1. 

Geipel  stated  that  in  a  series  of  16  cases  of  carcinoma  of  the  oesophagus  6  gave  metas- 
tases to  the  heart;  but  this  is  an  unusually  high  percentage,  and  Thorel  from  his  experi- 
ence does  not  regard  such  oesophageal  tumors  as  especially  liable  to  cardiac  metastases. 

Clinically  the  presence  of  a  tumor  in  the  heart  in  itself  exerts  little  influence,  unless, 
as  in  Luce's  case  of  sarcoma,  it  presses  upon  the  auriculoventricular  bundle  and  produces 
heart-block,  or  it  is  so  situated  as  to  produce  either  stenosis  or  regurgitation  at  a  valvular 
orifice.  The  benign  tumors  exert  little  or  no  effect  upon  the  force  or  rhythm  of  the  heart; 
the  malignant  tumors  give  rise  merely  to  signs  of  cachexia  in  which  the  cardiac  weakness 
seems  incidental  rather  than  primary.  In  cases  of  generalized  carcinosis  and  sarcomatosis, 
those  in  which  the  metastatic  nodules  are  most  common,  the  cachectic  myocardial  weak- 
ness is  still  more  intense  whether  the  tumors  affect  the  heart  or  not.  The  accidental  finding 
of  a  loud  harsh  murmur  suddenly  developing  and  progressing  with  the  metastasis  elsewhere 
in  the  body  is  very  suggestive;  but  this  is  rarely  encountered. 

In  some  cases  in  which  the  tumors  are  superficial,  pericarditis  may  set  in.  Effu- 
sion, especially  blood-stained,  is  rather  common  under  these  conditions 
and  the  signs  of  the  latter  may  be  the  first  and  only  sign  of  the  condition. 

In  1905  the  writer  aspirated  a  pericardial  exudate  which  contained  10  per  cent,  of 
haemoglobin  and  some  methsemoglobin.  The  patient  died  the  next  day,  and  autopsy 
revealed  carcinomatous  masses  in  the  myocardium  wall  and  pericardium,  which  were 
metastases  from  a  very  small  primary  carcinoma  of  the  bronchus  quite  unsuspected  during 
life.    The  finding  of  tumor  cells  in  such  an  exudate  would,  of  course,  give  the  diagnosis. 

Tumors  of  the  heart,  even  if  diagnosed,  would,  of  course,  be  inoperable. 

BIBLIOGRAPHY. 
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Boettcher,  A.,  and  Zenker.     Quoted  from  Krehl. 

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Romberg,  E.:  Ueber  die  Erkrankungen  des  Herzmuskels  bei  Typhus  abdominalis,  Schar- 
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Aschoff,  L.:  Zur  Myokarditisfrage,  Verh.  d.  Deutsch.  pathol.  Gesellsch.,  1904,  viii,  46. 

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Coombs,  O:  The  Myocardial  Lesions  of  Acute  Rheumatic  Infection,  Brit.  M.  J.,  Lond., 

1907,  ii,  1513.     Rheumatic  Myocarditis,  Quart.  J.  Med.,  Oxford,  190S-9,  ii,  26. 
Bracht,  E.,  and  Wachter:  Beitrage  zur  Aetiologie  und  pathologischen  Anatomie  der  Myo- 
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Freund,  G.:  Zur  Kenntniss  der  acuten  diffusen  Myocarditis,  Bed.  klin.  Wchnschr.,  Berl., 

1898,  xxv,  1077. 

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viii,  400. 
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De  la  Camp,  Moritz,  Dietlen,  Hornung.    See  Chapter  on  the  Physiology  of  Cardiac  Over- 
strain. 
Roily,  F.:  Ueber  die  Wirkung  des  Diphtheriegiftes  auf  das  Herz,  Arch.  f.  exper.  Pathol,  u. 

Pharmakol.,  Leipz.,  1899,  xlii,  283. 
V.  Stejskal,  K.  Ritter  :  Kritsch-experimentelle  Untersuchungen  ueber  den  Herztod  in 

Fogle  von  Diphtherietoxin,  Part  I,  Ztschr.  f.  klin.  Med.,  Berl.,  1902,  xliv,  367;    Part 

II,  ibid.,  1904,  li,  129. 
Mackenzie,  J.:  New  Methods  in  the  Study  of  Affections  of  the  Heart,  Brit.  M.  J.,  Lond., 

1905,  i,  521. 
Hibbard,  C.  M.:  Heart  Complications  in  Diphtheria,  M.  and  S.  Rep.,  Bost.  City  Hosp., 

Bost.,  1898. 
Forster,   Fr.:  Ueber  Myokarditis  und  Gefasserkrankungen  im   Kindesalter  insbesondere 

nach  akuten  Infektionskrankheiten,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  lxxxv, 

35. 
Hallwachs:  Ueber  die  Myocarditis  bei  Diphtherie,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1899,  lxiv,  770. 

Ziegler,  E.:  Lehrbuch  der  Pathologie  und  der  pathologischen  Anatomie,  9th  ed.,  Jena, 

189S. 
Huchard,  H.:  Etude  clinique  de  la  cardio-sclerose,  Rev.  de  med.,  Par.,  1892,  xii,  421. 
Dehio,  K.:  Myofibrosis  cordis,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1899,  lxii,  1. 
Radasewsky:  Ueber  die  Muskelerkrankungen  der  Vorhofe  des  Herzens,  Ztschr.  f.  klin. 

Med.,  Berl.,  1895,  xxvii,  529. 
Albrecht,  E.:  Der  Herzmuskel  und  seine  Bedeutung  fur  die  pathologische  Physiologie 

und  Klinik  der  Herzens,  Berl.,  1903. 
Aschoff,    L.,   and  Tawara,   S.:  Die   heutige  Lehre  von  den    pathologisch-anatomischen 

Grundlagen  der  Herzschwache,  Jena,  1906. 
Mackenzie,  Keith,  Wenckebach,  Schonberg.    Quoted  on  p.  21. 
Saigo:  Purkinjeschen  Muskelfasern  bei  Erkrankungen  des  Myokards.    Verhandl.  d.  deutsch. 

path.  Gesellsch.,  Jena,  1908,  xii,  165. 
Hering,  H.  E.:  Ueber  kontinuerliche  Herzbigeminie,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1904,  Ixxix,  175. 
Marev,  E.  J.:  La  circulation  du  sang  a  l'etat  phvsiologique  et  dans  les  maladies,  Paris, 

1881. 
Knoll,  Ph.:  Ueber  die  Veranderungen  des  Herzschlages  bei  reflectiorischer  Errazung  des 

vasomotischen  Nervensystems;    sowie  bei  Stiegerung  des  intracardial  Drucks  ueber- 

haupt,  Sitzungsber.  d.  k.  Akad.  d.  Wissensch.,  Wien,  Abth.  Ill  (Physiol.  Anat.  u. 

Med.),  1872,  lxv-lxvi,  195. 
Hering,  H.  E.:  Ueber  die  haufige  Kombination  von  Kammervenenpuls  mit  Pulsus  irreg- 
ularis perpetuus,  Deutsch.  med.  Wchnsch.,  Leipz.,   1906,  xxxii,   1. 
Gerhardt,  D.:  Arhvthmia  perpetua  des  Pulses,  Deutsch.  med.  Wchnschr.,  1907,  xxxiii, 

448. 
Theopold,  J.:  Ein  Beitrag  zur  Lehre  von  der  Arhythmia  perpetua,  Deutsch.  Arch.  f.  klin. 

Med.,   Leipz.,    1907,   xc,   77. 
Hewlett,  A.  W.:  The  Interpretation  of  the  Positive  Venous  Pulse,  J.  Med.  Research, 

Bost.,  1907,  xvii,  119. 
Mackenzie,  James,  and  Gibson,  G.  A.    Quoted  on  p.  95. 

Tuberculosis  of  the  Myocardium. 

Pollak,  S.:  Ueber  Tuberculose  des  Herzmuskels,  Ztschr.  f.  klin.  Med.,  Berl.,  1892,  xxi,  185. 
Brosch,  A.:  Ein  Fall  von  Herztuberkulose  mit  typischen  Weilschen  Symptomenkomplex, 
Wien.  med.  Pr.,  1896,  xxxvii,  985. 

22 


338  DISEASES   OF  THE   HEART   AND   AORTA. 

V.  Leyden,  E.:  Ueber  die  Affection  des  Herzens  mit  Tuberculose,  Deutsche  med.  Wchn- 

schr.,  Leipz.,  1896,  xxii,  1. 
V.  Tabora  and  Tilp:  Zur  Kasuistik  der  Herztuberkulose,  ibid.,  1908,  xxxiv,  Vereinsbeil  805. 

Cardiac  Syphilis. 

Grassmann:  Ueber  acquerirte  Syphilis  des  Herzens,  Miinchen.  med.  Wchnschr.,  1897, 
xliv,  473,  506,  522.  Klinische  Untersuchungen  an  den  Kreislauforganen  im  Fruh- 
stadium  des  Syphilis,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1900,  lxix,  58,  264. 

Mracek,  F. :  Die  Syphilis  des  Herzens  bei  erworbener  und  ererbter  Lues,  Arch,  f .  Dermatol, 
u.  Syph.,  Wien  and.  Leipz.,  1893,  xxv  (Erganzungshefte) ,  p.  279. 

Adler,  I.:  Observations  on  Cardiac  Syphilis,  Trans.  Assoc.  Am.  Phys.,  Phila.;  1898,  xiii, 
73;   and  N.  York  M.  J.,  1898,  lxviii,  577. 

Sacharjin:  Die  Lues  des  Herzen  von  der  klinischen  Seite  betrachtet,  Deutsches  Arch.  f. 
klin.  Med.,  Leipz.,  1889,  xlvi,  388. 

Le  Count,  E.  R.:  Gummata  of  the  Heart  in  a  Case  of  Congenital  Syphilis,  J.  Am.  M.  Assoc, 
Chicago,  1898,  xxx,  181. 

Huehard,  H.,  and  Fiessinger:  Syphilis  gommeuse  du  cceur,  Rev.  de  Med.,  Par.,  1907,  xxvii. 

Tumors  of  the  Heart. 

Thorel,  C:  Pathologie  der  Kreislaufsorgane,  Ergebn.  d.  allg.  Path.  u.  path.  Anat.  d.  Mensch. 

u.  d.  Tiere,  herausg.  v.  Lubarsch  u.  Ostertag.,  Wiesb.,  1903,  ix,  1  Part;    and  1907, 

xi,  Pt.  2.    With  excellent  bibliography. 
Hektoen,  L.:  Three  Specimens  of  Tumors  of  the  Heart,  etc.,  Med.  News,  Phila.,  1893, 

lxiii,  571. 
Berthenson,  L.:  Zur  Frage  von  der  Diagnose  primarer  Neoplasmen  des  Herzens,  Myxom 

des  linken  Vorhofs,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1893,  cxxxii,  390. 
Link  R.:  Klinik  der  primarer  Neubildungen  des  Herzens,  Ztschr.  f.  klin.  Med.,   Berk, 

1909,  lvii,  272. 
Knox,  J.  H.  M.,  and  Schorer,  E.:  A  Multiple  Rhabdomyoma  of  the  Heart  Muscle,  Arch. 

Ped.,  N.  York,  1906. 
Wolbach,  S.  B.:  Congenital  Rhabdomyoma  of  the  Heart,  J.  Med.  Research,  Bost.,  1907, 

xvi,  495. 
Geipel.     Quoted  from  Thorel. 
Luce.     Quoted  on  p.  576. 


X. 

ARTERIOSCLEROSIS.1 

NORMAL    CHANGES   IN    THE    ARTERIES    DURING    LIFE. 

A  certain  degree  of  progressive  change  in  the  walls  of  the  arteries 
occurs  normally  throughout  life,  and  is  therefore  not  to  be  considered 
pathological.  The  condition  of  the  arteries  normal  to  a  man  of  thirty 
would  be  thoroughly  abnormal  in  a  child,  and  those  normal  for  a  man  of 
seventy  would  in  turn  be  regarded  as  abnormal  in  a  man  of  forty. 

Thus,  Thayer  and  Fabyan  state  that  "at  birth  the  artery  (radial)  is  delicate, 
translucent,  extremely  thin,  and  collapsing.  The  surface  on  opening  is  perfectly  smooth. 
The  i  n  t  i  m  a  consists  of  a  single  endothelial  layer  lying  directly  on  the  surface  of  a  deeply 
undulating  elastica  interna.  The  media,  which  consists  of  transversely  arranged  smooth 
muscle-fibres  with  rather  large  vesicular  nuclei,  has  a  depth  of  seven  to  eight  layers  of  cells. 
Connective  tissue,  if  present  in  the  intima  and  media,  is  extremely  scanty,  none  being 
revealed  by  the  Mallory  or  Van  Gieson  stains.  There  is,  however,  a  relatively  large  amount 
of  elastic  tissue  which  appears  on  cross  section  as  very  thin,  parallel,  slightly  wavy  lines. 
The  elastica  externa  is  neither  as  coarse  nor  as  deeply  undulating  as  the  interna. 

"  The  adventitia,  considerably  thicker  than  the  media,  consists  of  compact  con- 
nective-tissue fibres  with  relatively  large  nuclei.    The  elastic  fibres  are  fairly  numerous. 

"  By  the  middle  of  the  first  decade,  the  intima  has  become  thicker  owing  to  the  appear- 
ance of  a  fresh  layer  of  elastica  interna,  while  more  muscle-fibres  appear  in  the  media. 

"10-20  years.  Walls  of  the  vessel  become  thicker  but  still  collapsed.  Intima 
and   media   thicker,   the  elastic  tissue  being  relatively  less  marked. 

"21-40  years.  Slight  further  general  thickening  of  intima  and  media.  A  sec- 
ond elastic  layer  appears  in  the  intima.  In  the  media  the  connective  tissue  begins 
to  be  demonstrable  by  Van  Gieson's  stain. 

"41-50  years.  Decided  change.  Lumen  of  the  vessel  remains  open.  Areas  of 
calcification  in  the  deep  layers  of  the  intima  are  frequent.  The  media  reaches  its 
maximum  thickness.    There  is  a  good  deal  of  connective  tissue. 

"After  the  fifth  decade  there  is  a  progressive  increase  in  the  thickness  of  the  intima 

....  and  a  diffuse  connective-tissue  thickening  becomes  the  common  type The 

media  after  the  fifth  decade  becomes  on  the  whole  rather  thinner;  there  is  a  marked 
increase  in  the  connective  tissue. 

"Calcification  in  the  deep  layers  of  the  intima  becomes  more  common  with 
age,  four  out  of  five  cases  in  the  eighth  and  ninth  decade  showing  this  change." 

PATHOLOGICAL    ANATOMY. 

Theoretical  Considerations.  —  Pathologically,  arteriosclerosis  is  char- 
acterized by  the  occurrence  of  changes  in  and  thickening  of  the  intima, 
which  was  supposed  by  Rokitansky  to  be  due  to  the  depositing  of  cells 
directly  from  the  blood  stream;  by  Virchow  to  be  a  true  inflammatory 
hyperplasia  as  the  result  of  some  "formative  stimulus";  and  by 
Thoma  to  be  a  compensatory  thickening  of  the  wall  in  order  to 
diminish  the  lumen  of  the  vessel  after  the  stretching  which  occurred  under 
■the  increased  blood-pressure  with  which  it  was  usually  associated.  Jores,  on 
the  other  hand,  regards  this  as  a   true   hyperplasia   resulting  from 

1apT7jpi.ai  artery;  ctO^puaiz,  hardening. 

339 


340  DISEASES   OF  THE   HEART   AND   AORTA. 

the  high  blood-pressure  but  independent  of  the  lumen  of  the  vessel,  return- 
ing to  a  certain  degree  to  the  view  of  Virchow.  These  observers  con- 
sidered the  changes  in  the  intima  as  primary,  and 
tended  rather  to  neglect  the  second  important  change  which  characterizes 
arteriosclerosis,  namely  inflammatory  changes  within  the  media. 

On  the  other  hand,  Koster  and  his  pupils  called  attention  to  the  im- 
portance of  degenerative  and  calcareous  changes  in 
the  media  and  adventitia  as  well  as  in  the  intima.  Koster 
studied  the  inflammatory  process  very  carefully  by  means  of  serial  sections 
and  injected  specimens,  and  claimed  that  the  arteriosclerotic  lesion  always 
took  its  origin  in  the  adventitia  as  an  infiltration  surrounding 
the  vasa  vasorum  like  a  sleeve.  This  infiltration  followed  the 
vasa  vasorum  into  the  media.  Koster  found  that  in  the  normal  artery 
the  vasa  vasorum  do  not  pass  deeper  than  the  outer  third  of  the  media, 
though  in  certain  arteries  (notably  those  of  the  brain  and  the  lungs)  there 
was  a  fine  capillary  network  penetrating  the  deeper  layers  of  the  media  as 
well  and  spreading  along  the  medial  surface  of  the  elastic  a  interna. 

Changes  in  Vasa  Vasorum.  —  This  view  is  confirmed  by  v.  Ebner 
(in  Kolliker's  Handbuch  der  Gewebelehre) ,  who  states  that  "the  media 
of  the  larger  arteries  and  veins,  according  to  the  consensus  of  opinion 
of  many  authors,  contains  blood-vessels,  though  in  small  numbers  and  only 
in  the  external  layers;  whereas  the  inner  layers  of  the  media  and  the  intima 
seem  to  be  always  free  from  vessels  (in  the  ox  the  wall  of  the  vena  cava  is 
richly  supplied  with  vessels  even  down  to  the  intima) . 

The  infiltration  about  the  vasa  vasorum  follows  these  paths,  setting  up  areas  of 
infiltration,  necrosis,  and  calcification  in  the  smooth  muscle  and  elastic  fibres  of  the  media. 
When  it  penetrates  to  the  elastica  interna  a  small  area  of  this  is  first  injured,  the  inflamma- 
tion acts  as  a  stimulus,  and  hyperplasia  of  the  intima  sets  in.  The  intima  becomes  thick- 
ened until  its  cells  undergo  spontaneous  fatty  degeneration,  after  which  they  either  calcify 
or  the  capillary  network  penetrates  through  the  elastica  interna  and  a  true  process  of  organ- 
ization and  proliferation  of  connective  tissue  goes  on. 

Koster  admits  that  it  is  possible  that  the  degenerative  and  hyperplastic  changes  in 
the  intima  may  go  on  without  the  entrance  of  blood-vessels,  as  do  those  seen  in  inflamma- 
tions of  the  cornea;  but  he  states  that  if  the  lesions  are  followed  in  serial  sections  there 
is  almost  always  a  demonstrable  continuity  between  the  patches  of  endarteritis,  mesar- 
teritis,  and  periarteritis. 

The  number  and  size  of  the  vasa  vasorum  and  the  richness  of  the  capil- 
lary network  are  always  increased  in  arteriosclerosis  and  in  phlebosclerosis. 
He  states  that  endarteritis  occurs  only  in  arteries  that  have  vasa  vasorum, 
that  is,  in  the  larger  arteries  and  in  the  smaller  arteries  of  the  brain  and 
the  lungs. 

These  observations  have  been  confirmed  by  Marchand,  Ophiils,  Klotz, 
and  a  host  of  other  writers.  Heller  and  his  pupils,  Dohle,  Moll  and  Isenberg, 
as  well  as  Marchand  and  Klotz,  have  shown  that  in  syphilitic  disease  of  the 
media  the  strands  of  infiltration  along  the  vasa  vasorum  are  much  thicker 
than  in  arteritis  (medial  arteriosclerosis)  due  to  other  causes.  As  far  as  the 
media  and  adventitia  are  concerned,  Koster's  findings  have  been  confirmed 
by  Ophiils,  whose  careful  study  constitutes  one  of  the  most  important  and 
clearest  of  the  recent  contributions  to  the  subject.  Ophiils,  however,  was 
unable  to  demonstrate  any  constant  relation  between  lesions  in  the  media 


ARTERIOSCLEROSIS.  341 

and  those  in  the  intima,  and  believes  that  they  are  produced  independently 
though  from  the  same  general  cause.  He  states  that  "  anatomically  arterio- 
sclerosis of  the  aorta  is  a  unit.  It  is  a  chronic  inflammatory  process  of  the 
vessel  wall  which  attacks  all  the  coats  simultaneously,  which  as  a  rule  first 
produces  changes  in  the  intima  and  adventitial  He  believes,  therefore,  that, 
as  Koster  suggested,  the  changes  in  the  intima  begin  as  parenchymatous 
changes  without  the  presence  of  blood-vessels,  like  the  inflammations  within 
the  cornea. 

Calcification. — In  degenerative  lesions  of  the  intima  and  media,  calcare- 
ous deposition  (atheroma)  is  very  common,  and  is  in  fact  a  phenomenon 
which  is  normal  for  the  eighth  and  ninth  decades  of  life.  These  deposits 
always  occur  in  areas  of  fatty  degeneration;  and  it  was  thought,  especially 
by  the  older  German  investigators,  that  certain  acids  within  the  tissues  acted 
as  lime-catchers  (Kalkf anger),  combining  with  the  calcium  and  precipitating 
it  in  situ. 

It  was  at  first  thought  that  phosphoric  acid  derived  from  autolysis  of 
the  cell  nucleoproteids  might  be  the  main  lime-catcher,  but  Gideon  Wells 
and  his  collaborators  have  shown  that  when  spleen  or  thymus  which  are  rich 
in  nucleoproteids  are  transplanted  into  another  animal  and  allowed  to  degen- 
erate, no  more  deposition  of  lime  occurs  than  in  the  degeneration  of  other 
tissues.  It  has  also  been  assumed  that  the  calcium  first  combines  with  the 
fatty  acids  produced  in  the  process  of  fatty  degeneration, — a  phenomenon 
which  may  actually  take  place  in  true  adipose  tissue.  This  theory  was  advo- 
cated by  Klotz  on  the  basis  of  the  histological  appearance  when  stained  with 
Sudan  III,  but  Baldauf  and  Aschoff  have  shown  that  exactly  these  appear- 
ances might  be  given  by  mixtures  of  oleic  acid,  triolein,  and  lecithin. 

The  analyses  of  Baldauf,  Selig,  and  Wells  have  failed  to  demonstrate 
the  presence  of  calcium  soaps;  but,  on  the  other  hand,  Baldauf  and  Wells 
have  found  that  the  calcium  phosphate  and  carbonates  which  are  the  main 
constituents  exist  in  the  same  proportions  as  are  found  in  bone  (about  85 
to  90  per  cent,  of  the  former  to  10  to  15  per  cent,  of  the  latter) .  However, 
Wells  has  shown  that  this  proportion  is  also  ex- 
actly the  proportion  in  which  the  phosphates  and 
carbonates  exist  in  the  serum,  and  his  own  observations,  as 
well  as  those  of  Hofmeister  and  Tanaka,  indicate  that  this  is  the  composi- 
tion to  which  any  calcium  salts  whatever  are  ultimately  reduced  by  the  mass 
action  of  the  lymph  and  serum.  Wells  believes  that  the  "  calcium  is  carried 
in  the  blood  in  amounts  not  far  from  the  saturation  point,  held  in  solution 
by  the  colloids  and  the  carbon  dioxide,  and  existing  probably  in  the  form 
of  an  unstable  double  salt  of  calcium  bicarbonate  and  dicalcium  phosphate. 
In  normal  ossification  and  in  most  instances  of  pathological  calcification  the 
deposition  is  probably  initiated  by  a  process  of  colloid  adsorption,  causing. a 
concentration  of  this  double  salt  in  the  hyaline  matrix  which  is  to  be  calcified 
and  which  has  a  strong  affinity  for  calcium  salts.  Calcium  deposition  seems 
to  depend  more  on  physico-chemical  processes  than  on  chemical  reactions." 

Ossification. — Virchow  and  subsequent  writers,  notably  Moenckeberg, 
Bunting,  Oppenheimer,  Poscharissky,  Klotz,  and  Wells,  have  called  atten- 
tion to  the  fact  that  not  only  plaques  of  calcification  but  even  true  bone  may 
be  deposited  in  the  walls  of  diseased  arteries,  and  even  in  calcified  portions 


342 


DISEASES  OF  THE  HEART  AND  AORTA. 


of  the  heart  itself.  Wells  has  shown  that  the  palcium  salts  act  as  a  stimulus, 
in  the  sense  of  Virchow's  formative  stimuli,  in  giving  rise  to  the  formation 
first  of  tissue  resembling  bone-marrow  in  structure  and  later  to  a  growth  of 


TOFDMBDAJEII150BUTQWB  ENDARTERITIS  OBLITERANS     ENDARTERITIS 


ANEURISM 


KRIARTEIIITISII0D05A 
MESARTERITI5  /£f&3?^  KORMAI 


Fig.  153. — Various  types  of  arteriosclerotic  lesions.     (Schematic.) 


true  bone.  Such  arterial  ossification  is  more  common  than  is  generally  sup- 
posed, especially  in  calcareous  mesarteritis. 

Classification  of  Arteriosclerotic  Lesions. — From  the  stand-point  of 
structure,  Ranvier  has  divided  the  arteries  into  two  great  groups : 

1.  Vessels  of  the  elastic  type,  the  aorta,  pulmonary,  carotid,  and  common 


ABC 

Fig.  154. — Types  of  aortic  lesions.  A,  fatty  degeneration  of  the  intima  from  a  patient  dying  of 
typhoid  fever;  B,  syphilitic  aortitis,  showing  the  sharp  demarcation  of  the  diseased  area;  C,  generalized 
non-luetic  arteriosclerosis  (atherosclerosis). 

iliac  arteries,  whose  media  is  made  up  of  lamellae  of  elastic  tissue  interwoven 
with  elastic  fibrils. 

2.  Arteries  of  the  muscular  type,  embracing  all  the  other  arteries  of  the 
body,  whose  media,  though  contaming  elastic  fibres,  is  composed  chiefly  of 
strands  of  smooth  muscle. 


ARTERIOSCLEROSIS.  343 

Diseases  of  the  arteries  occur  in  a  variety  of  forms,  which  affect  these  two 
types  of  vessels  somewhat  differently,  so  that  for  clinical  convenience  they  may 
be  divided  into  two  groups,  according  as  they  affect  the  vessels  of  the  elastic 
type,  and  especially  the  aorta,  or  the  muscle-walled  vessels  of  the  periphery. 

I.  Diseases  of  the  aorta  and  vessels  of  the  elastic  type. 

1.  Changes  in  the  intima: 

a.  Acute  aortitis,  with  fatty  degeneration  or  gelatinous  plaques  in  the  intima. 

b.  Atheroma,  with  formation  of  plaques  of  intimal  thickening,  fatty  degen- 

eration, and  calcification  (endarteritis  chronica  deformans,  Virchow; 
atherosklerose,  Marchand),  sometimes  syphilitic  associated  with  syph- 
ilitic mesaortitis. 

2.  Changes   in    the   media    (mesaortitis,    mesarteritis): 

a.  Syphilitic,  showing  large,  thick  strands  of  fibrous  tissue  with  destruction 

of  the  elastic  tissue. 

b.  Acute  and  chronic  inflammatory  mesarteritis  due  to  other  germs,  among 

them  the  tubercle  bacillus,  or  perhaps  to  the  results  of  clinical  poisons 
(lead,  alcohol,  etc.). 
II.  Diseases  of  the  peripheral  arteries   (muscular  type). 

1.  Acute  endarteritis: 

a.  Suppurative,  with  purulent  infiltration  of  all  the  coats  of  the  artery  and 

the  formation  of  small  abscesses  in  its  walls.  This  is  usually  attended 
with  thrombosis  within  the  lumen  as  well  (thromboangitis)  and  final 
suppuration  of  the  thrombus  itself. 

b.  Swelling  and  fatty  degeneration  of  the  intima,  as  the  result  of  bacteria 

or  toxic  substances  either  directly  from  the  blood  strain  or  reaching  it 
through  the  vasa  vasorum. 

2.  Atheroma  or  endarteritis  deformans  resulting  from  calci- 

fication of  degenerated  patches. 

3.  Changes  in  the  intima  (endarteritis,  productiva  or  oblit- 

erans). Inflammatory  changes  in  the  intima,  leading  to 
fatty  degeneration  and  swelling  of  the  intima  or  to  the 
proliferation  of  fibrous  and  also  of  elastic  tissue  within 
the  lumen,  so  that  the  latter  may  be  either  encroached 
on  or  completely  obliterated. 

4.  Thromboangitis  obliterans  (to   be  discussed   in   a   follow- 

ing  chapter),   in  which   spontaneous   endovascular   clot- 
ting  precedes    demonstrable    changes   in    the    artery   and 
the  clot  gradually  becomes  organized  with  solid  fibrous 
tissue  free  from  elastic  fibres 
III.  Diseases  affecting  the  media  (mesarteritis). 

1.  Hypertrophy  of  media. 

2.  Simple  medial  fatty  degeneration  with  calcification  or  ossification  (Marchand 

and  Moenckeberg) . 

3.  Infective  mesarteritis  with  infiltration  along  the  vasa  vasorum.     Syphilitic 

with  very  coarse  strands  of  fibrosis. 

4.  Bacterial  invasion  of  media : 

a.  Acute  septicsemic,  giving  rise  to  necrosis  of  media  and  mycotic  aneurisms. 

b.  Chronic,  as  in  typhoid  fever,  giving  rise  to  chronic  mesarteritis  with 

strands  finer  than  those  of  lues. 

c.  Tuberculous  arteritis  (rare). 

IV.  Diseases  affecting  the  adventitia  (periarteritis). 

a.  Diffuse  periarteritis  part  of  process  of  all  infection,  luetic  and  tubercu- 

lous arteries. 

b.  Periarteritis  nodosa  (Kussmaul  and  Mayer)    (supra-arterial  fibroid  nod- 

ules) : 

(a)  Acute. 

(b)  Chronic. 


344  DISEASES  OF  THE  HEART  AND  AORTA. 

Fatty  Degeneration  of  the  Intima.— The  mildest  form  of  disease  of  the 
intima  is  manifested  by  the  formation  of  small,  slightly  raised,  round  or  elon- 
gated patches,  white  or  yellow  in  color,  which  are  most  frequently  situated 
along  the  inner  surface  of  the  aorta  above  the  valves  or  about  the  mouths 
of  the  intercostal  arteries.  The  surface  is  smooth  and  lined  with  intact 
endothelium,  but  the  subendothelial  connective  tissue  is  swollen  and  filled 
with  granules  of  fatty  degenerated  material  rich  in  lecithin  and  cholesterin, 
thus  causing  the  surface  of  the  plaque  to  be  elevated  above  the  surrounding 
structure  (Fig.  154,  A;  Plate  XVII,  A). 

Such  patches  of  fatty  degeneration  are  common  at  all  ages,  especially 
in  conditions  of  anaemia,  chlorosis,  febrile  disease,  and  acute  intoxications; 
and  they  are  also  found  accompanying  the  various  types  of  arteriosclerosis 
and  atheroma. 

Calcification  of  the  Intima. — Endarteritis  chronica  deformans  (Virchow) 
(atheroma)  is  usually  the  result  of  a  more  chronic  process,  probably  the 
gradual  deposition  of  calcium  phosphate  and  carbonate,  in  a  preliminary 
focus  of  fatty  degeneration  in  the  intima.    Frequently  the  endothelial  surface 

becomes  ulcerated  over  the  calcification. 
A  similar  change  often  occurs  upon 
the  aortic  and  mitral  valves  (Fig.  155) 
and  also  in  the  heart  muscle  itself.  And 
the  mechanism  by  which  the  lesion  is 
produced  is  probably  the  same  in  all. 

This  form  of  arteriosclerosis  is  prob- 
ably the  most  common  form  of  all, 
for  it  is  the  arterial  disease  of  old  age, 
but  its  importance  in  the  causation  of 
signs  or  symptoms  depends  upon  the 
location  of  the  plaques.  Thus,  a  few 
Fig.  155.— Syphilitic  aortitis  (atheroscie-      plaques  along  the  course  of  the  descend- 

rosis)  with  deposition  of  calcined  plaques  just         • ■  v    ,       i 

above  and  upon  the  aortic  valves  mg     aorta     may     cause     n°     disturbance 

whatever,  not  even  a  rise  of  blood-pres- 
sure ;  while  a  plaque  upon  the  valvular  surface  of  a  sinus  of  Valsalva  may 
cause  active  insufficiency,  or  a  small  area  of  calcification  over  the  mouth 
of  one  of  the  coronary  arteries  may  keep  the  heart  from  receiving  a  sufficient 
supply  of  blood  and  give  rise  to  angina  pectoris. 

Klotz  has  claimed  that  the  degeneration  of  an  area  of  intima  is  due  to 
diminished  circulation  through  the  diseased  vasa  vasorum  supplying  nutri- 
ment to  the  corresponding  part.  Definite  proof  for  this  theory  is,  however, 
lacking;  and  the  older  theory,  that  the  intimal  cells  are  destroyed  by  toxic 
products  in  the  circulating  blood  or  in  the  lymph  that  bathes  them,  explains 
as  many  of  the  conditions. 

In  the  smaller  vessels  a  small  patch  of  calcification  or  even  an  area  of 
intimal  swelling  from  fatty  degeneration  has  much  more  effect  on  blood 
flow  than  in  the  aorta,  and  may  occlude  a  sufficiently  large  part  of  the  lumen 
to  cause  more  or  less  ischsemia  and  impairment  of  function  of  the  organ  sup- 
plied, which  is  permanent  in  the  case  of  calcification  but  may  be  temporary 
if  due  to  fatty  degeneration. 


ARTERIOSCLEROSIS.  345 

Acute  Aortitis  and  Acute  Arteritis. — In  septicemic  conditions  when  large 
numbers  of  virulent  cocci  or  bacteria  are  circulating  in  the  blood,  or  in  arteries 
in  the  vicinity  of  abscess-cavities  or  local  infections,  it  is  but  natural  that 
some  of  them  should  at  times  lodge  and  proliferate  in  the  vasa  vasorum,  and 
thus  give  rise  to  acute  inflammatory  processes  in  and  about  them,  following 
into  the  media  and  giving  rise  to  lesions  in  all  three  coats  of  the  artery.  The 
elastic  fibres  degenerate  exactly  as  in  luetic  arteritis,  and  mycotic  aneurisms 
may  result. 

The  intima  may  undergo  necrosis,  the  endothelium  degenerate,  fibrin  fer- 
ment be  liberated  from  it  into  the  lumen,  and  thrombosis  of  the  vessel  may 
take  place  (thromboarteritis  acuta,  Ziegler).  In  less  severe  infections  the 
lesions  may  heal,  and  the  areas  of  degeneration  be  replaced  by  fibrous  tissue. 

In  other  acute  infectious  diseases,  especially  those  which  are  severe,  the 
intima  alone  may  undergo  necrosis  and  be  covered  with  elevated  white 
gelatinous  patches  (acute  gelatinous  aortitis,  described  by  Cornil  and  Ranvier 
and  the  subsequent  French  writers). 

Vegetative  Endarteritis. — In  some  cases,  especially  in  those  in  which  there 
is  a  severe  endocardial  lesion  involving  several  valves  at  once,  the  vegetative 
process  may  extend  upward  into  the  aorta  and  give  rise  to  vegetations  which 
arise  out  of  the  intima  exactly  as  vegetations  upon  the  valves  arise  out  of  the 
endocardium  (endarteritis  verrucosa).  They  may  be  produced  during  the 
course  of  severe  infections,  as  in  one  case  reported  by  Nauwerck  and  Eyrich; 
they  may  be  found  in  cases  of  very  chronic  endocarditis  without  other  signs 
to  indicate  their  presence.  The  condition  is  homologous  with  endocarditis  of 
the  more  severe  grade,  notably  with  chronic  infectious  endocarditis. 

Endarteritis  Productiva  seu  Obliterans. — Complete  obliteration  of  the 
lumen  of  an  artery  by  the  proliferation  of  connective  tissue  which  passes  out 
from  the  intima  is  a  normal  process  in  certain  arteries,  notably  the  umbilical 
and  hypogastric  arteries  and  the  ductus  arteriosus;  and  it  also  represents 
the  normal  method  of  healing  a  wounded  vessel. 

The  studies  of  Thayer  and  Fabian  quoted  above  show  that  a  certain 
amount  of  thickening  of  the  intima  (endarteritis  productiva)  is  also  a  normal 
process  as  age  advances;  and  similar  changes  represent  one  of  the  most  com- 
mon forms  of  pathological  change  in  arteries  all  over  the  body,  particularly 
in  those  of  the  muscular  type,  in  which  it  is  frequently  accompanied  by 
mesarteritis.  The  lesion  consists  of  a  gradual  thickening  of  the  intima  by 
proliferation  of  both  the  fibrous  and  the  elastic  tissue  until  it  encroaches 
upon  the  lumen  of  the  artery  (endarteritis  productiva)  or  actually  obliterates 
it  (endarteritis  obliterans).  In  some  cases  the  lesion  is  secondary  to  a  mesar- 
teritis, the  infiltration  and  the  vasa  vasorum  penetrate  the  entire  media, 
destroy  the  el'astica  interna  and  penetrate  into  the  intima,  as  Koster  described, 
while  in  others  the  connective  tissue  is  laid  down  layer  by  layer  in  response 
to  some  chemical  stimulus  which  enters  from  either  the  lumen  of  the  artery 
or  the  lymph  spaces  that  bathe  the  intima.  Thoma's  theory,  that  this  pro- 
liferation is  a  compensatory  one  in  response  to  increased  pressure,  in  order 
to  retain  the  lumen  of  the  artery,  is  disproved  by  the  experiments  of  Jores, 
who  showed  that  dilating  the  vessels  of  the  leg  by  cutting  the  sciatic  nerve 
is  not  followed  by  sclerotic  changes. 


346  DISEASES  OF  THE  HEART  AND  AORTA. 

Endarteritis  productiva  occurs  to  a  somewhat  greater  extent  in  the 
peripheral  arteries  than  in  the  aorta,  in  the  latter  only  in  patches,  while  in 
the  former  it  may  be  diffuse. 

Hypertrophy  of  the  Media  (Arterial  Hypermyotrophy,  Savill). — While 
trying  to  explain  the  rise  of  blood-pressure  in  chronic  interstitial  nephritis 
upon  the  basis  of  diminished  blood  flow  through  the  kidneys,  George  Johnston 
in  1873  called  attention  to  the  fact  that  there  is  a  direct  relation  between 
hypertrophy  of  the  heart  and  hypertrophy  of  the  muscular  walls  (media) 
of  the  small  arteries  (the  arteriocapillary  fibrosis  of  Gull  and  Sutton),  not 
only  of  the  kidney  but  also  throughout  the  entire  body,  and  especially  those 
of  the  skin  and  mucous  membranes,  the  constriction  of  which  causes  the  high 
blood-pressure.  This  observation  has  received  ample  confirmation,  especially 
by  writers  of  the  British  school,  by  Savill,  Russell,  and  Sir  Clifford  Allbutt. 
F.  Parkes  Weber  claims  that  it  bears  the  same  relation  to  arteriosclerosis 
that  cardiac  hypertrophy  bears  to  cardiosclerosis. 

The  clinical  importance  of  this  arterial  hypertrophy  is  best  shown  by 
the  fact  that  hypertrophy  of  the  media  was  present  in  every  one  of  the  Savill's 
257  autopsies  on  patients  who  had  during  life  presented  circulatory  symptoms 
without  valvular  disease,  though  in  many  it  was  associated  with  other  forms 
of  arterial  lesion.  Savill  states  that  in  these  cases  without  marked  endarteritis 
"  the  vessel  loses  some  of  its  pliability,  remains  unduly  patent,  and  does  not 
collapse  as  a  normal  artery  should.  .  .  .  The  increase  in  muscular  tissue 
takes  place  in  length  as  well  as  in  thickness,  so  that  the  artery  becomes 
tortuous." 

The  hypertrophy  of  the  media  is  well  marked  in  the  radials,  but  best  in 
the  arteries  of  the  lower  extremity,  which,  owing  to  the  influence  of  gravity, 
are  under  the  highest  pressure;  and,  on  the  other  hand,  it  is  relatively  slight 
in  the  cerebral  vessels,  probably  owing  to  their  elevation  when  the  body  is 
erect.  Savill  believes  that  the  absence  of  hypermyotrophy  in  these  arteries 
is  responsible  for  the  relative  frequency  of  cerebral  hemorrhage.  Savill  dis- 
tinctly states  that,  though  common  in  chronic  nephritis,  arterial  hypermy- 
otrophy is  by  no  means  universal  in  that  condition. 

Jores,  on  the  basis  of  a  relatively  small  series  of  carefully  investigated 
cases,  has  claimed  that  hypertrophy  of  the  heart  and  the  presence  of  extremely 
high  blood-pressures  is  confined  to  the  cases  of  small  red  kidney  in  which  an 
intracapsular  fibrosis  about  the  loops  of  the  glomerular  capillaries  represents 
the  predominant  lesion,  and  the  lesions  of  the  tubules  are  less  marked.  In , 
primary  tubular  nephritis,  even  when  the  glomeruli  are  greatly  injured,  he 
finds  no  hypertrophy  of  the  heart  nor  elevation  of  blood-pressure. 

On  the  other  hand,  it  has  been  shown  by  W.  Russell,  and  later  by  Jane- 
way  and  Park,  that  changes  in  consistency  of  the  arterial  wall  may  be  respon- 
sible for  great  changes  in  the  compressibility  of  the  artery  and  therefore  for 
errors  in  the  determination  of  blood-pressure;  and  it  is  most  likely  that  this 
form  of  disease  is  largely  concerned.  It  is,  indeed,  not  impossible  that  the 
extremely  high  figures  for  blood-pressure  in  this  condition  may  be  due  in 
part  to  those  changes  in  the  internal  wall,  and  may  be  often  apparent  rather 
than  real. 

Syphilitic  Mesaortitis  and  Mesarteritis. — While  Lancisi  and  the  writers 
of  the  early  part  of  the  nineteenth  century  noticed  the  association  of  aneurism 


ARTERIOSCLEROSIS.  347 

and  weakening  of  the  arterial  wall  with  syphilis,  it  remained  for  Francis 
Welch  to  point  out  the  existence  of  a  well-defined  type  of  aortitis  of  syphilitic 
origin.  He  noted  that  these  lesions  were  usually  confined  to  definite  zones  of 
the  aorta,  most  commonly  near  the  sinuses  of  Valsalva  or  encircling  the  first 
part  of  the  aorta,  but  sometimes  confined  to  the  transverse  arch  or  to  the  de- 
scending aorta  just  above  the  diaphragm.  The  areas  of  change  in  the  aorta 
end  abruptly,  and  the  rest  of  the  vessel  is  almost  always  clear  (Fig.  154  B). 

These  lesions  are  composed  of  patches  over  which  opaque  elevated 
nodules  alternate  with  punched-out  depressions,  which,  as  Dohle  puts  it,  are 
as  uniform  as  if  punched  out  with  a  stamp.  The  fibrous  plaques  are  elevated 
above  the  areas  in  which  the  media  is  normal. 

Heller  and  his  pupils  Dohle,  Moll,  and  Isenberg  have  shown  that  the 
histological  picture  of  these  lesions  is  quite  as  characteristic  as  their  gross 
appearance.  They  represent  the  prototype  of  the  form  described  by  Koster, 
sleeve-like  infiltrations  about  the  vasa  vasorum,  along  which,  as  the  recent 
observations  of  Schmorl,  Klotz,  and  Wright  and  Richardson  have  recently 
shown,  the  spirochetes  (treponema  pallidum)  lodge  in  the  vessel  wall.  When 
this  invasion  is  recent,  the  lesions  consist  chiefly  of  small  areas  of  necrosis 
infiltrated  with  lymphocytes,  plasma  cells,  and  here  and  there  a  few  giant 
cells  and  miliary  gummata.  According  to  the  observations  of  Wright  and 
Richardson,  the  spirochsetes  (treponemata)  are  most  numerous  in  the  areas 
of  necrotic  tissue,  and  "  their  numbers  and  distribution  in  the  lesions  would 
suggest  that  they  rapidly  multiply  at  a  given  point,  produce  necrosis,  and  then 
degenerate  and  disappear."  The  necrosis  is  especially  marked  hi  the  elastic 
tissue  and  muscle-fibre  of  the  media,  which  fragment,  degenerate  and  are 
then  absorbed.  As  the  spirochsetes  disappear,  the  cellular  infiltration  is 
replaced  by  fibroblasts  and  these  in  turn  by  fibrous  tissue,  so  that  in  the  older 
lesions  the  media  is  seen  to  be  broken  up  by  coarse  bands  of  fibrous  tissue 
which  pass  along  the  vasa  vasorum  and  may  reach  into  the  intima.  Miliary 
or  submiliary  gummata  are  sometimes  present  in  the  areas  of  fibrosis.  The 
elastic  and  muscle  fibres  are  fragmented,  entirely  destroyed  in  the  path  of 
the  invasion  and  are  replaced  by  the  above-mentioned  fibrous  tissue.  The 
latter  is  entirely  rigid;  but  the  intervening  areas  of  elastic  or  muscular 
tissues  contract,  and  when  the  artery  is  opened  "  appear  as  areas  of  depres- 
sion between  the  elevated  areas  of  fibrosis.  This  is  the  exact  opposite  of 
the  conditions  in  inflammations  of  the  intima,  in  which  the  diseased  portions 
are  the  elevated  ones;  and  moreover  it  applies  only  to  pure  mesarteritis,  for 
in  many  cases  the  latter  is  accompanied  by  plaques  of  endarteritis  as  well  as 
fibrosis.  When  the  blood  is  circulating  through  the  artery,  however,  condi- 
tions are  reversed,  for  then  the  strong  elastic  and  muscular  tissue  resists  the 
pressure  better  than  the  weaker  and  distensible  elastic  tissue;  and  the  areas 
of  the  latter  bulge  outward  or  may  even  appear  as  definite  aneurisms,  for  it 
is  this  form  of  arteriosclerosis  from  which  aneurisms  arise. 

The  process  of  fibrosis  may  also  be  accompanied  by  a  gradual  prolifera- 
tion or  obliterating  of  the  vasa  vasorum,  by  which  the  nutrition  of  the  corre- 
sponding areas  of  arterial  wall  is  still  further  cut  off.  This,  as  Klotz  has 
claimed,  probably  causes  ischaemia  and  secondary  changes  in  the  corre- 
sponding areas  of  intima,  so  that  necrosis,  atheroma,  and  in  the  more  slowly 
developing  cases  proliferation  of   connective  tissue  (endarteritis  progressiva 


348  DISEASES  OF  THE  HEART  AND  AORTA. 

seu  obliterans)  results^  There  is  thus  an  endarteritis  of  the  vasa  vasorum 
giving  rise  to  endarteritis  of  the  vessel  itself. 

Clinically,  as  Welch,  Heller,  and  a  host  of  subsequent  observers  have 
shown,  syphilitic  mesaortitis  is  particularly  likely  to  affect  the  first  part  of 
the  aorta,  especially  in  young  men,  and  to  be  confined  to  this  zone  or  at  least 
to  extend  no  further  than  the  transverse  arch.  The  lesions  are  especially 
prone  to  extend  downward  into  the  sinuses  of  Valsalva  and  produce  constric- 
tions about  the  mouths  of  the  coronary  arteries,  thus  giving  rise  to  cardiac 
weakness  and  angina  pectoris.  Somewhat  more  commonly  the  same  process 
extends  over  to  involve  the  cusps  of  the  aortic  valves  themselves,  causing 
deformation  and  shrinkage  of  the  latter  with  the  development  of  the  very 
common  syphilitic  form  of  aortic  insufficiency.  Syphilitic  aortitis  is  therefore 
of  great  clinical  importance,  and,  though  less  common  than  endarteritis,  is 
more  prone  to  give  rise  to  striking  clinical  entities,  and  thus  to  attract  the 
attention  of  the  clinician. 

Another  common  form  of  the  luetic  lesion  is  the  formation  of  a  band  or 
collar  about  the  descending  aorta  just  above  the  attachment  of  the  diaphragm, 
leaving  the  rest  of  the  aorta  clear.  This  is  the  zone  from  which  aneurisms 
of  the  descending  aorta  often  arise. 

Moreover,  common  as  are  the  luetic  involvements  of  the  aorta,  it  is 
still  more  common  for  the  spirochete  to  be  filtered  out  in  the  smaller  periph- 
eral, visceral,  and  cerebral  arteries,  where  their  distribution  determines  the 
various  pleomorphic  lesions  of  the  disease.  In  these  arteries  the  histological 
picture  is  quite  similar  to  that  in  the  aorta,  except  that,  as  the  media  is  thinner, 
the  necrotic  and  sclerotic  processes  extend  more  readily  to  the  intima  and  a 
more  severe  grade  of  endarteritis  results,  often  to  the  complete  obliteration 
of  the  lumen. 

Non-syphilitic  infective  mesaortitis  and  mesarteritis  also  occur,  but,  as  in 
the  non-syphilitic  cirrhosis  of  the  liver,  the  strands  of  infiltration  and  fibrosis 
are  much  less  coarse  than  in  those  of  syphilitic  origin,  giving  rise  to  less  weak- 
ening of  the  arterial  wall,  and  are  less  striking  in  the  pictures  which  they 
present. 

In  the  arteries  of  rheumatic  patients  Klotz  has  found  "  small  areas  of 
medial  fibrosis  which  in  many  respects  simulate  the  sclerotic  patches  in  the 
heart  described  by  Aschoff.  During  the  progressive  stage  of  these  lesions 
narrow  lines  of  cellular  infiltration  are  seen  along  the  small  capillaries  in  the 
adventitia  and  also  in  the  media.  The  larger  arteries  and  arterioles  of  the 
media  do  not  share  this  infiltration.  Moreover,  the  inflammatory  process 
is  limited  to  a  narrow  zone  just  along  the  vasa  vasorum.  Frequently  this 
infiltration  is  only  a  few  cells  deep."  As  healing  goes  on  this  becomes  replaced 
by  a  strand  of  fibrosis. 

Arterial  changes  affecting  all  three  coats  have  been  described  in  typhoid 
fever  by  Landouzy  and  Siredey,  Thayer,  and  numerous  other  observers. 
The  cells  of  the  intima  become  raised,  swollen,  and  desquamated;  the  elastica 
interna  is  injured.  The  layers  of  the  media  are  infiltrated  with  mononuclear 
cells;  and  the  vasa  vasorum  of  the  adventitia  are  surrounded  with  dense 
infiltrations,  similar  to  those  seen  in  myocardial  lesions. 

Klotz  has  found  that  in  this  disease  the  mesarteritis  is  less  extensive  than 
in  rheumatism,  but  a  different  light  is  thrown  upon  his  findings  by  the  over- 


ARTERIOSCLEROSIS.  349 

whelming  mass  of  clinical  evidence  brought  forward  by  Landouzy  and  Siredey 
and  by  Thayer.  The  apparent  discrepancy  is  probably  due  to  the  fact  that, 
as  Landouzy  and  Siredey  have  claimed,  typhoid  fever  not  only  produces 
immediate  lesions  but  exerts  an  especially  marked  effect  in  lowering  the 
resistance  of  the  arterial  wall  to  subsequent  infections  and  intoxications. 

In  scarlet  fever  Klotz  found  small  areas  of  necrosis  of  the  media  lying 
about  the  vasa  vasorum  which  had  been  obstructed  by  agglutinative  thrombi ; 
and  these,  on  subsidence  of  the  infection,  are  readily  replaced  by  areas  of 
fibrosis.  Similar  infiltrative  and  fibrous  changes  occur  in  other  infectious 
diseases. 

Degeneration  and  Calcification  of  the  Media. — Marchand  and,  later, 
Moenckeberg  have  called  attention  to  the  fact  that  the  ordinary  rigid  "  pipe- 
stem,"  "  beaded,"  or  "  goose-neck  "  arteries  of  old  are  produced  by  a  special 
form  of  arteriosclerosis,  which  occurs  only  in  arteries  of  the  muscular  type. 
This  type  is  characterized  by  a  pure  medial  sclerosis  (mesarteritis)  or,  more 
accurately,  a  necrosis  (arterionecrosis),  most  marked  in  the  deeper  layers 
of  the  media,  accompanied  by  fatty  changes,  necrosis  of  the  elastic  and  muscle 
fibres  and  especially  by  the  deposition  of  calcifications  in  masses  in  the  necrotic 
areas  and  in  rows  of  fine  granules  between  the  elastic  and  muscle  fibres.  These 
calcifications  often  follow  the  transverse  fibres  around  the  artery  in  rings, 
which  cause  it  to  give  to  the  palpating  finger  a  sensation  like  that. of  a  goose's 
trachea. 

Occasionally,  especially  when  the  calcification  is  of  long  duration,  ossi- 
fication takes  place  in  the  calcified  areas,  with  the  formation  of  true  bone  in 
the  walls  of  the  arteries. 

Calcareous  mesarteritis  is  very  common  in  the  femoral,  radial,  temporal, 
and  dorsalis  pedis  arteries,  and,  owing  to  the  striking  changes  in  the  walls 
of  the  arteries,  it  represents  the  most  easily  diagnosed  of  all  the  forms  of  arterio- 
sclerosis. On  the  other  hand,  since  it  attacks  only  the  arteries  of  the  muscular 
type,  its  presence  furnishes  no  clue  to  the  condition  in  the  aorta.  It  is  usually 
much  more  marked  in  some  arteries  than  in  others,  and  hence,  although 
changes  of  this  type  may  go  on  in  the  coronary  arteries,  these  also  cannot 
be  prophesied  from  the  condition  of  the  radials.  For  the  same  reason,  the 
most  extreme  changes  of  this  type  may  be  noticed  in  the  radials  of  patients 
whose  blood-pressure  is  absolutely  normal,  or  even  below  normal,  owing  to  the 
fact  that  the  changes  in  the  arteries  are  purely  local  ones. 

Periarteritis. — The  most  striking  form  of  inflammation  of  the  adventitia 
is  the  so-called  periarteritis  nodosa  (Kussmaul  and  Mayer,  1865),  or  supra- 
arterial  fibroid  nodules;  small  grayish  nodules  1-2  mm.  in  diameter,  located 
along  the  course  of  the  vessels  affected,  most  commonly  the  coronary,  renal, 
or  mesenteric  arteries,  though  it  also  occurs  along  the  arteries  of  the  muscles, 
the  stomach,  the  genitalia,  diaphragm,  peritoneum,  and  more  rarely  in  the 
cervical  arteries,  bladder,  adrenals,  brain,  lungs,  and  pleura  (Moenckeberg). 
The  lesions  are  frequently  accompanied  by  the  formation  of  small  multiple 
aneurisms,  owing  to  the  weakness  of  the  medial  coat. 

Histologically  the  lesions  consist  of  areas  of  fibrous  tissue  occurring  along 
the  course  of  the  vasa  vasorum  and  represent  processes  very  similar  to 
those  which  occur  within  the  media  in  infective  mesarteritis.  The  strik- 
ing difference  is  that,  whereas  the  fibrosis  of  mesarteritis  replaces  a  dense 


350 


DISEASES  OF  THE  HEART  AND  AORTA, 

PLATE  XVII. 

A. 


INT. 


MED. 


ADV. 
Endarteritis  with  thickening  of  intima  in  a  patient  dying  from  typhoid  fever  without  complications 


B. 


Degeneration  of  the  media  of  a  cerebral  artery,  showing  destruction  of  the  elastic  fibres* 
which  are  stained  black. 


Radial  artery  showing  great  hypertrophy  of  tunica  media.     (After  W.  Russell.) 


ARTERIOSCLEROSIS. 
PLATE  .XVII  (Continued). 
D.  E. 


351 


INT 


MED 


ADV 


ADV 


MED 


Syphilitic   aortitis   showing  destruction 
of  the  elastic  fibres  in  the  media  and  their  Mononuclear   infiltration   along  the  course 

replacement  by  fibrous  tissue:  INT,  intima;  of  the  vasa  vasorum  of  adventitia  and  media  in 

MED,  media;  ADV,  adventitia.  syphilitic  aortitis. 


F. 


G. 


WHmmSSm'^mSKBr^MM^BX^m 


4l*gj 

.  0 

i    . 

■  M '  ■ 

* 

; 

■  ■  £ 

Endarteritis  productiva  et  obliterans  in  the 
vasa  vasorum  and  periarteritis  of  the  latter  in  a 
case  of  syphilitic  aortitis. 


Treponemata  (spiro- 
chatffi)  from  the  wall  of  an 
aneurism.  (After  Wright 
and  Richardson.) 


352 


DISEASES  OF  THE  HEART  AND  AORTA. 


tissue  already  formed,  the  fibrosis  of  periarteritis  represents  a  new  formation 
which  is  located  in  a  very  scant  amount  of  loose  tissue  and  rises  exuberantly 
above  it. 

The  inflammation  usually  extends  further  along  the  vasa  vasorum  into 
the  media,  whose  elastic  and  muscle  fibres  it  destroys,  and  passes  into  the 
intima  to  produce  an  area  of  proliferative  endarteritis. 

As  regards  etiology,  Kussmaul  and  Mayer,  Chvostek  and  Weichselbaum, 
Miiller  and  Graf,  regard  syphilis  as  the  most  common  cause,  while  Fletcher, 
v.  Kahldan  and  a  host  of  others,  among  them  Moenckeberg,  describe  cases 

in  which  lues  could  not  have  played  a  role.  Intes- 
tinal intoxication,  congenital  weakness  of  the  vascu- 
lar tissues,  polymyositis  and  polyneuritis,  all  seem 
to  play  roles  in  certain  cases  (Moenckeberg). 

Tuberculous  Arteritis  and  Aortitis.  —  In  the 
ordinary  forms  of  chronic  tuberculosis  the  only 
change  in  blood-vessels  outside  the  area  of  the 
lesion  is,  as  a  rule,  the  presence  of  small  areas  of 
fatty  degeneration  in  the  cells  of  the  intima  and 
media  (Frothingham) .  It  is  only  in  the  more  severe 
forms  of  tuberculous  infection  when  the  germs  are 
circulating  freely  in  the  blood  that  diffuse  arteritis 
occurs. 

In  localized  tuberculous  lesions  the  bacilli  may 
gradually  invade  the  walls  of  the  smaller  vessels 
per  extensionem,  and  it  is,  as  a  rule,  the  rupture 
of  tubercles  in  the  intima  of  one  of  the  smaller  vessels 
that  gives  rise  to  generalized  tuberculosis.  In  the 
latter  condition  the  presence  of  miliary  tubercles 
in  the  walls  of  the  vessels  is  not  infrequent,  particu- 
larly in  the  small  pulmonary  vessels  and  in  the 
small  meningeal  branches  in  tuberculous  meningitis. 
Tubercles  in  the  wall  of  the  aorta,  on  the  other  hand, 
are  rare,  and  Woolley,  who  has  recently  reviewed 
the  subject,  has  found  accounts  of  only  ten  cases 
besides  his  own. 

In  most  of  these  cases  the  tuberculosis  arose  by 
extension  from  tuberculous  lymph-glands,  but  in 
several  the  lesions  existed  in  the  form  of  solitary 
tubercles  of  the  intima,  measuring  from  one  to  four 
centimetres  and  occasionally  surmounted  with  polypoid  growths.  In  all  these 
cases  the  tubercles  contained  very  large  numbers  of  tubercle  bacilli,  so  that 
their  rupture  might  easily  give  rise  to  a  wide-spread  infection. 


Fig.  156. — Arteriosclerosis 
of  the  descending  aorta,  show- 
ing atheromatous  plaques. 


ETIOLOGY. 


The  most  important  etiological  factors  in  the  production  of  arterio- 
sclerosis in  man  are  age,  hard  work,  alcohol,  syphilis,  and  the  more  acute 
infectious  diseases,  especially  typhoid  fever.  The  relative  frequency  of 
these  causal  factors,  as  indicated  by  the  palpability  of  the  radial  artery  in 


ARTERIOSCLEROSIS.  353 

4000  consecutive  cases  admitted  to  the  Johns  Hopkins  Hospital,  has  been 
made  the  subject  of  a  careful  study  by  Thayer  and  Brush. 

These  observers  found  palpable  arteries  in  the  following  percentage  of  the  patients 
under  fifty  years  who  had  been  subject  to  various  etiological  factors: 

After  scarlatina,  radials  palpable  in 16.4  per  cent. 

No  causal  factor,  radials  palpable  in 16.5  per  cent. 

Pneumonia,  radials  palpable  in 17     per  cent. 

Diphtheria,  radials  palpable  in 17     per  cent. 

Malaria,  radials  palpable  in 20     per  cent. 

Typhoid  fever,  radials  palpable  in 26     per  cent. 

Rheumatism,  radials  palpable  in 34     per  cent. 

Alcohol,  radials  palpable  in 46.8  per  cent. 

Hard  work,  radials  palpable  in 57.5  per  cent. 

Richard  Cabot  takes  exception  to  these  findings  of  the  high  frequency  of  arteriosclerosis 
after  alcohol,  basing  his  conclusions  upon  autopsies  of  dipsomaniacs  under  fifty,  in  whom 
he  says  arteriosclerosis  was  not  present  in  more  than  twenty  per  cent.  His  exceptions  to 
Thayer's  findings  are,  however,  somewhat  against  the  general  consensus  of  opinion,  as  well 
as  against  the  experimental  evidence  of  Aubertin,  who  produced  arteriosclerosis  and  cardiac 
hypertrophy  in  rabbits  by  the  injection  of  alcohol.  On  the  other  hand,  Cabot  is  supported 
by  Fahr,  who  performed  309  autopsies  on  habitual  drunkards  dying  at  the  Harbor  Hospital 
of  Hamburg  and  found  arteriosclerotic  changes  no  more  common  than  in  abstemious  indi- 
viduals, occurring  in  95  cases,  82  of  whom  were  over  40  years  of  age.  Only  7  drunkards  in 
his  series  died  before  40  from  causes  referable  to  arteriosclerosis.  Similar  changes  existed  in 
only  six  other  persons  under  40.  Unlike  Aubertin,  Fahr  was  unable  to  produce  arterio- 
sclerosis in  rabbits  by  administration  of  alcohol  for  over  two  years.  From  this  it  would 
appear  that  the  evil  effects  of  alcohol  have  been  considerably  exaggerated,  at  least  as  far 
as  the  arteries  are  concerned.  It  must  be  borne  in  mind  that  indulgence  in  a  certain 
amount  of  alcohol  is  almost  universal,  especially  in  those  persons  who  do  hard  work,  hence 
it  is  extremely  difficult  to  segregate  these  factors  in  any  large  number  of  cases.  If,  for 
example,  a  patient  has  had  typhoid  fever,  has  used  alcohol,  and  has  done  hard  work,  it  is 
not  logical  to  enter  his  name  into  each  of  the  three  columns,  for  it  is  not  possible  to  deter- 
mine which  of  the  factors  is  the  most  important. 

Fortunately,  however,  for  the  decision  of  these  doubtful  points,  the  experiments 
of  Pic  and  Bonnamour  (1.  c.)  upon  experimental  adrenalin  arteriosclerosis  have  shown 
that  where  two  factors  are  acting  together,  arteriosclerosis  may  be  pro- 
duced in  conditions  in  which  it  could  not  be  brought  about  by  one  of  them  alone. 
Thus,  tuberculosis  +  adrenalin  yielded  arteriosclerosis  in  young  rabbits  which  would 
not  have  shown  arteriosclerosis  after  adrenalin  alone,  and  there  is  no  doubt  that  the 
same  is  true  in  man. 

Syphilis,  as  stated  above,  is  an  important  factor,  especially  in 
persons  under  the  age  of  thirty-five.  Pearce  (Arch.  Int.  Med.,  1910,  vi,  478) 
has  tabulated  the  results  of  a  large  number  of  observers,  showing  the  Wasser- 
mann  reaction  positive  in  57  cases  of  mesaortitis,  negative  in  70;  positive 
in  29  cases  of  endaortitis,  negative  in  214;  in  aortic  insufficiency,  positive  in 
85,  negative  in  122.  Collins,  Sachs,  Clough,  Guthrie,  Longcope,  and  others 
call  attention  to  its  great  frequency  in  the  sclerotic  form. 

Worry  and  continued  pain  have  long  been  regarded  by 
clinicians  as  causes  of  arteriosclerosis,  but  a  physiological  basis  for  this  belief 
was  not  found  until  Cannon  and  de  la  Paz  (Am.  J.  Physiol.,  1911,  xxviii,  64) 
showed  that  the  blood  obtained  by  catheter  from  the  adrenal  vein  of  a  cat 
excited  by  the  presence  of  a  dog  contained  more  adrenalin  than  that  obtained 
when  the  animal  was  quiet. 
23 


354  DISEASES  OF  THE  HEART  AND  AORTA. 

Lead  poisoning  (especially  chronic  plumbism)  and  gout  are 
important  etiological  factors,  as  is  also  chronic  nephritis.  Overeating 
is  thought  to  play  an  important  r61e;  especially  when  the  diet  is  rich  in  meats, 
sweetbreads,  livers,  kidneys,  etc. — in  other  words,  in  purin  bodies  and  in 
kreatin.  The  exact  role  of  these  substances  has  not  been  carefully  studied, 
although  Croftan  found  that  long-continued  injection  of  0.5  to  5.0  mg.  xanthin 
into  rabbits  caused  a  rise  of  forty  millimetres  in  blood-pressure,  as  well  as 
sclerotic  changes  at  least  in  the  renal  arteries.  (He  does  not  describe  the 
condition  of  the  other  arteries.)  Barger  and  Walpole  (Jour.  Physiol.,  1909, 
xxxviii,  pages  xxii  and  xxiii)  find  that  the  pressor  amines  which  are  found  in 
protein  putrefaction  by  the  liberation  of  C02  from  the  amino-acids  have  an 
intense  action  upon  the  vasomotor  mechanism  and  blood-pressure.  It  is 
therefore  quite  natural  that  overeating  would  rank  with  hard  work  as  a 
main  cause  of  arteriosclerosis,  but  the  exact  extent  of  its  occurrence  is  more 
difficult  to  determine  in  a  large  series  of  cases  than  in  an  individual  case 
in  private  practice. 

Lastly,  and  still  more  important,  in  the  etiology  of  arteriosclerosis,  are 
age  and  heredity  (Israel). 

Thus,  Osier  states  that  "entire  families  sometimes  show  this  tendency  to  early 
arteriosclerosis,  a  tendency  which  cannot  be  explained  in  any  other  way  than  that  in  the 
make-up  of  the  machine  bad  material  was  used  for  the  tubing."  This  is  especially  true  as 
regards  alcoholism,  as  has  been  shown  in  a  recent  statistical  study  by  Emerson,  who  found 
that  this  factor  was  of  more  importance  than  the  drinking  of  alcohol  by  the  individual 
himself  in  determining  arteriosclerosis  and  longevity,  and  that  an  alcoholic  ancestry  was 
very  frequently  followed  by  a  generation  with  a  tendency  to  early  arteriosclerosis. 

Experimental  Arterionecrosis  in  Animals. — A  most  interesting  side 
light  upon  the  genesis  of  arteriosclerosis  has  been  thrown  by  attempts  to 
produce  it  experimentally  in  animals,  especially  in  rabbits  and  guinea- 
pigs.  The  lesions  which  have  been  produced  cannot  be  termed  true  arterio- 
sclerosis like  that  seen  in  man,  but  are  confined  to  the  media  and  adventitia, 
the  intima  always  remaining  clear.  The  reason  for  this  is  not  evident. 
Even  the  possibility  that  in  these  small  animals  the  blood  supply  of  the 
arterial  wall  is  different  from  that  in  man,  and  that  owing  to  this  difference 
lesions  occur  most  readily  in  the  media,  does  not  hold,  since  Ophuls  has 
demonstrated  the  occurrence  of  spontaneous  endarteritis  in  rabbits.  The 
experimental  and  clinical  conditions  seem  to  be  closely  analogous,  but  it 
is  not  possible  to  draw  an  absolute  parallelism  between  them. 

Gilbert  and  Lion  have  been  able  to  produce  arteriosclerosis  experimentally  in  ani- 
mals by  the  injection  of  bacterial  toxins,  and  this  has  been  confirmed  by  Klotz. 
This  fact  is  of  great  importance,  not  only  from  the  stand-point  of  experimental  arterio- 
sclerosis, but  also  because  it  establishes  the  importance  of  bacterial  disease  in  the  etiology 
of  arteriosclerosis  met  with  clinically. 

The  earliest  observation  of  arteriosclerosis  brought  about  by  toxic  action  of  organic 
compounds,  and  one  which  establishes  beyond  doubt  the  deleterious  action  of  tobacco 
upon  the  arteries,  is  that  of  Isaac  Adler,  demonstrating  sclerosis  in  the  smaller  peripheral 
arteries  of  rabbits  as  a  result  of  feeding  them  with  infusions  of  tobacco.  Boveri  confirmed 
these  results  by  giving  infusion  of  tobacco  by  stomach-tube,  and  obtained  atheromatous 
plaques  or  thickening  at  the  base  of  the  aorta  in  ten  out  of  sixteen  rabbits,  while  Baylac 
obtained  sclerosis  in  each  of  eight  rabbits  into  which  tobacco  infusion  was  injected  eithe! 
intravenously  or  subcutaneously.  Jebrowsky  and  later  W.  E.  Lee  have  produced  it  in 
rabbits  made  to  inhale  tobacco  smoke.    From  Baylac's  experiments  it  would  appear  that 


ARTERIOSCLEROSIS.  355 

in  general  the  liability  to  occurrence  bears  some  relation  to  the  channel  by  which  it  enters 
the  body.  This  may  explain  the  very  marked  action  of  tobacco  inhaled  and  entering  the 
heart  directly  from  the  pulmonary  circulation  in  smokers,  as  compared  with  the  somewhat 
milder  effects  of  chewing  tobacco,  under  which  condition  the  nicotine  passes  through  and 
is  perhaps  somewhat  attenuated  in  the  liver  before  entering  the  systemic  circulation, 
and  has  still  to  pass  through  the  venae  cavae,  right  heart,  and  pulmonary  circulation  before 
reaching  the  coronary  circulation.  In  smoking,  however,  the  nicotine  enters  through 
the  lungs  and  strikes  its  first  blow  at  the  coronary  arteries  and  base  of  the  aorta,  where  the 
elastic  fibres  are  under  the  greatest  tension  and  hence  most  liable  to  degeneration.  It  is, 
therefore,  easy  to  understand  why  smoking  of  heavy  cigars  should  be  one  of  the  most 
potent  factors  in  the  etiology  of  arteriosclerosis  and  coronary  sclerosis. 

An  almost  new  era  in  the  study  of  arteriosclerosis  was,  however,  introduced  by  the 
discovery  of  Josue  that  the  repeated  intravenous  injection  of  adrenalin 
into  rabbits  brought  about  sclerosis  and  calcification  in  the  aorta  within  a  few  weeks. 
This  was  very  soon  confirmed  by  W.  Erb,  Jr.,  who  produced  the  lesions  in  a  large  number 
of  animals,  and  demonstrated  the  considerable  uniformity  with  which  such  lesions  fol- 
lowed the  injections.  Similar  results  have  been  obtained  in  rabbits  by  Fischer  by  the 
intravenous  injection  of  a  very  large  number  of  substances, — hydrochloric  acid, 
phosphoric  acid,  lactic  acid,  calcium  phosphate,  c  hlo  r  alamide, 
mercuric  chloride,  trypsin,  diuretin,  and  physiological  salt  solu- 
tion, so  that  the  effect  can  scarcely  be  considered  as  specific  for  adrenalin.1 

On  the  other  hand,  Pic  and  Bonnamour,  as  well  as  Adler  and  Hensel,  have  called 
attention  to  the  fact  that  in  none  of  the  series  of  experiments  published  did  more  than  a 
certain  number  of  the  animals  injected  show  lesions,  and  in  a  very  large  series  the  latter 
showed  that  it  was  practically  impossible  to  produce  arteriosclerosis  in  rabbits  by  these 
poisons  until  they  had  attained  a  certain  age.  After  that  age  arteriosclerosis  occa- 
sionally occurred  spontaneously,  but  could  be  brought  on  with  considerable  frequency  by 
the  injection  of  toxic  substances.  As  stated  above,  Pic  and  Bonnamour  have,  however, 
been  able  to  produce  it  in  young  animals  whose  vitality  was  diminished  by  tuberculosis, 
etc.,  indicating  that  disease  may  be  an  accessory  factor  in  diminishing  the  resistance  of 
the  arteries  to  toxic  influences  which  ordinarily  leave  no  traces.  This  carries  the  clinical 
corollary  that  persons  liable  to  arteriosclerotic  changes  should  particularly  avoid  all  con- 
tributing factors  (alcohol,  tobacco,  hard  work,  etc.)  for  some  time  after  infectious  diseases. 

Hypercholesterinsemia. — Anitschkow  (Beitr.  z.  path.  Anat.,  1914,  lix,  306J  claims  to 
have  been  able  to  produce  endarteritis  by  feeding  cholesterin  to  rabbits,  but  these  observa- 
tions lack  confirmation.  However,  H.  B.  Schmidt  (Arch.  Int.  Med.,  1914,  xiii,  121)  finds 
hypercholestersemia  in  arteriosclerotics  with  hypertension,  but  that  hypercholesterin- 
semia also  occurs  in  jaundice  and  other  conditions  without  high  blood-pressure. 

Mechanism  Producing  Experimental  Arteriosclerosis.  —  The  mechanism  by  which 
arteriosclerosis  is  produced  has  been  the  object  of  considerable  study.  In  the  case  of 
adrenalin  at  least,  Erb  believes  that  a  spasm  of  the  vasa  vasorum  takes 
place,  bringing  about  an  insufficient  blood  supply  to  the  coats  of  the  vessels,  and  thereby 
ischaemic  degeneration  of  the  latter,  especially  of  the  tunica  media.  This  view  was  also 
shared  by  Pearce  and  Stanton  and  other  observers,  but  Fleisher  and  Loeb  have  shown 
that  considerable  areas  of  aorta  may  be  kept  ischaemic  by  com- 
pression without  producing  arteriosclerosis.  The  factor  must ,  therefore, 
be  toxic.  It  is  possible  that  in  some  cases  with  high  blood-pressure  actual  rupture  of  the 
weakened  elastic  fibres  takes  place,  which  serves  as  a  centre  for  areas  of  necrosis.  W.  H. 
Harvey  has  shown  that  if  bits  of  excised  aorta  are  filled  with  agar  under  various  pressures 
and  then  transplanted  into  subcutaneous  tissue,  those  under  tension  degen- 
erate more  rapidly.  The  same  is  probably  true  of  the  fibres  within  the  artery. 
Moreover,  Josue  has  shown  that  repeated  injections  of  adrenalin  in  the  rabbit  are  followed 
by  permanent  rise  in  blood-pressure.  An  increase  in  blood-pressure  is  indeed  the  rule  in 
arteriosclerosis,  although,  as  Hasenfeld  has  pointed  out,  it  occurs  mainly  in  persons  whose 
sclerosis  involves  the  splanchnic  arteries.  Neither  increase  in  blood-pressure  nor  hypertro- 
phy of  the  heart  necessarily  occurs  in  patients  where  these  vessels  are  not  involved.    The 

XA  summary  of  the  recent  literature  upon  this  point  will  be  found  in  the  papers  of 
Saltykow,  Adler,  and  Benda. 


356 


DISEASES   OF  THE  HEART   AND  AORTA. 


reason  for  this  may  be  that  the  cutting  down  of  the  circulation  of  so  large  an  area  as  the 
splanchnic  region  in  itself  increases  the  resistance  to  blood  flow  and  thereby  raises  pressure. 
There  is  also  no  doubt  that,  besides  the  single  artery  involved  in  the  sclerosis,  the  latter  is 
often  the  result  of  prolonged  vasomotor  spasm  in  the  femoral  artery,  etc.  On  the  other 
hand,  such  spasm  may  be  transitory  and  be  accompanied  by  temporary  rise  of  blood-pres- 
sure and  sensory  phenomena  which  cause  the  syndromes  described  by  Pal  as  vasomotor 
crises  (see  page  368).  Aubertin,  Vaquez,  and  Wiesel  have  found  hyperplasia  of  the 
adrenals  in  arteriosclerotic  persons,  while  A.  E.  Cohn  found  the  same  in  patients  without 
arteriosclerosis.  Moreover,  Fraenkel  (Arch,  of  Exper.  Path.  u.  Pharmakol.,  1909,  lx,  394) 
found  increased  adrenalin  in  blood  of  only  a  small  percentage  of  hypertension  cases.  It 
therefore  seems  quite  possible,  in  the  light  of  these  findings,  that  hypertrophy  of  the  heart 
and  arteriosclerosis  may  often  be  the  result  of  a  hypersecretion  of  adrenalin, 
perhaps  also  of  some  other  internal  secretions.  Why  this  should  be  associated  with 
splanchnic  arteriosclerosis  is  easy  to  see.  The  latter  condition  tends  to  diminish  the  circu- 
lation through  the  abdominal  viscera,  and  more  blood  is  thus  shunted  through  the  adrenal 
arteries  which  lie  just  above  the  mesenteries,  thus  bringing  about  an  increase  in  adrenal 
secretion. 

It  may  be  added  that  Bayer,  in  Krehl's  clinic,  has  shown  that  some- 
times the  high  blood-pressure  is,  in  part  at  least,  dependent  upon  the  amount 
of  salt  in  the  food,  being  low  on  salt-free  and  high  on  diet  rich  in  salt,  though 
this  is  by  no  means  the  rule. 

DISTRIBUTION    OF   ARTERIOSCLEROTIC   LESIONS. 

As  regards  the  distribution  of  arteriosclerotic  lesions  and  its  relations 
to  etiology,  Harlow  Brooks  has  given  the  following  statistical  summary  based 
upon  the  notes  of  autopsies  on  400  cases: 


Artery. 


Etiological  factors. 


Aorta 

Visceral  trunks 

Coronary  arteries 

Brain 

Renal 

Pancreas  

Hepatic 

Splenic 

Lungs 

Cceliac  axis  and  branches. 

Spinal  vessels 


Alcohol  149,  among  laborers  118,  nephritis  51,  syph- 
ilis 38,  old  age  38.     Males  275,  females  125. 


Alcohol  107,  nephritis  35,  syphilis  27,  excessive 
tobacco  9. 

Alcohol  48,  nephritis  21,  syphilis  19. 

Alcohol  43,  nephritis  10,  syphilis  10. 

Alcohol  19,  syphilis  9,  senility  9. 

Alcohol  12,  nephritis  8,  syphilis  6,  senility  3. 

Alcohol  9,  syphilis  7,  nephritis  4,  endocarditis  2, 
senility  2,  tuberculosis  2. 

Syphilis  5,  senility  5,  alcohol  4,  tuberculosis  4, 
nephritis  2. 

Most  of  them  with  alcoholism.  Sclerosis  of  mesen- 
teric, all  cases  with  adiposis. 

Alcoholic  4,  syphilitic  4,  most  of  the  rest  in  primary 
spinal  diseases. 


ARTERIOSCLEROSIS   IN   THE   YOUNG. 

Arteriosclerosis  in  infants,  children,  and  young  persons  while  rare  is 
not  extremely  so. 

According  to  Fremont  Smith,  who  has  given  an  excellent  review  of  the  subject, 
congenital  syphilis  is  the  cause  in  about  forty  per  cent,  of  the  cases,  and  diphtheria,  scarlet 
fever,  and  typhoid  fever,  as  well  as  infections  in  the  mother  during  pregnancy,  are  impor- 
tant factors.  The  blood-pressure  is  not  usually  elevated,  often  being  as  low  as  70  mm. 
Hg.    The  writer  has  seen  one  case  of  a  boy  aged  six  suffering  from  acute  nephritis,  com- 


ARTERIOSCLEROSIS.  357 

plicated  by  lobar  pneumonia,  large  bacillus  coli  abscess  of  the  buttocks,  cystitis  caused  by 
the  same  germ,  who  in  spite  of  continuously  low  blood-pressure  developed  tortuous  and 
apparently  thickened  temporal  and  thickened  radial  arteries.  After  a  few  months  these 
arteries  were  no  longer  palpable.  It  is  possible  that  these  changes  may  have  been  merely 
mononuclear  infiltration  about  the  vessels  of  the  adventitia. 

CLINICAL   MANIFESTATIONS   OF   ARTERIOSCLEROSIS. 

Clinically,  the  symptoms  due  to  arteriosclerosis  usually  express 
themselves  in  several  groups  dependent  upon  the  arteries  most  affected. 

(1)  Cardiac,  associated  with  myocarditis  and  coronary  sclerosis; 
often  with  renal  symptoms  (see  Chapter  IX).  As  shown  by  Fleisher  and 
Loeb,  the  myocarditis  may  be  produced  by  the  same  cause  and  may  be  more 
severe  than  the  arteriosclerosis  itself. 

(2)  Simple  coronary  sclerosis,  paroxysmal  dyspnoea,  angina 
pectoris,  Adams-Stokes  syndrome,  paroxysmal  tachycardia,  sudden  death. 

(3)  Cerebral    symptoms. 

(4)  Aneurism. 

(5)  Intermittent  claudication. 

(6)  Vasomotor  crises  (Pal) : 

(a)  Abdominal  pain  from  vasoconstriction; 

(6)  Raynaud's  disease; 

(c)  Pain  down  arms  and  legs. 
The  clinical  characteristics  of  the  cardiac  and  renal  cases  have  been 
discussed  in  Chapter  I X  under  the  head  of  the  myocarditis  which 
invariably  accompanies  them.  They  may  be  briefly  summarized  as  short- 
ness of  breath,  especially  on  exertion,  often  asthmatic  or  paroxysmal 
in  character;  palpitation;  weakness  ;  occasionally  a  considerable  degree 
of  nervousness,  loss  of  memory,  and  insomnia.  In  advanced  cases 
with  some  sclerosis  of  cerebral  arteries  there  may  be  more  or  less  transient 
irrationality,  especially  at  night  or  on  awakening.  There  may  be 
pains  over  the  precordium,  in  the  shoulders,  or  down  the  arms,  or  in  the 
abdomen  or  legs,  which  may  be  definitely  associated  with  periods  of  high 
blood-pressure  (the  vasomotor  crises  of  Pal) ;  there  may  be  sudden  pain 
and  sudden  paralysis  of  a  leg,  disappearing  on  rest,  reappearing 
after  a  few  steps  are  taken  (intermittent  claudication,  Charcot,  Erb);  or 
there  may  be  severe  precordial  pain  with  a  feeling  of  weight  and  constriction 
over  the  sternum  and  an  utterable  fear  of  impending  death  (angina  pectoris). 
On  the  other  hand,  the  hand  or  foot  may  become  cold  or  numb,  the 
pulsation  disappear  from  the  arteries,  intense  pain  set  in  (Raynaud's  disease), 
or  finally  be  followed  by  gangrene  (thromboangitis  obliterans).  Still  further 
the  patient  may  suffer  from  all  the  signs  and  symptoms  of  aneurism. 

On  physical  examination  the  radial  arteries  may  or  may  not  be 
found  to  be  thickened  or  beaded  (atheromatous),1  dependent 
partly  upon  the  distribution  of  the  sclerosis,  since  the  radial  artery  may  be 
spared.  Some  writers  state,  however,  that  in  men  who  do  hard  manual  labor 
the  radial  arteries  are  the  first  attacked,  while  in  those  who  lead  a  sedentary 
life  sclerosis  may  appear  very  early  about  the  base  of  the  aorta,  and  the 
radial,  nevertheless,  may  be  perfectly  normal. 

1  Wertheim  Salamonson  (Arch,  des  malad.  du  cceur,  1910,  iii,  688)  recommends  feel- 
ing the  wall  of  the  artery  with  the  finger-nail  instead  of  the  finger. 


358 


DISEASES   OF   THE   HEART    AND    AORTA. 


The  artery  in  which  the  sclerosis  is  next  most  readily  observed  is  the 
temporal,  which  usually  stands  out  like  a  cord  or  is  very  tortuous,  and  when 
pressed  against  the  bone  feels  thickened  and  leathery.  This  tortuosity 
may  also  be  present  in  the  brachials  and  even  in  the  abdominal  aorta,  and 
is  probably  brought  about  by  the  stress  of  the  arterial  tension  exerted  upon 
the  walls,  which  are  in  some  places  weaker  and  less  elastic  than  in  others; 
so  that  we  have  a  force  (blood-pressure)  which  is  exerted  equally  on  all 
sides  against  walls  which  interpose  a  greater  resistance  on  one  side  than  on 
the  other,  hence  the  curvature  results.    As  might  be  expected,  the  tortu- 

ousness  is  therefore  greater  when  the  disturbing 
force  is  high  (high  blood-pressure)  and  less  when 
it  is  low,  as  shown  in  the  figure  (Fig.  157). 

Other  superficial  arteries  which  may  be  felt 
are  the  brachials,  axillaries,  facials,  popliteals,  and 
dorsalis  pedis. 

Changes  in  the  Retinal  Vessels.  —  Hirschberg 
in  1882  called  attention  to  the  fact  that  changes 
in  the  retinal  vessels  constitute  an  early  sign  of 
arteriosclerosis,  and  later  demonstrated  that  this 
change  was  normal  in  old  persons  and  usually  began 
in  the  fifth  decade.  Friedenwald  and  Preston  exam- 
ined twenty-three  persons  suffering  from  general 
arteriosclerosis,  and  found  only  seven  normal  reti- 
nas among  them. 

De  Schweinitz  gives  the  following  criteria  for  sclerosis  of 
the  retinal  vessels : 

(1)  Suggestive  Signs. — Uneven  caliber  and  undue  tortu- 
ousness  of  the  retinal  arteries  (corkscrew  form),  increased  dis- 
tinctness of  the  central  light  streak,  an  unusually  light  color  of 
the  artery,  and  alterations  in  the  course  and  caliber  of  the  veins. 

(2)  Pathognomonic  Signs. — Changes  in  si/e  and  breadth 
of  the  arteries,  loss  of  translucency,  lesions  in  the  arterial  walls 
consisting  of  white  stripes  in  the  form  of  perivasculitis,  inden- 
tation of  the  veins  by  the  stiffened  arteries,  tortuousness  of 

veins  and  white  stripes  or  varicosities  along  their  courses,  cedema  of  the  retina  in  the 
form  of  gray  opacity  around  the  disk  or  following  the  course  of  the  vessels,  hemorrhages 
as  linear  extravasations  or  roundish  infiltrations.  Sometimes  very  sudden  changes  in 
the  caliber  of  the  retinal  arteries  may  be  seen  accompanying  vasomotor  crises. 


Fig.  157. — Tortuous  radial 
artery.  (After  Pal.)  Solid  line, 
course  of  the  radial  artery  at 
200  mm.  Hg  blood-pressure. 
Broken  line,  course  of  the  ar- 
tery at  95  mm.  blood-pressure, 
after  amyl  nitrite. 


X-ray  Examination. — Absolute  proof  of  arteriosclerosis  is  also  given 
by  the  X-ray,  by  which  calcified  plaques  along  the  course  of  deeply  situated 
arteries  (popliteals,  femorals,  abdominal  aorta,  etc.)  may  be  discerned  as 
distinct  shadows  ranged  along  the  course  of  the  artery.  These  may  be 
brought  out  more  distinctly  by  using  two  stereoscopic  pictures  instead  of 
Unfortunately,  it  has  not  been  possible  to  discern  sclerosis  of  the 


one 


coronary  arteries  in  this  way. 

Sclerosis  of  the  Abdominal  Aorta. — Arteriosclerosis  of  the  abdominal 
aorta  and  splanchnic  vessels  is  very  common,  as  has  been  shown  by  Hasen- 
feld,  Bond,  Brooks,  Ortner,  and  Gilbride.  In  fact,  it  may  almost  be  diagnosed 
with  certainty  when  the  blood-pressure  is  elevated.  Occasionally  the  course 
of  the  abdominal  aorta  may  be  felt  to  be  tortuous.    Sclerosis  of  the  abdom- 


Fig.  158. — Retinal  changes  in  arteriosclerosis.  A,  Normal  fundus.  B  to  F,  successive  changes 
occurring  in  arteriosclerosis,  including  pallid  arteries  (B),  later  assuming  a  silver-wire  appearance  (C); 
indented  veins  (B,  C),  afterward  showing  ampulliform  enlargements  (D,  E);  corkscrew  capillaries  (C,  D); 
corkscrew  arteries  and  veins  (D,  E);  perivasculitis  (C.  D);  sclerosis  of  vessels  (F);  cedema  of  disk 
(B,  C,  D,  E),  hemorrhages  (C  F).— D.     (After  de  Schweinitz.) 


ARTERIOSCLEROSIS. 


359 


inal  vessels  is  not  infrequently  accompanied  by  great  flatulence  with  pains 
not  unlike  those  of  tabes  (abdominal  vasomotor  crises),  but  these  may 
also  be  present  from  simple  pulsation  of  the  abdominal  aorta  when  tugging 
upon  loose  peritoneal  moorings.  Sclerosis  of  the  pancreatic  artery  is  often 
accompanied  by  diabetes  mellitus. 

BLOOD-PRESSURE    AND    PULSE. 

In  arteriosclerosis  the  mechanical  factors  affecting  blood-pressure 
tend  to  approach  those  in  a  system  of  rigid  tubes, — a  high  pressure  through- 
out systole,  a  low  pressure  in  diastole.  In  such  a  system  we  should  have, 
as  a  rule,  a  greater  difference  between  pressure  in  systole  and  in  diastole 
than  when  the  normal  elasticity  tends  to  keep  up  the  diastolic  pressure, 
so  that  the  pulse-pressure  is  often  more  than  50  to  60  mm.  rather  than  being 
nearer  30  or  40  mm.  as  in  the  normal  individual. 


r  ig.  159. — Effect  of  arteriosclerosis  upon  the  circulation.  I,  normal.  II,  arteriosclerosis,  with 
high  peripheral  resistance  and  anacrotic  form  of  pulse  wave;  the  arrow  points  to  a  rise  in  maximal  and 
minimal  pressure  and  increased  pulse-pressure.  Ill,  arteriosclerosis  with  low  peripheral  resistance, 
showing  low  blood-pressure  and  increased  pulse-pressure  and  collapsing  pulse.    (Compare  with  Fig.  26.) 

Pulse. — The  pulse  may  assume  any  form  whatever,  from  collapsing 
and  almost  water-hammer  in  character  to  an  anacrotic  plateau,  or  even 
in  rare  cases  to  a  pulsus  tardus.  These  depend  upon  the  relation  between 
strength  and  size  of  beat  and  outflow  through  the  arterioles.  Thus,  if  the 
peripheral  arteries  or  any  large  areas  of  blood-channels  are  dilated  and 
lacking  in  elasticity,  there  will  be  a  momentary  rise  in  pressure  at  the  begin- 
ning until  the  pressure  wave  is  transmitted  from  the  aorta  to  the  periphery. 
When  it  reaches  this  point  there  is  a  sudden  outflow  through  those  vessels 
and  a  sudden  fall  or  collapse,  which  is  greater  than  it  would  be  in  a  more 
elastic  system  (see  Fig.  159).  On  the  other  hand,  if  the  peripheral  outflow 
is  small,  the  pressure  in  the  non-elastic  system  quickly  rises  higher  than 
in  an  elastic  system  and  remains  so  throughout  systole,  forming  a  systolic 
plateau  (anacrotic  pulse)  with  a  large  rapid  rise  and  plateau  reaching  to 
the  end  of  systole,  then  a  gradual  fall  during  diastole.  The  pulse  form 
accordingly  gives  us  the  information  in  arteriosclerosis  as  in  other  condi- 
tions (see  page  66),  — namely,  indicates  low  peripheral  resistance  when 
it  is  collapsing  and  high  peripheral  resistance  when  it  is  anacrotic  or  sus- 


360 


DISEASES  OF  THE  HEART  AND  AORTA. 


tained.  The  pulse  may  either  be  quite  large  or  very  small,  dependent  upon 
the  degree  either  of  vasoconstriction  or  of  endarteritis.  Its  character  may 
be  very  variable ;  it  may  be  quite  quick  and  collapsing,  corresponding  to  a 
general  rigidity  of  the  whole  vascular  system,  or  the  vessel  may  fill  rapidly, 
remain  well  sustained  with  long  systolic  plateau,  and  may  then  decline 
either  rapidly  or  slowly.  However,  the  lumen  of  the  radial  artery  may 
have  decreased  so  much  from  an  endarteritis  that  the  filling  of  the  artery 
is  slow  and  the  up-stroke  on  the  pulse-tracing  very  oblique,  just  as  would 
be  typical  of  aortic  stenosis.  This  is  not  extremely  common,  and  the  very 
quick  up-stroke  is  the  form  most  frequently  seen.  On  the  other  hand,  in 
rarer  cases  when,  as  Romberg  and  also  Hasenfeld  have  pointed  out,  the 
splanchnic  vessels  are  not  involved,  the  maximal  blood-pressure  may  be 
quite  normal  (110-120  mm.)  and  the  minimal  also  (90  mm.). 

Blood=pressure.  —  The  blood-pressure  is  often  high.  Thayer  found 
in  his  studies  of  post-typhoid  arteriosclerosis  that  the  maximal  blood- 
pressure  was  usually  20-30  mm.  higher  than  for  normal  individuals  of 
corresponding  age. 

Romberg  and  Sawada,  on  the  other  hand,  found  that  this  occurred  in  only 
12.5  per  cent,  of  all  arteriosclerotics,  while  Groedel  found  hypertension  in  only  37 
per  cent,  of  446  cases  of  arteriosclerosis  free  from  chronic  nephritis.  Dunin  found 
similar  results.  Israel,  however,  found  hypertension — over  140  mm.  Hg  or  180  cm. 
H20  (v.  Recklinghausen  apparatus) —  in  64.4  per  cent,  of  45  cases  of  arteriosclerosis.  The 
minimal  pressure  was  also  increased,  but  less  than  the  maximal.  Israel  gives  the 
following  average  figures: 


Normal — 

cm.  H20 

mm.  Hg 

Arteriosclerosis — 

cm.  H20 

mm.  Hg 

Average  increase — 

mm.  Hg 


Max. 

Min. 

Mean. 

170 

110 

140 

125 

81 

103 

240 

140 

190 

177 

103 

140 

52 

23 

37 

Pulse- pressure 
(amplitude). 


60 

44 

100 

74 

30 


Israel's  figures  accord  well  with  the  writer's  experience  (using  the  Erlanger  apparatus). 
The  highest  of  these  blood-pressures  are  seen  in  cases  with  chronic  nephritis  (Israel,  Jane- 
way,  Horner).  The  writer  has  often  found  a  maximal  pressure  of  220  mm.  Hg  with  a  mini- 
mal of  160,  though  usually  in  association  with  nephritis.1 

As  has  been  seen  under  cardiac  overstrain,  the  presence  of  arterio- 
sclerosis has  a  marked  effect  in  impairing  the  bodily  strength  and  the  ability 
to  withstand  strain.  The  diminution  in  arterial  bed  increases  the  total 
work  of  the  heart,  and  the  patches  of  arterial  fibrosis  prevent  the  arteries 
from  dilating  under  functional  activity.  On  the  other  hand,  the  loss  of 
arterial  elasticity  removes  a  factor  which  tends  to  propel  the  blood  during 
diastole  and  thus  to  maintain  the  blood  flow  at  the  least  expenditure  of 
energy  by  the  heart.  As  a  result  of  this  factor,  the  heart  is  compelled  to 
increase  its  systolic  output  (increased  pulse-pressure)  under  normal  condi- 

1  Russell  has  shown  that  these  determinations  may  be  too  high  in  thick-walled  arte- 
lies  (see  page  28). 


ARTERIOSCLEROSIS.  361 

tions  and  hence  has  little  ability  for  further  increase  in  reserve.  Muscular 
effort  therefore  gives  rise  to  signs  of  greater  strain  than  in  normal  individ- 
uals, greater  increase  in  blood-pressure,  and  greater  fatigue. 

The  intensity  of  vasomotor  reactions  varies  considerably  in  different 
cases  of  arteriosclerosis.  In  some  cases,  as  Romberg  has  shown,  the  vaso- 
motor reaction  of  the  arm  vessels  to  cold  may  entirely  disappear;  while  in 
others  (vasomotor  crises)  the  reactions  are  so  intense  as  to  produce  ischsemia 
of  the  parts. 

The  Second  Aortic  Sound. — Corresponding  to  the  high  blood-pressure 
there  is  also  accentuation  of  the  second  aortic  sound,  which  on  the  one  hand 
may  be  due  to  the  heightened  blood-pressure  and  the  greater  tension  of  the 
aortic  valves,  or,  on  the  other,  to  the  thickening  and  partial  calcification 
of  the  valves  themselves,  which  gives  rise  to  a  louder  sound  than  usual 
when  the  valves  strike  together,  even  under  the  usual  pressure.  A  marked 
accentuation  of  the  aortic  second  sound  therefore  always  leads  to  the 
suspicion  of  arteriosclerosis,  even  in  the  absence  of  thickening  in  the  walls 
of  the  superficial  vessels.  However,  it  is  not  pathognomonic,  since  it  may 
often  be  heard  in  cases  where  no  special  sclerosis  is  present,  especially  at 
times  when  the  heart  is  acting  strongly  and  probably  giving  forth  a  larger 
output  into  the  aorta  at  each  systole,  as  in  typhoids  with  dicrotic  pulse 
or  in  perfectly  healthy  young  persons  during  attacks  of  palpitation.  In 
such  cases  the  accentuation  of  the  second  sound  is  transitory. 

BLOOD    COUNT    IN    ARTERIOSCLEROSIS. 

The  blood  count  may  vary  considerably,  first  on  account  of  the  great 
variety  of  diseases  associated  with  arteriosclerosis,  and  secondly,  because 
the  latter  is  sometimes  accompanied  by  polycythemia  or  erythremia. 

There  are  no  blood  changes  which  in  themselves  can  be  said  to  be  defi- 
nitely associated  with  arteriosclerosis. 

AORTIC    SCLEROSIS. 

When  the  aortitis  near  the  base  of  the  aorta  is  marked,  and  especially 
if  calcified  plaques  are  present,  the  first  sound  as  well  as  the  second  may  be 
changed  and  may  be  accompanied  by  a  loud  murmur  which  is  usually  trans- 
mitted to  the  carotid  and  brachial  arteries,  resembling  that  heard  in  aortic 
stenosis  but  less  intense.  Since  the  condition  is  much  more  common  than 
the  latter,  this  murmur  is  also  more  commonly  due  to  this  cause,  but  in 
the  absence  of  the  characteristic  pulse  it  is  quite  indistinguishable  from 
that  of  aortic  stenosis,  for  both  arise  at  the  same  site  at  the  same  time  and 
are  transmitted  in  the  same  way.  The  murmur  is  often  accompanied  by 
a  marked  thrill  having  the  same  distribution  and  is  followed  by  a  distinct 
diastolic  shock. 

As  regards  sclerosis  of  the  aorta  alone,  Bittorf  has  found  that  it  frequently  occurs  at 
an  average  age  of  fifty-five  (forty-five  in  syphilitics)  as  a  result  of  the  usual  factors;  some- 
times a  single  trauma  to  the  chest  may  seem  to  be  the  important  moment  in  the  etiology. 
It  is  especially  common  in  syphilitics  and  fat  persons,  and  is  frequently  associated  with 
pale,  ashy-gray  color,  very  high  blood-pressure  (170  to  220  mm.),  occasionally  difference 
in  size  of  the  pupils,  pains  over  the  chest  and  down  the  arms,  oedema  over  the  sternum, 


362  DISEASES  OF  THE  HEART  AND  AORTA. 

unilateral  dilatation  of  veins  in  second  and  third  interspaces,  ringing  aortic  second  sound 
without  diastolic  murmur,  hypertrophy  of  the  heart,  often  pulsus  celer,  rarely  pulsus 
tardus  or  pulsus  paradoxus.  Cardiac  pain  may  be  present,  often  felt  just  after  percus- 
sion, and  described  as  something  boring  through  the  sternum,  sometimes  with  a  feeling  of 
constriction,  sometimes  radiating  to  the  arms  and  neck.  Occasionally  spells  of  weakness 
in  the  arms  may  be  felt  not  unlike  intermittent  claudication. 

The  differential  diagnosis  from  aortic  stenosis  is  made  by  the  gradual 
up-stroke  on  the  pulse  tracing  in  the  latter  case,  as  contrasted  with  the  sudden  up-stroke 
and  plateau  in  the  former;  from  aortic  insufficiency  by  the  diastolic  murmur  and  high 
pulse-pressure;  from  aneurism  by  the  percussion  and  fluoroscopic  findings.  R.  Knox  (Arch. 
Roentg.  Ray,  1910,  147)  has  been  able  to  recognize  atheromatous  plaques  in  the  aorta  with 
the  X-ray. 

SCLEROSIS  OF  THE  PULMONARY  ARTERY. 

Sclerosis  of  the  pulmonary  artery  may  occur  whenever  there  is  increased  work  of  the 
right  heart,  especially  in  mitral  stenosis,  emphysema,  and  phthisis.  Giroux  (Arch,  des 
malad.  du  cceur,  1910,  iii,  595)  finds  that  the  lesion  usually  consists  of  opaque  yellow  ath- 
eromatous patches  in  the  arteries  near  the  hilus,  rarely  in  the  main  trunks;  but  in  the  latter 
there  may  be  a  mesarteritis  which  may  lead  to  pulmonary  insufficiency.  Clinically,  the 
cases  are  characterized  by  headaches,  giddiness,  shortness  of  breath,  a  tendency  to  pulmo- 
nary hemorrhage,  and  a  peculiar  purplish  cyanosis  of  hands  and  face.  The  pulmonic 
second  sound  is  very  loud;  but  a  systolic  murmur  may  be  present  over  the  pulmonary 
area  or  a  diastolic  (pulmonary  insufficiency)  be  transmitted  down  the  left  sternal  margin. 

Case  of  Primary  Pulmonary  Sclerosis. 

Romberg  reports  the  case  of  a  man,  aged  24,  who  had  had  no  infectious  diseases 
except  measles  as  a  child  and  a  recent  slight  muscular  rheumatism,  three  months  after 
which  he  began  to  have  gradually  increasing  shortness  of  breath,  epigastric 
pressure,  occasional  headaches  and  giddiness,  and  his  color  became  very  blue.  On  exami- 
nation he  showed  marked  cyanosis  over  the  face,  body,  and  limbs.  There  was 
a  pulsation  due  to  the  right  ventricle'in  the  fourth  interspace  4  cm.  inside  the  mammillary 
line  and  thence  inward  to  the  sternum,  also  a  smaller  pulsation  (left  ventricle)  in  the  fifth 
interspace  mammillary  line,  cardiac  dulness  7  cm.  to  right,  15  cm.  to  left.  Both  pulmonic 
sounds  were  louder  than  the  aortic.  Pulse  small,  regular,  116.  Liver  enlarged;  spleen 
enlarged.    No  cedema;  no  swelling  of  vessels  of  neck. 

Probable  diagnosis  (Curschmann),  congenital  heart  lesion.  Patient  gradually  became 
worse;  digitalis  was  without  effect.    Died  one  month  after  admission. 

Autopsy  showed  enlarged  heart;  right  ventricle  hypertrophied 
and  forms  the  entire  apex,  and  the  conus  arteriosus  and  right  auricle  are 
especially  hypertrophied.  All  the  valves  intact  and  normal;  aorta  free  from  sclero- 
sis, but  unusually  small.  Ductus  arteriosus  closed.  Tremendous  sclerosis  and 
atheroma  of  the  pulmonary  artery  and  all  its  branches.1 

Sanders  has  recently  collected  similar  cases  from  the  literature. 

TREATMENT. 

The  general  treatment  of  arteriosclerosis  is  mainly  prophylactic,  hygienic, 
and  dietetic,  and  actual  specific  treatment  is  of  far  less  value. 

Diet. — Carefully  selected  diet  is  a  most  important  factor,  restriction 
being  in  both  quality  and  quantity.  The  general  diet  given  in 
heart  cases  (see  page  235)  is  of  great  benefit  here,  or  equivalent  diets  with 

1  Notes  of  a  case  of  pulmonary  arteriosclerosis  (O.  A.  K.)  secondary  to  mitral  stenosis 
are  given  on  p.  453. 


ARTERIOSCLEROSIS.  363 

this  as  a  basis.  However,  in  simple  arteriosclerosis  the  quantity  taken  at 
a  time  need  not  be  so  greatly  restricted;  but  the  total  quantity  in  twenty- 
four  hours  should  not  exceed  twenty-five  hundred  calories,  and  should 
always  be  near  the  lower  level  for  proteids,  and  as  free  as  possible  of  purin 
bodies  (nitrogenous  extractives  such  as  are  found  in  meat),  creatinin,  etc., 
and  also  of  salt.  The  more  recent  studies  quoted  above  seem  to  indicate 
that  excess  in  salt  is  almost  as  injurious  as  are  excesses  in  alcohol,  and  that 
the  salt  mackerel  of  Boston  is  as  dangerous  as  the  beer  of  Milwaukee.  For 
the  sclerotic  danger  probably  lurks  in  the  Smithfield  ham  or  the  cold  smoked 
tongue  as  well  as  in  the  Baltimore  rye  or  the  Martini  cocktail  (Beyer,  Barie, 
Hadfield).  The  patient's  safety  lies  in  milk,  eggs,  potatoes,  bread,  other 
carbohydrates,  butter,  and  the  simpler  fruits. 

Restriction  of  Liquids.  —  On  the  other  hand,  the  liquid  intake  also 
should  not  be  excessive,  since  drinking  large  amounts  either  of  water  or 
of  beer  seems  to  favor  sclerosis  (Krehl),  but  the  amount  ingested  should 
remain  in  the  vicinity  of  fifteen  hundred  cubic  centimetres  a  day,  some 
persons  thriving  best  at  five  hundred  cubic  centimetres  above,  some  at 
five  hundred  cubic  centimetres  below  this  level. 

Tobacco  and  alcohol  should  be  dispensed  with  entirely  if  possible; 
if  the  patient  insists  on  taking  small  quantities,  one  or  two  light  dry  cigars, 
as  thin  as  possible  (Lee),  or  "stogies,"  a  day  are  perhaps  the  mildest  that 
one  may  prescribe.  Cigarette  smoke  is  usually  inhaled  and  pipes  are  very 
heavy.     Thick  Havana  cigars  should  be  entirely  prohibited. 

As  to  alcohol,  if  the  patient  insists  upon  taking  a  small  quantity, 
this  should  be  limited  to  an  occasional  glass  of  claret  or  white  wine,  or 
perhaps  a  single  glass  of  beer  at  rare  intervals.  The  latter  in  large  quan- 
tities is  especially  undesirable,  both  on  account  of  the  large  amounts  of 
liquid  taken  and  because  it  contains  both  alcohol  and  proteid  and  purin 
substances  extracted  from  the  yeast.  Gin  is  perhaps  more  dangerous 
than  whiskey. 

Coffee  and  tea  should  be  taken  in  only  small  quantities,  since 
the  vasoconstrictor  action  of  the  caffeine  favors  the  onset  of  spasmodic 
vasoconstriction  (vasomotor  crises),  and,  on  the  other  hand,  the  increase  of 
blood-pressure  itself  brought  on  by  caffeine  is  damaging  to  the  arteries. 
However,  it  must  be  stated  that,  in  contrast  to  nicotine,  lead,  adrenalin, 
etc.,  injections  of  caffeine  into  animals  have  thus  far  failed  to  bring  on 
arteriosclerosis  and  that  perhaps  the  deleterious  effect  of  caffeine  may  be 
overestimated. 

Hydrotherapy. — Systematic  hydrotherapy  is  of  considerable  value  in 
arteriosclerosis,  especially  the  use  of  warm  baths,  warm  douches 
(Brieger),  or  alternating  warm  and  cold  douches  (Riley)  applied  both  locally 
and  generally.  They  owe  their  efficacy  to  the  vasodilatation  which  they 
bring  about,  and  hence  must  be  classed  in  effect  with  the  drugs  of  the  nitrite 
group.  In  most  cases  the  effect  of  a  good  warm  douche  or  warm  bath  is 
more  marked  and  more  lasting  than  that  of  any  of  these  drugs,  and  it  is 
further  devoid  of  that  certain  residuum  of  deleterious  effect  which  all 
drugs  leave  behind  them.  So  that,  while  one  cannot  agree  with  Brieger 
that  arteriosclerosis  can  be  entirely  cured  symptomatically  by  proper 
hydrotherapy,  nevertheless  warm   baths    and   warm   showers 


364  DISEASES   OF  THE   HEART   AND    AORTA. 

once  or  twice  a  day  should  be  an  indispensable  part 
of  the  treatment  of  every  arteriosclerotic.  Cold  baths 
should  be  avoided,  since  they  precipitate  vasomotor  reactions,  which  in 
the  arteriosclerotic  may  amount  to  vasoconstrictor  spasm. 

Drugs.  —  Potassium  Iodide. — As  to  drugs,  universal  experience  points 
to  the  efficacy  of  potassium  iodide  in  doses  ascending  from  0.3 
Gm.  (gr.  v)  t.i.d.,  p.c,  to  as  high  as  4  Gm.  (5i);  some  clinicians  favor- 
ing the  smaller,  some  the  larger  doses.  In  the  writer's  experience  doses 
under  1  Gm.  (gr.  xv)  seem  to  have  some  effect  in  alleviating  symptoms; 
and  when  there  is  a  suspicion  of  lues  the  dose  should  be  increased  still 
further.  (The  therapeutic  action  and  its  limitations  are  discussed  in 
Chapter  V.) 

It  has  been  attempted  to  settle  the  question  experimentally  by  deter- 
mining the  effect  of  potassium  iodide  upon  the  course  of  adrenalin  atheroma 
in  rabbits.  Koranyi,  Boveri,  and  Cummins  and  Stout,  who  were  the  first 
to  undertake  these  investigations,  all  reported  that  potassium  iodide  or 
iodipin,  when  injected  during  the  time  that  adrenalin  was  being  injected, 
inhibited  the  production  of  atheroma.  However,  it  must  be  borne  in  mind 
that  Biland,  Loeb  and  Githens,  Adler  and  Hensel  found  that  large  doses 
of  potassium  iodide  seemed  to  increase  rather  than  inhibit  the  atheromatous 
changes.  For  persons  who  cannot  tolerate  iodides  in  sufficient  doses,  sajodin, 
iodipin,  or  some  other  iodine  derivative  which  has  fewer  unpleasant  gastric 
and  cutanteous  effects  may  be  used,  often  with  great  satisfaction. 

Salvarsan. — Salvarsan  is  as  dangerous  a  remedy  in  most  cases  of  arterio- 
sclerosis as  in  myocarditis,  and  the  indications  and  contraindications  are 
about  the  same  (see  pages  273  and  274). 

Nitrites. — Next  to  the  iodides  in  general  use  is  the  group  of  nitrites, — 
amyl  nitrite,  nitroglycerin,  sodium  nitrite,  erythrol  tetranitrate.  These 
drugs  are  of  value  for  symptomatic  treatment,  to  relieve  pain  or  discomfort 
for  the  time  being,  but  they  exercise  no  inhibitory  influences  upon  the  prog- 
ress of  the  arteriosclerosis,  as  has  been  shown  for  adrenalin  arteriosclerosis. 
On  the  other  hand,  their  effect  upon  the  symptoms  due  to  arteriosclerosis, 
the  pain  of  intermittent  claudication,  of  angina  pectoris,  of  the  abdominal 
and  peripheral  vascular  crises,  is  most  remarkable,  and  in  this  regard  they 
are  invaluable  (Lauder  Brunton).  However,  in  their  administration  it 
must  be  borne  in  mind  that  persons  with  arteriosclerosis  seem  to  have 
considerable  tolerance  for  nitrites  (page  270),  and  to  bring  about  vasodila- 
tation and  fall  in  blood-pressure  much  larger  doses  must  be  given  than  is 
necessary  to  produce  the  effect  in  normal  individuals.  Accordingly,  as 
indicated  in  Chapter  V,  the  drug  should  be  administered  in  increasing 
doses  until  the  physiological  effect  (flushing,  throbbing  in  head,  ringing 
of  the  ears)  is  obtained,  and  then  continued  in  a  close  just  a  little  smaller 
than  this.  One  need  not  be  surprised,  however,  to  find  that  this  dose  for 
a  person  with  arteriosclerosis,  particularly  a  colored  person,  may  be  ten 
or  even  twenty  times  the  average  dose  for  a  normal  individual.  When 
such  is  the  case  the  blood-pressure  is  probably  a  beneficial  compensatory 
phenomenon,  and  the  nitrites  should  be  discontinued. 

In  the  chronic  hypertension  of  arteriosclerosis  venesection  is 
not  only  useless  but  often  harmful. 


ARTERIOSCLEROSIS.  365 

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Thayer,  W.  S.,  and  Brush,  C.  E.:  The  Relation  of  Acute  Infectious  Diseases  to  Arterio- 
sclerosis, J.  Am.  M.  Assoc,  Chicago,  1904,  xliii,  726. 
Cabot,  R.  C:  The  Relation  of  Alcohol  to  Arteriosclerosis,  ibid.,  1904,  xliii,  774 
Fahr:  Zur  Frage  des  chronischen  Alcoholismus,  Verhandl.  d.  deutsch.  Path.  Gesellsch., 

Jena,  1909,  xhi,  162;  abstracted  in  editorial:  The  Pathology  of  Chronic  Alcoholism, 

J.  Am.  M.  Assoc,  Chicago,  1909,  Ihi,  1824. 
Heiberg,  Heller.    Quoted  from  Ophuls. 
Croftan,  A.  C. :  The  Role  of  Alloxuric  Bases  in  Nephritis,  Am.  J.  M.  Sci.,  Phila.,  1900,  cxx, 

593. 
Israel:  Ueber  erworbene  Storungen  in  den  Elasticitatsverhaltnissen  der  grossen  Gefasse, 

Arch.  f.  path.  Anat.,  etc.,  Berl.,  1886,  ciii,  461. 
Osier,  W.:  The  Principles  and  Practice  of  Medicine,  N.  York  and  Lond.,  5th  ed.,  1903. 
Emerson,  C.  P. :  Personal  communication. 
Brooks,  H.:  A  Preliminary  Study  of  Visceral  Arteriosclerosis,  Am.  J.  M.  Sci.,  Phila.  and 

N.  York,  1906,  cxxxi,  778. 
Gilbert,  A.,  and  Lion,  G.:  Arterites  infectueuses  experimentales,  Compt.  rend.  Soc  de 

Biol.,  Par.,  1889,  583;  Arch,  de  med.  exper.,  Par.,  1904,  xvi,  73. 
Adler,  I.:  Remarks  on  Arteriosclerosis,  Med.  Rec,  N.  York,  1902,  lxi,  721;  J.  M.  Research, 

Bost.,  1902,  vih,  309.    The  Present  Status  of  Experimental  Arterial  Disease,  Am.  J. 

M.  Sc,  Phila.  and  N.  York,  1908,  cxxxvi,  241. 
Benda,  C:  Ergebn.  d.  Pathol.,  herausg.  v.  Lubarsch  und  Ostertag,  Leipz.,  1907-08,  xi. 

Die  Arteriosklerose  (Atherosklerose),  Therap.  d.  Gegenw.,  Berl.,  1909,  1,  121. 
Saltykow:  Experimentelle  Forschung  in  der  Lehre  der  Arteriosklerose,  Zentralbl.  f.  d. 

ges.  Physiol,  u.  Path.  d.  Stoffwechsels,  Berl.,  1908,  iii,  654. 
Baylac:  Atherome  experimental  de  l'aorte  consecutif  a  Faction  du  tabac,  Compt.  rend. 

Soc  de  Biol.,  Paris,  1906,  lx,  935. 
Jebrowsky  and  Lee.    See  p.  717. 
Josue,  O.:  Atherome  aortique  experimental  par  injections  repetees  d'adrenaline  dans  les 

veines,  Compt.  rend.  Soc.  de  Biol.,  Par.,  1903,  lv,  1374,  and  Presse  med.,  1903,  ii,  798. 
Fischer,  B.:  Ueber  Arterienerkrankungen  nach  Adrenalininjektionen,  Verhandl.  d.  Kong. 

f.  innere  Med.,  Wiesbaden,  1905,  xxii,  235. 
Pic  and  Bonnamour:  Contribution  a  l'etude  du  determinisme  de  1'atheroma  aortique 

experimental,  Compt.  rend.  Soc.  de  Biol.,  Par.,  1905,  lviii,  219. 
Adler,  I.,  and  Hensel,  O.:  Studies  on  So-called  Experimental  Arteriosclerosis,  Trans.  Asso. 

Am.  Physicians,  Phila.,  1907,  xxii,  683. 
Erb,  W.,  Jr.:  Experimentelle  und  histologische  Studien  ueber    Arterienerkrankung   nach 

Adrenalininjektionen,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,    1905,  liii,    173. 
Harvey,  W.  H. :  Studies  on  the  Influence  of  Tension  in  the  Degeneration  of  Elastic  Fibres 

of  Buried  Aorta,  J.  Exper.  Med.,  N.  York,  1906,  viii,  388. 
Pearce,  R.  M.,  and  Stanton,  E.  McD. :  Experimental  Arteriosclerosis,  J.  Exper.  M.,  N.  York, 

1906,  viii,  74. 


ARTERIOSCLEROSIS.  367 

Hasenfeld,  A.:   Ueber  die  Herzhypertrophie  bei  Arteriosklerose,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  lix,  193. 
Bond,  C.  S.:  Clinical  Observations  of  Arteriosclerosis  from  Alimentary  Toxins,  Trans. 

Asso.  Am.  Phys.,  Phila.,  1906,  xxi,  73. 
Ortner,  N.:    Zur  Klinik  der  Angiosklerose  der  Darmarterien,  Volkmann's  Samml.  klin. 

Vortr.,  Leipz.,  N.  S.  No.  347. 
Gilbride,  J.  J.:  Gastrointestinal  Disturbances  due  to  Arteriosclerosis,  J.  Am.  M.  Asso., 

Chicago,  1909,  lii,  955. 
Hamburger,  W.:  Beitrage  zur  Atherosklerose  der  Magenarterie,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1909,  xcvii,  49  (with  excellent  bibliography). 
Hasenfeld.    Quoted  on  p.  398. 
Pal,  J. :  Die  Gefasskrisen,  Leipz. >  1905. 
Vaquez,  Aubertin,  Wiesel.    See  p.  291. 
Bayer,  R.:  Ueber  den  Einfluss  des  Kochsalzes  auf  die  arteriosklerotische  Hypertonic, 

Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1907,  Ivii,  162. 
Fremont-Smith,  F. :  Arteriosclerosis  in  the  Young,  Am.  J.  M.  Sc,  Phila.  and  N.  Y.,  1908, 

cxxxv,  199. 
Hirschberg:  Centralbl.  f.  prakt.  Augenheilk.,  1882,  vi,  329.    Quoted  from  de  Schweinitz. 
Raehlmann:  Ueber  ophthalmoskopisch  sichtgare  Erkrankung  des  Netzhautgefasse  bei 

allgemeiner  Arteriosklerose,  Ztschr.  f.  klin.  Med.,  Berl.,  1889,  xvi,  606. 
Friedenwald,  H.:  Report  on  the  Ophthalmoscopic  Examination  of  Dr.  Preston's  Cases 

of  Arteriosclerosis,  J.  Am.  Asso.,  Chicago,  1891,  xvi,  623. 
De  Schweinitz,  G. :  Intra-ocular  Angiosclerosis,  and  its  Prognostic  and  Diagnostic  Sig- 
nificance, Internat.  Clinics,  Phila.,  1907,  17th  Ser.,  vol.  i,  177. 
Romberg  and  Hasenfeld.    Quoted  on  p.  291. 

Romberg,  E.:  Ueber  Arteriosklerose,  Verh.  d.  Kong.  f.  innere  Med.,  Wiesb.,  1904,  xxi,  60. 
Sawada:  Blutdruckmessung  bei  Arteriosklerose,  Deutsch.  med.  Wchnschr.,  1904,  xxx,  425. 
Groedel:  Ueber  den  Wert  der  Blutdruckmessung  fiir  die  Behandlung  der  Arteriosklerose, 

Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb.,  1904,  xxi,  113. 
Israel,  A.:  Klinische  Beobachtungen  ueber  das  Symptom  der  Hypertension,  Samml.  klin, 

Vertr.,  Leipz.,  1907.    Innere  Med.,  Nos.  135-136. 
Janeway  and  Horner.    Quoted  on  p.  54. 
Bittorf,  A.:  Zur  Symptomatologie  der  Aortensklerose,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1904,  lxxxi,  65. 
Romberg,  E. :  Ueber  Sklerose  der   Lungenarterie,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1891,  xlviii,  197. 
Sanders,  W.  E.:  Primary  Pulmonary  Arteriosclerosis  with  Hypertrophy  of  the  Right 

Ventricle,  Arch.  Int.  Med.,  Chicago,  1909,  iii,  257. 
Rogers,  L. :  Extensive  Atheroma  and  Dilatation  of  the  Pulmonary  Arteries,  without  Marked 

Valvular  Lesions,  as  a  not  very  Rare  Cause  of  Cardiac  Disease  in  Bengal,  Quart. 

J.  Med.,  Oxford,  1908-9,  ii,  1. 
Brieger,  L.:  Clinical  Lectures  at  the  Hydrotherapeutische  Anstalt  der  Kgl.  Poliklinik, 

Berlin,  1906. 
Riley:  Blatter  f.  klin.  Hydrotherap.,  1898;  cited  from  Buxbaum,  B.,  Lehrbuch  der  Hydro- 

therapie,  Leipz.,  1903. 
Senator,  H.:    Ueber  die  Arteriosklerose  und  ihre  Behandlung,  Therap.  d.  Begenw.,  Berl., 

1907,  xlviii,  97. 
Koranyi,  V.:  Ueber  die  Wirkung  des  Iods  auf  die  durch  Adrenalin  erzeugte  Arterione- 

krose.  Deutsch.  med.  Wchnschr.,  Leipz.,  1908,  xxxii,  679. 
Boveri,  P.:  Contributo  alio  studio  degli  ateromi  aortici  sperimentali,  Clin.  med.  ital., 

Milano,  1906,  xlv,  41. 
Cummins,  W.  T.,  and  Stout,  P.  S.:  Experimental  Arteriosclerosis  by  Adrenalin  Inocula- 
tions and  the  Effect  of  Potassium  Iodide,  Univ.  Penn.  M.  Bull.,  Phila.,  1906-7,  xLx,  101. 
Biland,  J. :  Ueber  die  durch  Nebennierenpraparate  gesetzten  Gefass-  und  Organverander- 

ungen,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  lxxxvii,  413. 
Loeb,  L.,  and  Githens,  T.  C:  The  Effect  of  Experimental  Conditions  on  the  Vascular 

Lesions  Produced  by  Adrenalin,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1905,  cxxx,  568. 
Loeb,  L.,  and  Fleisher,  M.  S.:  Influence  of  Iodine  Preparations  on  the  Vascular  Lesions 

Produced  by  Adrenalin,  ibid.,  1907,  cxxxiii,  903. 


XI. 

VASOMOTOR  CRISES  AND  THE  ANGIONEUROTIC  LESIONS. 

VASOMOTOR     CRISES. 

GENERAL    CONSIDERATIONS. 

The  general  clinical  manifestations  of  arteriosclerosis  bear  a  close 
relation  to  the  condition  described  by  Pal  as  "  vasomotor  crises/'  under 
which  he  includes  all  conditions  which  are  associated  with  more  or  less 
sudden  constriction  or  dilatation  of  the  arteries,  and  whose  symptoms  and 
signs  disappear  or  markedly  diminish  as  soon  as  this  paroxysmal  change  in 
the  blood-vessels  passes  off.    There  are  accordingly 

(1)  Vasoconstrictor  crises,  usually  associated  with  hypertension. 

(2)  Vasodilator  (hypotension)  crises. 

The  vasoconstrictor  crises  Pal  divided  into 

(1)  Abdominal  type.  (2)  Pectoral  type.  (3)  Cerebral  type.  (4)  Crises  in  the  ex- 
tremities.   (5)  Crises  in  the  large  arteries. 

The  vasodilator  crises  according  to  Pal  include 

(1)  Ordinary  syncope.  (2)  Surgical  shock.  (3)  Collapse  after  infectious  disease 
or  most  poisonings.  (4)  Erythromelalgia  and  many  other  "trophic"  skin  disease.1  (5) 
Occasional  cases  of  tabes  with  lancinating  pains  and  low  blood-pressure.  (6)  Various 
attacks  of  weakness  in  Addison's  disease. 

Probably  no  unit  cause  exists  for  the  crises  themselves;  the  visceral 
crises  and  lancinating  pain  in  tabes,  the  painter's  colic,  the  ursemic  con- 
vulsion, the  delirium  of  the  cerebral  sclerotic,  the  pain  of  angina  pectoris, 
and  the  attack  of  cardiac  asthma  seem  to  have  little  etiology  in  common 
except  their  relation  to  the  sympathetic  nerves.1  However,  all  manifest 
high  blood-pressure,  and,  according  to  Pal,  all  are  relieved  by  artificial 
depression  of  blood-pressure.  It  is,  therefore,  not  unlikely  that,  however 
diverse  the  ultimate  causes  of  the  condition,  the  cause  of  the  symptoms 
is  high  blood-pressure  with  localized  vasoconstriction.  The  variation  in 
the  areas  of  constriction  in  regions  whose  arteries  are  already  sclerotic 
accounts  for  the  occurrence  of  the  different  symptom  complexes. 

As  to  treatment,  the  statements  of  Pal  would  lead  one  to  believe  that 
they  are  all  relieved  by  vasodilators,  especially  nitro- 
glycerin and  the  nitrites,  occasionally  by  sodium  thiocyanate, 
and  that  marked  improvement  results  while  the  blood-pressure  is  lowered. 
The  symptoms  return  if  the  blood-pressure  again  rises.  (Pal,  also  Heitz, 
and  Norrero.)  However,  Prof.  Barker's  experience  at  the  Johns  Hopkins 
Hospital  does  not  warrant  such  sweeping  conclusions. 

1  The  cardinal  signs  of  sympathicotonic  should  be  carefully  tested  for  (see  page  19). 
368 


VASOMOTOR   CRISES. 


363 


Case  of  Abdominal  Vasomotor  Crises.     (Quoted  from  Pal.) 

P.  V.,  sausage  maker,  aged  57,  had  rheumatism  14  years  ago,  and  for  the  past  year 
pain  and  pressure  in  the  epigastrium,  especially  on  taking  a  deep  breath.  Has  occa- 
sional paroxysms  of  extreme  dyspnoea  and  palpitation  of  the  heart,  but 
always  has  some  shortness  of  breath.  He  was  formerly  a  heavy  drinker,  now  drinks  two 
or  three  litres  of  beer  a  day  as  well  as  a  half  litre  of  wine  and  some  whiskey!  He  also 
smokes  in  moderation. 

On  admission,  April  7,  1904,  he  was  found  to  be  a  well-nourished  man,  slightly  cyanotic. 
Lungs  clear,  respiration  34.  Heart.  Maximum  impulse  in  sixth  interspace  two  fingers' 
breadth  beyond  mammillary  line.  Dulness  extends  to  third  rib  above  and  two  fingers' 
breadth  beyond  the  right  margin  of  the  sternum.  Sounds  quite  clear  at  apex  and  base, 
second  aortic  sound  not  accentuated.  Pulse 
68;  radial  walls  stiff;  blood-pressure  225. 
Liver  enlarged;  spleen  not  palpable.  Slight 
cedema  of  feet  and  legs.  Urine  2600  c.c;  sp. 
gr.  1010;  albumin  1.5  Gm.  per  litre. 

Patient  was  given  0.5  Gm.  (gr.  viii)  so- 
dium thiocyanate  t.i.d.  to  diminish  his  blood- 
pressure. 

April  21.  Patient  delirious;  blood-pres- 
sure 110.  Thiocyanate  discontinued,  where- 
upon delirium  disappears.  The  chart  in  Fig. 
160  shows  the  course  of  the  blood-pressure, 
pulse-rate,  and  respiration.  The  patient  was 
free  from  other  exceptional  symptoms  from 
April  7  to  May  1.  May  1,  8.00-11.30  a.m. 
Feels  hot  and  cold.  11.30.  Sudden  attack 
of  severe  pain  and  great  feeling  of  pressure 
in  epigastrium.  11.35.  Pains  in  back  and 
third  to  seventh  vertebra?.  Cries  out  with 
pain,  and  also  cries  "I  am  choking."  Lungs 
clear.  Cardiac  dulness  only  to  right  sternal 
margin  and  to  two  fingers'  breadth  within 
left  mammillary  line.  11.40.  Symptoms 
diminish  but  pressure  in  epigastrium  still 
present.  11.41.  Symptoms  reappear.  11.42. 
Diminution  of  symptoms,  pains  less. 


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Fig.  160- 


-Blood-pressure  chart  of  P.  V.    Typical 
vasomotor  crisis. 


A  second  severe  attack  as  before.  11.55. 
After  a  few  minutes  patient  has  a  third  momentary 
attack  with  blood-pressure  over  200  mm.  Hg,  which  then  subsides.  12.10. 
Feels  better.  12.55.  Still  better.  Free  from  attacks  until  May  3,  during  which  time  he 
receives  0.5  Gm.  (gr.  vii)  diuretin  t.i.d.  On  May  18,  sodium  thiocyanate  was 
again  given,  which  lowered  blood-pressure  but  caused  delirium. 
From  that  time  until  discharged  frequent  attacks  of  pain  and  hypertension. 

Pal  reports  similar  hypertensive  crises  in  association  with  the  colic  of 
lead  poisoning  and  also  with  the  visceral  crises  of  tabes,1  the  pain  being 
always  relieved  when  the  blood-pressure  is  brought  down  by  amyl  nitrite 
or  nitroglycerin;  as,  for  example,  in  the  following  case. 

Case  of  Abdominal  Crisis  in  Lead  Poisoning. 

X.  J.,  painter,  aged  31,  has  had  lead  colic  twice  before.  Was  free  from  it 
on  change  of  occupation,  but  it  returned  when  he  again  wTorked  in  lead.  Drinks  little; 
denies  lues.     He  has   had  abdominal  pain  for  three  weeks.     During  past  few  days  has 


1  The  claim  of  Pal  that  a  similar  association  of  pain  with  high  blood-pressure  exists 
with  the  lancinating  pains  of  limbs  cannot  be  maintained,  since  the  pains  in  his  own  cases 
are  sometimes  associated  with  hypotension,  sometimes  with  hypertension. 
24 


370 


DISEASES    OF   THE   HEART   AND    AORTA. 


had  continuous  cramps,  loss  of  appetite,  and  no  stool.  He  is  pale  and  has  a 
marked  lead  line.  Pupils  react  readily.  Lungs  clear.  Heart  normal;  pulse  rather  hard. 
Abdominal  walls  tense,  tender  on  both  sides.     Spleen  just  palpable. 

July  23.  8.30  p.m.    B.  P.  130.    Slight  pain. 

P.  170.     Increased  pain. 
Amyl   nitrite    inhalation. 
No   pain. 

Pain  again,  lasting  then  over  one-half  hour  with  same  B.  P. 
After  amyl  nitrite,  which  again  gave  relief. 
Pains  return. 
Further  increase  of  pain. 

Pains   diminish   under   amyl   nitrite. 
They  return  again,  but 
6.30a.m.     B.  P.    85.    Pains    disappear   under   amyl     nitrite. 
After  July  25,  blood-pressure  was  always  under  130  (during  last  four  days  under 
110),  the  patient  was  free  from  pain,  and  bowels  were  regular. 


8.30  p.m. 

B. 

P. 

130. 

9.10  p.m. 

P. 

68 

.    B. 

9.13  p.m. 

9.15  p.m. 

B. 

P. 

105. 

9.17  p.m. 

B. 

P. 

165. 

9.45  p.m. 

B 

P. 

95. 

9.48  p.m. 

B. 

P. 

140. 

12  M. 

160. 

4.20  a.m. 

B 

P. 

135. 

Case  Illustrating  the  Cerebral  Crises. 

The  following  case,  illustrating  what  Pal  terms  the  cerebral  type  of  vascular  crisis, 
was  under  the  writer's  care  at  the  Johns  Hopkins  Hospital: 

J.  M.  C.j  grocer,  aged   52,    who   had   suffered   repeatedly  with  myocarditis,- 
hypertrophied  heart,   irregular   pulse,    and  general   anasarca,    entered   the   Johns 

Hopkins  Hospital  in  September,  1903. 
290 
280 
270 
260 
250 


Oct.  24.  Restless  at  night.  Left  pupil 
larger  than  right:  both  react  normally. 
Nov.  2.  Very  weak.  Pulse  weak  and  irregu- 
lar.    Liver  enlarged. 

Nov.  5.  At  12.30  p.m.  began  to  complain 
of  general  discomfort  with  numbness  in  legs; 
complained  of  nervousness  and  restlessness. 
At  12.45  p.m.  the  restlessness  became 
very  .marked;  he  began  to  strike  out  with 
his  hands  and  to  try  to  get  out  of  bed.  Was 
at  this  time  conscious  and  able  to  understand 
questions.  (Blood-pressure  curve  shown  in 
Fig.  161.)  No  aphasia.  Pupils  equal  and 
dilated.  Head  and  eyes  drawn  to  right  and 
rigid.  There  was  some  twitching  of  muscles 
of  both  arms  and  hands.  Reflexes  of  right 
arm  slightly  exaggerated.  Soon  became  cya- 
notic and  vessels  of  neck  stood  out.  Be- 
came unconscious.  Respiration  stertorous. 
Blood-pressure  270  mm.  Hg.  After 
600  c.c.  of  blood  had  been  withdrawn  from  left  arm,  cyanosis  slowly  subsided,  respira- 
tion becoming  less  stertorous  and  blood-pressure  falling  to  180  mm.  Hg. 

Becomes  conscious  after  catheterization  at  7.30  p.m.  Still  picking  at  bedclothes, 
which  continued  until  next  morning.  He  was  then  mentally  clear  by  11  a.m.  and  pupils 
reacted  to  light. 

Nov.  6.  9  p.m.  Remained  clear  and  recalled  hallucinations  of  previous  night, 
realizing  them  as  hallucinations.    Blood-pressure  160. 

Had  no  further  attacks  of  this  kind  and  blood-pressure  remained  below  190. 
Died  March  28,  1904.    Autopsy  showed  chronic  myocarditis  (heart  1000  Gm.),  chronic 
adhesive  pericarditis,  coronary  sclerosis,  hydronephrosis,  and  stone  in  right  kidney.1 


SEF 

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230 

220 

210 

200 

190 

180 

170 

160 

150 

Fig.  161. — Blood-pressure  chart  showing  a  vascu- 
lar crisis  of  the  cerebral  type. 


1  It  is  possible  that  this  attack  may  have  been  due  to  transitory  cerebral  cedema 
like  that  described  by  H.  Gushing  and  James  Bordley  (Subtemporal  Decompression  in  a 
Case  of  Chronic  Nephritis  with  Uraemia;  with  Especial  Consideration  of  the  Neuro retinal 
Lesion,  Am.  J.  M.  Sc,  1908,  cxxxvi,  484). 


VASOMOTOR   CRISES.  371 


INTERMITTENT    CLAUDICATION. 


This  condition  is  always  associated  with  sclerosis  of  the  femoral, 
popliteal,  or  one  of  the  other  arteries  of  the  leg  which  are  usually  pipe-stem 
in  character.  Often  the  atheromatous  changes  are  readily  demonstrable 
by  the  X-ray.  Owing  to  the  narrowed  lumen  of  the  artery,  the  amount 
of  blood  that  can  flow  through  it  is  limited, 

but  this  is  sufficient  to  supply  the  muscle  when  jj  ha^" 

at    rest.     During   slow  walking  the    C02   pro-  Jl  S& 

duced  by  the  muscle  and  the  oxygen  needed  /*  t^^^* 

by  it  increase  greatly.     If  the  arterial  flow  is  /'       ,rJa* 

sufficient,    no    symptoms    appear;    but    when  i %ejs^ 

rapid  walking  or  running  is  begun,  there  is  a  /J%3 

sudden  increase  in  the  oxidation  in  the  muscle,      Jj£-* t 

and,  since  the  blood  supply  cannot  keep  pace  fig.  i62  —  Diagram  to  illustrate 
with  it,  asphyxia  of  both  the  muscle  and  its  ^^^ZfS^^S^. 
nerve  endings  sets  in,  accompanied  by  paralysis     SoiM  line  indicates  co2  formation 

j., TTT  ii-j_         •     ±  ■  •    •  £  during    halts    and    while    walking. 

of  the  limb  and  often  intense  pain  arising  from  Broken  ]ine  represent3  the  rapidity 
stimulation  of  the  sensory  fibres  by  the  CO,.      of  c°2  elimination.    *  indicates  the 

m,  ,.       ,.  niiiij  -r\-  »i  degree  of  CO2  accumulation  at  which 

lhe  patient  is  compelled  to  halt.  During  the  pain  sensations  set  in. 
rest  the  C02  production  falls,  and  the  slow  cir- 
culation is  able  to  carry  off  the  excess  and  to  supply  fresh  oxygen  to  the 
tissues.  With  the  renewed  aeration,  function  returns.  The  patient  is  able 
to  walk  again  until  local  asphyxia  sets  in;  and,  since  this  will  be  brought 
about  by  the  same  amount  of  C02  as  before,  his  walking  will  be  limited  to 
the  same  distance.    He  must  travel  in  stages.     (Fig.  162.) 

Case  of  Intermittext  Claudication. 

H.  E.,  carpenter,  aged  74,  complains  of  pain  in  right  foot,  drinks  beer  and  whiskey 
in  moderation,  smokes  very  little,  and  has  always  been  healthy.  In  October  toe  was  red 
and  ached.  For  the  past  ten  or  fifteen  years  patient  has  been  at- 
tacked by  severe  pains  in  both  feet,  causing  him  to  stop  in  his 
walks.  Knees  never  gave  way.  The  attacks  came  on  oftenest  during  exercise.  On 
examination,  thorax  is  emphysematous;  heart  slightly  enlarged  to  left.  Blowing  systolic 
murmur  heard  over  the  tricuspid  area,  becoming  musical  over  the  apex,  well  heard  in  the 
axilla,  but  faint  and  blowing  in  the  pulmonary  area,  where  the  second  sound  is  accentuated. 
Pulse  slightly  irregular.  Right  radial  more  sclerotic  than  left.  Blood-pressure  165  mm. 
General  reddening  from  tarsometatarsal  joints  to  the  toes  of  right  foot,  where  pulsa- 
tion of  dorsalis  pedis  is  not  felt.  Both  tibials  are  palpable,  but  pulsation 
is  well  felt.     Left  foot  normal,  artery  pulsating  well.     Both  popliteals  are  very  sclerotic. 

Given  nitroglycerin  mg.  1  (gr.  -£$)  t.i.d.,  alternating  with  sodium  nitrite  0.2  Gm. 
(gr.  hi)  t.i.d.  He  was  somewhat  improved  by  treatment,  but  left  the  hospital  a  few 
days  later. 

Prognosis. — Since  the  claudication  is  simply  part  of  the  general  arterio- 
sclerosis, the  prognosis  is  bad,  for  the  coronary  arteries,  aorta,  and  cerebral 
arteries  may  be  involved.  Sometimes,  however,  the  arterial  change  is 
confined  to  the  limbs,  occurring  simply  as  degeneration  of  the  media  with 
atheroma,  exactly  as  is  found  in  experimental  adrenalin  arteriosclerosis. 
In  that  case  the  prognosis  as  to  life  is,  of  course,  better. 


372  DISEASES   OF   THE   HEART   AND    AORTA. 


HYPOTENSIVE    VASOMOTOR    CRISES. 

The  so-called  "hypotensive"  crises  seem  to  bear  no  relation  to  arterio- 
sclerosis, but  rather  to  trauma,  action  of  toxic  substances,  and  perhaps 
to  cutaneous  diseases.  They  are  in  the  main  associated  with  depression 
of  the  vasomotor  system  and  have  been  discussed  elsewhere.  The  one 
condition  with  paroxysmal  depression  of  the  blood-pressure  which  may 
owe   its  origin  to  arteriosclerosis   is   paroxysmal   tachycardia. 

ANGEIONEUROSES. 

Maurice  Raynaud  in  1862  described  many  cases  of  this  group,  espe- 
cially of  the  condition  which  bears  his  name.  He  showed  that  the  three 
phenomena  manifested  in  these  conditions  are: 

1.  Local  syncope,  i.e.,  blanching  from  absence  or  diminution 
of  blood  in  the  arteries  of  the  .part  affected; — Raynaud's  disease  a  spas- 
modic vasoconstriction.  This  is  usually  symmetrical  in  its  distribution, 
affecting  the  ends  of  the  extremities,  i.e.,  toes,  hands  or  feet,  arms  or  legs. 
The  trouble  in  one  extremity  is  frequently  more  intense  than  in  the  other. 
Often  it  leads  to  formation  of  bullae,  ulceration,  and  to  symmetrical  gangrene 
(Raynaud's  disease). 

2.  Local  asphyxia,  i.e.,  presence  of  a  venous  blood,  that  is  to 
say  of  a  blood  insufficiently  oxygenated,  causing  blueness  of  the  part  (now 
designated  as  acrocyanosis)  with  a  distribution  corresponding  to  that  of 
Raynaud's  disease. 

3.  Local  hyperaemia,  giving  rise  to  redness  (as  in  the  condi- 
tion termed  erythromelalgia  by  Weir  Mitchell). 

Later  investigations  have  enabled  Cassirer  as  well  as  Barker  and 
Sladen  to  epitomize  the  symptoms  of  vasomotor  disease  as  follows: 

The  vasomotor  symptoms  include  (1)  hyperaemia,  (2)  syncope,  and  (3) 
asphyxia;  the  sensory,  (1)  pain,  (2)  hyperaesthesia,  (3)  anaesthesia,  (4) 
paraesthesia;  the  trophic,  (1)  ulceration,  (2)  gangrene,  (3)  dystrophies 
of  the  skin  (Barker  and  Sladen) .  They  affect  the  fingers  and  particularly 
the  toes.  The  chief  types  of  disease  are  acrocyanosis  (Cassirer),  erythro- 
melalgia (Weir  Mitchell),  and  Raynaud's  disease. 

The  symptoms  may  be  arranged  as  follows  in  ascending  scale  (Barker 
and  Sladen) : 

1.  Acrocyanosis. 

Vasomotor   symptoms — venous   stagnation   and    hyperaemia   in   fingers  and 
toes  with  cyanosis;    sensory  and  trophic  disturbances  absent. 

2.  Acroparsesthesia. 

Acrocyanosis — sensory  symptoms  (paresthesia) ,  numbness,  pain,  and  tingling. 

3.  Erythromelalgia. 

Vasomotor — hyperaemia  (arterial).     Sensory — pain. 

4.  Raynaud's  disease  (all  the  symptoms). 

Vasomotor — hyperaemia,  syncope,  and  asphyxia.     Sensory — pain,  anaesthesia, 
paraesthesia.     Trophic — gangrene  and  scleroderma. 

As  might  be  expected,  there  are  many  cases  with  symptoms  inter- 
mediate between  these  groups  and  many  transitions  from  one  to  the  other 
(Sachs). 


ANGEIONEUROSES.  373 

Pathology. — Raynaud  realized  that  the  gangrene  in  the  disease  which 
bears  his  name  differed  from  ordinary  gangrene  and  directed  his  first  inves- 
tigations to  the  state  of  the  arteries.  He  found  that,  though  the 
pulse  became  very  small  or  impalpable  during  the 
attacks  of  blanching,  it  returned  to-  normal  volume 
between  attacks.  He  made  very  careful  pathological  studies  of 
the  extremities  in  a  number  of  cases,  and  finding  the  arteries  clear  con- 
cluded that  the  trouble  was  of  vasomotor  origin,  a  view  which  he  supported 
by  demonstrating  transitory  changes  of  caliber  in  the  radial,  popliteal, 
and  retinal  arteries,  associated  with  the  attacks.  In  accordance  with  these 
studies  of  Raynaud  the  vasodilation  of  erythromelalgia  corresponds  to  a 
period  of  paralysis  of  the  vasoconstrictor  nerves  (sympathetic  paralysis) 
quite  similar  to  the  active  hypersemia  which  Claude  Bernard  produced  in 
the  rabbit's  ear  by  cutting  the  cervical  sympathetic.  Just  such  a  local 
paralysis  of  the  vasomotors  produced  by  the  overheating  of  a  hand  or  foot 
benumbed  by  cold  gives  rise  to  the  condition  of  "chilblains."  The  latter 
condition  is  always  associated  with  overheating  after  exposure  to  cold 
and  often  with  formation  of  blebs,  while  attacks  of  erythromelalgia  may 
occur  spontaneously  from  slight  emotional  or  nervous  disturbances  or  from 
slight  exposure  to  cold  without  overheating.  There  is  rarely  bleb  forma- 
tion. An  attack  of  chilblains  induced  by  overheating  may  thus  be  con- 
tinued in  spontaneous  attacks  of  erythromelalgia. 

Raynaud's  disease,  on  the  other  hand,  corresponds 
to  an  extreme  vasoconstriction,  like  that  produced 
in  ergotism.  Raynaud  himself  was  so  much  impressed  with  this 
similarity  that  he  made  searching  inquiries  in  all  his  cases  regarding  the 
character  of  rye  bread  taken,  and  conducted  an  extensive  series  of  experi- 
ments upon  ergotism  in  various  animals.  He  was  forced  to  discard  the  ergot 
hypothesis  by  the  absence  of  any  obtainable  evidence  of  ergot  ingestion, 
but  the  parallelism  between  the  two  conditions  remains. 

Case  op  Mild  Raynaud's  Disease. 

A.  S.,  a  trained  nurse,  aged  30,  was  always  healthy  until  the  age  of  nineteen,  when 
during  her  period  of  training  she  was  compelled  to  have  a  small  ovarian  cyst  and  one 
ovary  removed.  For  some  years  she  suffered  considerable  pain  from  adhesions,  so  that 
three  years  ago  these  were  broken  up  by  a  second  operation.  She  bore  the  operation 
well,  but  during  convalescence  three  weeks  later  had  a  fainting  spell,  since  when  she 
suffers  from  severe  palpitation.  For  the  past  two  years  she  has  found  that  in  cold  weather 
both  her  hands  and  forearms  become  absolutely  white,  cold,  and  numb.  This  condition  is 
soon  relieved  by  rubbing  or  by  laying  them  in  a  basin  of  warm  water,  but  is  sufficiently 
severe  to  prevent  her  from  accepting  a  very  desirable  appointment  in  a  colder  climate. 

Between  attacks  the  patient  seems  perfectly  healthy,  has  a  good  color.  All  the  arteries 
are  soft.  They  appear  to  be  of  normal  caliber  and  pulsate  normally.  The  heart  is  normal 
in  size  but  moves  7  cm.  from  left  to  right  as  the  patient  turns  from  one  side  to  the  other. 
The  right  kidney  is  also  palpable  and  very  movable.  The  rest  of  the  abdomen  and  the 
lungs  are  clear.  The  blanching  of  the  hands  occurs  less  frequently  and  less  intensely  when 
the  patient's  health  is  good,  but  it  occurs  much  more  frequently  when  the  patient  is  excited. 

Nitrites,  belladonna,  digitalis,  bromides,  and  a  large  number  of  cardiac  stimulants 
have  been  tried  by  the  patient  without  marked  effect. 


374 


DISEASES    OF   THE   HEART   AND    AORTA. 


THROMBOANGITIS     OBLITERANS. 

In  recent  years  Weiss  and  v.  Winiwarter,  and  especially  L.  Buerger, 
have  discovered  a  group  of  cases  in  which  symptoms  at  times  simulating 
those  of  the  vasomotor  trophoneuroses  are  produced  by  complete  occlu- 
sion of  the  arteries  or  veins  with  spontaneous  thrombosis  (thromboangitis 
or  thrombophlebitis  obliterans).  In  such  cases  the  largest  artery  and 
sometimes  both  artery  and  vein  become  occluded  by  a  thrombotic  process 
of  considerable  extent.  After  a  short  time  the  fresh  red  thrombi  within 
the  vessels  undergo  organization,  usually  with  permanent  obliteratipn  of 
the  lumen  by  white  fibrous  tissue.  There  is  no  proliferation  of  new  elastic 
fibres  encroaching  on  the  lumen  as  is  the  case  in  arteriosclerosis 
(Fig.  163),  though  a  few  elastic  fibres  are  found  in  the  newly  formed  blood- 
vessels. 

A  B 


•*S  "V 


W®  * 


Fig.  163. — Thromboangitis  obliterans  (A)  and  endarteritis  obliterans  (B).  (After  Buerger.)  The 
elastic  fibres  (stained  black)  are  absent  from  the  organized  thrombus  in  A  but  present  in  large  numbers  in 
the  arteriosclerotic  lesion  B. 


This  was  the  condition  first  sought  for  by  Raynaud  to  explain  the 
origin  of  symmetrical  gangrene,  and  described  by  him  under  the  head  of 
senile  gangrene.  In  Buerger's  experience  of  over  70  cases,  however,  it  is 
most  frequent  in  Russian  and  Polish  male  Hebrews  between  twenty  and 
thirty-five  or  forty,  and  hence  is  usually  a  " presenile"  gangrene.  In 
such  cases  the  local  syncope  and  ulceration  are  due  to  arterial  occlusion. 
The  red  blush  is  due  to  compensatory  capillary  dilatation  (termed  eryth- 
romelia  by  Buerger,  in  contrast  to  erythromelalgia) .  Cyanosis  of  the  limb 
occurs  when  the  venous  circulation  is  slowed  from  any  cause. 

The  sensory  disturbances  found  in  the  trophoneuroses  are  also  found 
in  thromboangitis  obliterans. 

The  clinical  picture  produced. by  thromboangitis  obliterans  is  some- 
times so  similar  to  that  of  Raynaud's  disease  (spasmodic  vasoconstriction) 
that  Buerger  has  found  some  undoubted  cases  of  the  former  condition 
reported  in  the  literature  as  cases  of  the  latter. 

Differentiation  between  Thromboangitis  Obliterans  and  Angeioneuroses. — Dr.  Buerger 
has  informed  the  writer  that  he  finds  the  following  points  useful  for  clinical  differentiation: 

1.  There  is  always  at  least  one  vessel  which  remains  permanently 
pulseless,    while  in  Raynaud's  disease  the  pulse  soon  returns  to  normal. 


THROMBOANGITIS  OBLITERANS. 


375 


2.  Intermittent   claudication   is  present  in  most  of  the  cases. 

3.  Usually   one   limb   is   affected   a  considerable  time  before  the  other,  and 
the  disease  usually  attacks  the  lower  extremities. 

4.  There  are  exacerbations,  but  they  come  on  and  subside  rather 
gradually  and  are  not  paroxysmal  like  Raynaud's  disease. 

5.  Limbs  which  are  red  (erythromelia)  or  blue  in  the  dependent  position  become 
blanched    and   ischaemic    when   elevated. 

6.  Migrating  phlebitis  is  not  infrequently  associated  with  thromboangitis  obliterans. 

7.  He  has  seen  over  70  cases  in  Russian  and  Polish  male  Hebrews,  but  never  in  a 
female.    Raynaud's  disease  occurs  more  often  in  females. 

8.  Onset   is   usually  gradual,  while  it  is  sudden  in  Raynaud's  disease. 

9.  The  circulatory   phenomena  are  for  the  most  part  not  of  "vasomotor"  origin, 
but  are  due  to  occlusion  of  vessels.    They  therefore  bear  the  stamp  of  permanency. 

Nevertheless,  Dr.  Buerger  has  found  a  number  of  cases  in  which  the 
clinical  differentiation  from  Raynaud's  disease  was  very  difficult.  Dr. 
Bernard  Sachs,  on  the  other  hand,  believes  that  the  vasomotor  neuroses 
manifest  themselves  in  diseased  blood-vessels  as  well  as  in  healthy  ones, 
and  that  the  pathological  diagnosis  of  endarteritis  or  thromboangitis  does 
not  exclude  the  clinical  diag- 
nosis of  erythromelalgia  or 
Raynaud's  disease.  Indeed  it 
is  readily  conceivable  that 
thrombosis  should  occur  more 
readily  in  somewhat  diseased 
arteries  than  in  normal  ones. 
Even  Dr.  Buerger  has  found 
some  intimal  changes  in  his 
cases.  Moreover,  vasoconstric- 
tion, arterial  disease,  and  the 
formation  of  agglutinative 
thrombi  may,  as  is  seen  in  ergot 
poisoning,  be  produced  by  the 
action  of  a  single  toxic  agent.1 

Case  op  Thromboangitis 
Obliterans. 

The  following  is  the  history  of 
a  case  which,  though  at  the  time 
diagnosed  as  Raynaud's  disease  in  the 
light  of  Buerger's  investigations,  ap- 
pears to  be  one  of  thromboangitis 
obliterans. 

H.   F.,  tailor,  aged  32,   admitted  JIG- 164— Hands  and  feet  of  a  patient  with  thrombo- 

..  '  '     °.    .    .     '       .  angitis    obliterans,    showing    gangrenous    ulcers    and    the 

April  14,  1903,   complaining  OI   Sore      stumps  of  amputated  toes.     The  arrows  point  to  the  gan- 

t  o  e  s  and  sore  fingers.     Had     grenous  ulcers. 

rheumatism  at   12  years;  otherwise  well.     Smokes  ten  cigarettes  daily.     In   December, 

1899,  cold  began  to  cause  a  burning  sensation  in  big  toe  of  right  foot.     In  March, 

1900,  pus  collected  under  the  base  of  nail.  The  nail  was  removed,  and  four 
months  later  the  entire  toe.  Wound  did  not  heal  well.  After  this,  tingling  in  other 
toes  when  out  of  doors,  never  when  indoors.  In  April,  1902,  the  fingers  and 
thumb  of  the  right  hand  began  to  tingle  and  become  painful,  and  a  little  later  on  those 
of  the  left  hand.    In  January,  1903,  the  left  big  toe  began  to  become  gangrenous. 

1W.  H.  Howell  (Arch.  Int.  Med.,  1914,  xiii,  76)  found  that  there  was  a  lack  of  the  anti- 
thrombin  of  the  blood  in  a  case  of  thromboangitis  obliterans. 


376  DISEASES   OF  THE   HEART   AND   AORTA. 

Physicial  examination  on  entrance,  negative  except  for  the  extremities.  Both 
hands  are  flushed,  not  blue,  not  tender,  but  there  is  some  deformation  of  the 
second  phalanx  of  the  middle  fingers.  Right  big  toe  missing;  sloughs  between  third  and 
fourth  digits.     Left  great  toe  necrotic;    tenderness  and  pain  over   both  first  metatarsals. 

Patient  complains  of  paroxysms  of  intense  pain  during  the  night,  lasting 
five  to  ten  minutes.  Elevation  of  the  limb,  warm  dressings,  massage,  were  all  without 
effect.  Condition  became  worse  in  spite  of  hot  HgCh  compresses,  etc.,  and  the  left  great 
toe  had  to  be  removed.  The  stump  did  not  heal  for  several  months.  There 
was  never  pulsation  in  either  popliteal;  very  little  in  either 
femoral.     Patient  discharged  in  February,  1904,  unimproved. 

During  this  time  blood  count:  red  blood-corpuscles  5,000,000-5,500,000.  Haemo- 
globin 100  per  cent.    Urine  normal.    Blood-pressure  100  to  130  mm.  Hg.    Pulse  80. 

The  following  history  represents  a  more  typical  case  of  thromboan- 
gitis  obliterans  (quoted  from  Buerger). 

M.  K.,  44  years,  Russian  Hebrew,  father  of  three  healthy  children,  was  admitted  to 
Mt.  Sinai  Hospital  on  December  8,  1908.  His  limbs  never  troubled  him  until  about  a  year 
ago,  when  he  felt  the  presence  of  tender  spots  on  the  inner  side  of  the  right  foot.  Soon  other 
hard  "lumps"  and  "cords"  appeared;  some  of  these  in  the  neighborhood  of  the  ankle,, 
others  higher  up  on  the  leg.  After  two  months  these  disappeared,  only  to  recur  after  a  very 
short  interval.  Since  then  he  has  never  been  absolutely  free  from  peculiar  "painful  spots," 
and  now,  on  admission,  he  still  has  signs  of  some  of  them.  About  three  months  after  the 
onset  of  these  symptoms  he  experienced  pain  in  the  big  toe,  especially  on  walking.  This 
has  become  gradually  worse,  so  that  he  has  been  unable  to  get  about  properly  for  almost 
two  months.  Of  late  he  has  often  had  cramps  in  the  calf  and  instep  of  the  right  leg  after 
walking  for  a  short  distance.  His  chief  complaint,  however,  is  the  painful  condition  of  the 
inner  side  of  his  right  leg. 

Physical  examination  showed  evidences  of  circulatory  disturbance  in  the  right  lower 
extremity.  Both  the  dorsalis  pedis  artery  and  the  anterior  tibial  were  pulseless,  although 
pulsation  of  both  the  femoral  and  posterior  tibial  artery  could  be  easily  detected. 

Over  the  inner  border  of  the  right  foot  there  is  a  red  streak  about  one-half  inch  in 
length.  This  corresponds  to  a  tender  indurated  mass  which  thins  out  and  is  lost  as  it  is 
traced  upward.  A  short  distance  below  the  middle  of  the  leg  the  upper  end  of  a  hard  cord 
can  be  palpated.  This  extends  down  behind  the  border  of  the  tibia  for  more  than  two 
inches,  is  adherent  to  the  skin,  somewhat  nodulated,  and  marks  the  centre  of  an  area  of 
hypersensitive,  swollen,  turgid  skin.  There  are  no  trophic  disturbances.  Diagnosis: 
thromboangitis  and  thrombophlebitis  of  the  internal  saphenous  and  some  of  its  tributaries. 

On  December  15,  1908,  a  portion  of  the  thrombosed  saphenous  was  removed  for 
pathological  examination. 

On  December  26,  1908,  the  physical  examination  was  recorded  as  follows:  In  the 
horizontal  position,  the  right  foot  has  a  light  shade  of  red;  this  is  most  marked  over  the 
big  toe  and  fades  off  towards  the  ankle.  In  the  web  between  the  third  and  fourth  toes 
there  is  a  superficial  ulcer.  On  the  inner  side  of  the  foot  almost  two  inches  from  the  internal 
malleolus  there  is  a  hard,  cord-like  nodule  which  is  adherent  to  the  skin.  Behind  the  tibia 
there  is  the  scar  left  after  removal  of  a  portion  of  the  saphenous  vein.  The  saphenous  can 
no  longer  be  felt. 

On  elevation  of  the  foot  blanching  sets  in  rapidly  and  pain  becomes  intense.  The 
pendent  foot  turns  very  red  (marked  erythromelia) . 

Further  Course. — February  15,  1909,  the  pain  in  the  foot  has  been  getting  steadily 
worse,  and  the  fourth  toe  is  beginning  to  turn  black.  On  the  23d  of  February  amputation 
at  the  knee  was  done,  at  the  request  of  the  patient,  for  early  gangrene  of  the  fourth  toe. 

TREATMENT. 

In  the  light  of  Buerger's  pathological  studies,  treatment  should  be 
directed  toward  keeping  up  a  rapid  circulation  through  the  part  and  dimin- 
ishing the  tendency  to  coagulate.  To  bring  about  the  former  the  vasodilator 
drugs,  especially  the  nitrites,  should  be  freely  used,  but  most  of  all  the 


THROMBOANGITIS  OBLITERANS.  377 

mechanical  methods  of  inducing  arterial  hyperemia, — hot  poultices,  mustard 
foot  or  hand  baths,  or  the  Bier's  hypersemia  by  suction  in  vacuo  (not  Bier's  stag- 
nation hyperemia).  Exsanguination  of  the  limb  with  the  Esmarch  bandage, 
administration  of  sodium  citrate  in  the  hope  of  reducing  coagulation,  etc., 
have  proved  of  little  avail.  From  the  time  of  Raynaud  to  the  present  excellent 
results  have  been  reported  from  the  use  of  warm  (but  not  too  hot)  poultices. 
Arteriovenous  Anastomosis. — The  recent  advances  in  vascular  surgery, 
introduced  by  Carrel,  have  made  it  possible  to  anastomose  the  artery  with  the 
vein  and  to  lead  blood  to  the  limb  through  the  vein  instead  of  the  artery 
(reversal  of  the  circulation) .  Bernheim,  whose  operative  results  are  the  best 
thus  far  obtained,  has  reported  four  operations  upon  cases  of  Raynaud's  dis- 
ease, three  done  by  himself  and  one  by  Quenu.  In  Quenu's  case  partial  success 
was  obtained,  but  the  limb  had  to  be  amputated  four  months  later.  Two  of 
Bernheim's  operations  were  followed  by  complete  success,  but  in  the  third  no  re- 
lief was  afforded.  Of  fifty-two  cases  of  gangrene  from  various  causes  collected 
by  the  same  writer,  fifteen  were  successful,  while  among  his  own  cases  the  satis- 
factory result  was  obtained  in  five  out  of  six.  Bernheim  insists  upon  the  impor- 
tance of  operating  early,  before  all  the  vessels  supplying  the  part  have  become 
so  thrombosed  as  to  render  recovery  impossible.  The  importance  of  perfect 
technique  and  of  much  practice  in  vascular  surgery  cannot  be  overestimated. 
All  but  one  of  Bernheim's  anastomoses  were  end-to-end  anastomoses ;  the  other 
was  a  lateral  anastomosis  done  by  the  method  of  Bernheim  and  Stone. 

BIBLIOGRAPHY. 

Vasomotor  Crises  and  Angioneuroses. 

Pal,  J.:  Die  Gefasskrisen,  Leipz.,  1905. 

Charcot,  J.  M.:  Sur  la  claudication  intermittente  observee  dans  un  cas  d'obliteration  com- 
plete de  l'une  des  arteres  iliaques  primitives,  Compt.  rend.  Soc.  de  Biol.,  Paris,  1857, 
2  serie,  xii,  225.  Sur  la  claudication  intermittente  par  obliteration  arterielle,  Progres 
Med.,  Paris,  1887. 

Erb,  W. :  Ueber  das  "intermittirende  Hinken"  und  andere  nervose  Storungen  infolge  von 
Gefasserkrankungen,  Deutsch.  Ztschr.  f.  Nervenheilk.,  xiii,  1.  Ueber  Dysbasia  angio- 
sclerotica,  Munchen.  med.  Wchnschr.,  1904,  li,  905. 

Barker,  L.  F.,  and  Sladen,  F.  J. :  On  Acrocyanosis  Chronica  Anaesthetica  with  Gangrene, 
etc.,  J.  Nerv.  and  Ment.  Dis.,  N.  York,  1907,  xxxiv,  745. 

Cassirer,  R.:  Die  Vasomotorische  Trophoneurosen,  Berl.,  1901. 

Mitchell,  S.  Weir:  Phila.  M.  Times,  1872;  quoted  from  Sachs.  Mitchell,  S.  W.,  and  Spiller, 
W.  G. :  A  Case  of  Erythromelalgia  with  Microscopical  Examination  of  the  Tissue 
from  an  Amputated  Toe,  Am.  J.  M.  Sc,  Phila.,  1899,  N.  S.  cxvii,  1. 

Raynaud,  A.  G.  M.:  De  1'asphyxie  locale  et  de  la  gangrene  symmetrique  des  extremites, 
Par.,  1862;  also,  On  Local  Asphyxia  and  Symmetrical  Gangrene  of  the  Extremities, 
Transl.  by  T.  Barlow,  Lond.,  1888. 

Buerger,  L.:  Thromboangiitis  Obliterans;  a  Study  of  the  Vascular  Lesions  leading  to  Pre- 
senile Gangrene,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1908,  cxxxvi,  567.  The  Veins 
in  Thromboangiitis  Obliterans,  with  Particular  Reference  to  Arteriovenous  Anas- 
tomosis as  a  Cure  for  the  Condition,  J.  Am.  M.  Asso.,  Chicago,  1909,  lii,  1319. 

Sachs,  B.:  Raynaud's  Disease,  Erythromelalgia,  and  the  Allied  Conditions,  in  their  Relation 
to  Vascular  Disease  of  the  Extremities,  Am.  J.  M.  Sc,  Phila.  and  N.Y.,  1908,  cxxxvi,  560. 

Also,  Strauss,  H. :  Ueber  ans;iospastische  Gangran  (Raynaud'sche  Krankheit),  Arch.  f. 
Psychiat.,  Berl.,  1905,  xxxix,  109. 

Bernheim,  B.  M.:  Arteriovenous  Anastomosis — Reversal  of  the  Circulation — as  a  Preven- 
tive of  Gangrene  of  the  Extremities,  Ann.  Surg.,  Phila.,  1912, 195;  Bernheim,  B.  M.,  and 
Stone,  H.  B. :  Lateral  Vascular  Anastomosis,  an  Improved  Method,  ibid.,  1911,  497. 


XII. 

SCLEROSIS   OF  THE  CORONARY  ARTERIES,   AND   ANGINA 

PECTORIS. 

PHYSIOLOGY   OF   THE   CORONARY  CIRCULATION. 

The  coronary  arteries  have  usually  been  considered  to  be  terminal  arteries  in  the 
sense  of  Cohnheim;  that  is,  that  their  branches  did  not  anastomose  with  one  another  suffi- 
ciently to  maintain  an  adequate  circulation,  and  infarction  follows  their  occlusion.  This 
is  correct  under  most  clinical  conditions;  and  Porter  has  found  experimentally  that  the 
infarction  is  proportional  to  the  size  of  the  ligated  branch.  In  many  cases  ligation  of  a  coro- 
nary gives  rise  to  fibrillary  contractions  and  sudden  death  (Porter,  Magrath  and  Kennedy, 
Kronecker) ;  in  others  death  may  follow  within  a  few  minutes  (Cohnheim  and  v.  Schulthess- 
Rechberg),  within  an  hour  (Panum),  or  the  animal  may  live  several  weeks  or  more 
(Baumgarten)  if  the  operation  is  done  aseptically.    Death  even  then  often  occurs  suddenly. 


Fig.  165.- 


-Effect  of  ligation  of  a  large  coronary  artery  upon  the  blood-pressure. 
Schulthess-Rechberg.)     Coronary  artery  ligated  at  a. 


(After  Cohnheim  and  v. 


Distribution  of  the  Coronary  Arteries. —  Walter  Baumgarten  in  Porter's  laboratory 
was  able  to  ligate  the  various  coronary  branches  of  cats  and  dogs  under  aseptic  precau- 
tions and  produced  infarcts  in  the  corresponding  areas  of  the  myocardium.  He  found 
the  following  effects  by  ligating  the  various  branches: 

Ramus  descendens:'  Anterior  wall  of  left  ventricle,  anterior  papillary  mus- 
cle, left  half  of  the  thickness  of  the  interventricular  septum. 

Ramus  circumflexus:  Posterior  wall  of  left  ventricle,  apex,  posterior  papil- 
lary muscle,  a  certain  extent  of  the  right  ventricle,  posterior  wall  of  left  atrium,  posterior 
third  of  the  septum. 

Ramus  septi:  This  is  given  off  in  the  dog  near  the  origin  of  the  ramus  descen- 
dens or  independently  of  it.  Ligature  produces  a  triangular  infarction  with  the  apex  of  the 
triangle  towards  the  ligature. 

Right  coronary:  Greater  part  of  right  ventricle,  posterior  portion  of  the 
appendix  atrii.     (The  smaller  branches  of  the  atria  are  not  caught  in  the  ligature.) 

Baumgarten  also  excised  the  anaemic  area  and  perfused  it  with  defibrinated  blood, 
and  found  this  region  was  able  to  resume  contractions  when  the  cir- 
culation was  renewed  within  six  to  eleven  hours  after  the  artery  had  been  ligated.  The 
region  of  the  centre  of  the  infarct  lost  its  contractility  before  that  near  the  periphery, 
indicating  that  a  certain  degree  of  collateral  circulation,  perhaps  through  the  vessels  of 
Thebesius,  had  taken  place.  This  work  explains  why  it  is  that  a  certain  time  elapsed 
between  the  obstruction  of  the  artery  and  the  sudden  cessation  of  beat  in  the  experi- 

378 


SCLEROSIS  OF  THE  CORONARY  ARTERIES.  379' 

ments  of  Panum  and  of  Cohnheim  and  v.  Schulthess-Rechberg.  Many  of  Baumgarten's 
animals  survived  for  long  periods;  and  two  of  them  died  with  sudden  heart  failure,  one  in 
the  midst  of  violent  exertion. 

Wassiliewski  (Ztschr.  f.  exper.  Path.  u.  Therap.,  1911,  ix,  146)  injected  lycopodium 
spores  into  the  coronary  arteries,  producing  dilatation  and  weakness  of  the  heart,  often 
with  a  rise  of  blood-pressure.  Administration  of  nitroglycerin  then  caused  fall  of  blood- 
pressure  and  dilatation  diminished. 

Hirsch  and  Spalteholz  found  that,  though  infarcts  were  produced  by  ligation  of  the 
coronary  artery,  the  infarcts  were  smaller  than  the  area  supplied  anatomically  by  the 
artery,  and  there  was  a  not  inconsiderable  amount  of  anastomosis,  especially  between  the 
branches  near  the  surface  of  the  heart.  In  man  Chiari  has  found  complete  occlusion  of 
the  right  coronary  artery  without  infarction,  and  Pagenstecher  has  ligated  that  artery 
in  an  operation  without  evil  result.  These  are  the  main  facts  regarding  the  coronary  circu- 
lation which  throw  light  upon  the  clinical  conditions  observed. 

Pratt  has  shown  that  the  excised  mammalian  heart  can  be  nourished 
through  the  veins  of  Thebesius  sufficiently  to  carry  out  forcible  contrac- 
tions for  a  considerable  time,  though  this  probably  is  not  the  case  in  the 
living  animal. 

It  has  long  been  a  matter  of  debate  whether  the  heart  muscle  was 
nourished  with  blood  during  the  systolic  or  during  the  dias- 
tolic period;  the  earliest  contention  being  that  of  Scaramucci  (1689)  that  the  coro- 
nary vessels  are  squeezed  empty  by  the  contraction  of  the  heart  muscle-fibres  during  systole 
and  fill  from  the  larger  and  more  superficial  coronary  vessels  during  diastole.  After  a  long 
controversy,  during  which  Rabatel  showed  that  the  curve  of  coronary  blood-pressure  and 
apparently  also  the  curve  of  blood  velocity  were  exactly  similar  to  the  curve  in  the  aorta, 
the  question  was  definitely  settled  upon  the  excised  heart  by  Porter  and  his  pupils 
in  favor  of  the  old  view  of  Scaramucci. 

Martin  and  Sedgwick  (Studies  from  Biol.  Lab.,  Johns  Hopkins  Univ., 
1882-3,  ii,  322)  observed  sudden  changes  in  calibre  in  the  coronary  arteries, 
and  ascribed  this  to  the  action  of  vasomotor  nerves.  Tracings  by  Porter  (Bost. 
M.  and  S.  J.,  1896)  and  Maass  (1899)  confirm  this  view. 

This  was  confirmed  by  O.  Langendorff  and  Wiggers,  who  found  also  that  adrenalin 
exerted  a  vasodilator  action  upon  the  coronary  arteries  of  the  exc'sed  heart  instead  of  its 
usual  vasoconstrictor  action.  Both  Wiggers  and  G.  S.  Bond  have  found  that  the  outflow 
through  the  coronary  veins  of  the  dog's  heart  in  situ  is  increased  by  the  administration 
of  adrenalin.  As  a  rule,  the  blood  flow  through  the  coronaries  follows  the  general  blood- 
pressure  but,  as  shown  on  page  269,  certain  substances,  such  as  the  nitrites,  may  cause  the 
coronary  arteries  to  dilate  visibly  even  when  the  general  blood-pressure  falls.  This  dilata- 
tion is  so  intense  that  small  vessels  previously  invisible  spring  into  view  and  seem  to  shoot 
across  the  surface  of  the  ventricles.  This  phenomenon  is  also  noted  with  adrenalin  and  the 
latter  drug  seems  to  be  an  even  better  dilator  of  coronary  arteries  than  are  the  nitrites. 

Ida  Hyde  in  Porter's  laboratory  found  that  the  coronary  blood  flow  was  diminished 
by  distention  of  the  heart,  a  fact  which  may  account  for  the  weaker  contraction  of  over- 
dilated  hearts. 

SCLEROSIS    OF    THE    CORONARY    ARTERIES. 

PATHOLOGICAL    ANATOMY. 

While  the  sclerosis  of  the  coronary  arteries  does  not  differ  in  its  pathol- 
ogy from  the  sclerosis  of  arteries  elsewhere,  nevertheless  the  action  upon 
the  heart  gives  rise  to  clinical  and  to  secondary  pathological  conditions 
which  are  quite  different  from  those  of  general  arteriosclerosis,  and  which 
therefore  deserve  special  consideration. 


380 


DISEASES   OF  THE   HEART   AND    AORTA. 


Another  important  condition  which  is  very  common  is  arterioscle- 
rotic or  atheromatous  change  arising  in  the  aorta  with  or  without  associated 
involvement  of  the  coronaries  themselves,  but  spreading  so  as  to  involve 
the  mouths  of  the  coronaries  as  they  arise  from  the  aorta,  and  strangu- 
lating these  vessels  as  they  pass  through  the  aortic  wall  (see  Fig.  166). 
This  has  the  same  effect  as  a  metal  band  constricting  an  artery  would  have; 
namely,  of  diminishing  the  blood-pressure  and  the  velocity  of  flow  in  the 
artery  beyond  it,  of  allowing  the  walls  of  the  artery  to  contract  down  and 
hence  of  producing  a  further  permanent  secondary  narrowing  of  the  lumen, 
with  progressive  diminution  in  the  blood  supply  to  the  part  (Halsted). 
The  course  of  the  artery  may  show  patches  of  hardening  with  indentations 
and  wiclenings,  collar-like  constrictions,  or  uniform  widenings;  or,  on  the 
other  hand,  the  arteries  may  be  converted  into  uniform  tubes  whose  walls 

may  give  the  sensation  of  rubber 
tubes  on  the  one  hand  (uniform 
fibrous  sclerosis),  or  of  absolute 
pipe-stems  (complete  calcification) 
on  the  other.  This  condition  is,  of 
course,  particularly  common  in 
arteriosclerosis  affecting  the  base 
of  the  aorta,  i.e.,  luetic  aortitis  and 


Fig.  166. — Sclerosis  of  a  coronary  artery,  producing  an  area  of  infarction  near  the  apex.  A.  Show- 
ing the  entire  specimen.  B.  The  sclerotic  coronary  artery,  camera  brought  closer;  a  wire  has  been  passed 
through  the  mouth  of  the  coronary  artery. 

luetic  aortic  insufficiency,  and  may  account  for  many  of  the  symptoms  to 
be  discussed  later  (see  page  381). 

Since  the  heart  muscle  requires  much  more  blood  when  it  is  beating 
forcibly  and  rapidly  than  when  it  is  beating  slowly  and  quietly,  it  is  easily 
seen  that  this  collateral  circulation  may  be  sometimes  adequate  and  some- 
times not.  Also,  since  in  different  individuals  of  the  same  species  there  are 
variations  both  in  the  structure  and  disposition  of  the  minute  arteries  and 
in  the  needs  of  the  muscle-fibres  for. nourishment,  it  is  but  natural  that  the 
results  of  coronary  disease  should  vary  greatly. 


CLINICAL    MANIFESTATIONS. 


The  clinical  pictures  associated  with  coronary  sclerosis  are  character- 
ized by  some  or  all  of  the  following  features:  pain  over  the  precordium 
or  down  the  arms,  feelings  of  suffocation  or  of  impending  death, 


SCLEROSIS   OF  THE   CORONARY   ARTERIES.  381 

paroxysms  of  most  intense  dyspnoea  with  palpitation,  enlargement 
and  pulsation  of  the  liver,  general  weakness,  sudden  death. 

A  considerable  grade  of  arteriosclerosis  may  be  present  in  both  young 
and  old  individuals  without  giving  any  symptoms  whatever,  as  shown  in 
the  case  of  J.  L.  (page  573).  Another  example  of  this  was  a  colored  boy 
under  the  writer's  care  who  after  very  vigorous  life  died  at  the  age  of  nine- 
teen in  the  fifth  week  of  typhoid  fever.  Neither  before  nor  during  the  fever 
had  he  had  any  cardiac  symptoms.  However,  his  coronary  arteries  were 
found  to  be  very  sclerotic. 

Sudden  Death. — S  udden  death  is  frequently  the  first  manifesta- 
tion of  the  condition,  and  examples  are  almost  daily  in  the  newspapers  of 
persons,  usually  men  past  middle  life,  who  drop  dead  without  warning  and 
with  no  previous  illness,  due  to  sudden  thrombosis  of  the  sclerotic  coro- 
nary arteries,  or  perhaps  merely  to  the  fact  that,  though  the  sclerotic 
process  has  been  going  on  gradually,  the  instant  has  passed  at  which  the 
cardiac  nutrition  becomes  insufficient  and  ischsemia  sets  in  with  sudden 
functional  insufficiency,  just  as  occurs  in  the  leg  in  intermittent  claudica- 
tion. This  must  be  the  case  in  many  hearts  in  which  no  actual  thrombosis 
or  embolism  can  be  found  post  mortem. 

Paroxysms  of  dyspnoea  such  as  those  described  on  page  216,  the  so- 
called  cardiac  asthma,  are  also  extremely  common  in  coronary  sclerosis, 
especially  when  combined  with  aortic  insufficiency  (vide  page  468),  in 
which  case  they  are  no  doubt  due  to  the  dilatation  and  weakening  of  the 
left  heart  and  the  consequent  accumulation  of  C02  in  the  blood.  It  has 
been  suggested  by  Drs.  C.  M.  Cooper  and  E.  0.  Jellinek  of  San  Francisco 
that  this  was  always  an  accompaniment  of  sclerosis  of  the  right  coronary 
artery  and  dilatation  of  the  right  heart,  but  in  autopsies  of  two  cases  under 
the  writer's  care  who  had  suffered  from  such  attacks  the  right  coronary 
was  absolutely  free  from  sclerosis. 

Sensations  of  pain  in  the  precordium,  and  especially  behind  the  sternum, 
as  well  as  pains  and  tenderness  over  various  interspaces  and  radiating  down 
the  arms,  are  especially  common  in  coronary  sclerosis. 

Paroxysmal  Tachycardia.  —  Attacks  of  tachycardia  beginning  with 
sudden  doubling  of  the  pulse-rate  and  ending  in  sudden  halving  of  the  latter, 
just  as  is  present  in  essential  paroxysmal  tachycardia,  have  been  described 
by  Romberg  as  manifestations  of  coronary  sclerosis,  and  Krehl  also  cites 
similar  findings. 

In  Romberg's  case  the  pulse-rate  rose  suddenly  from  100  to  200,  while  the  respira- 
tion remained  at  20.  The  attack  lasted  two  days  and  then  the  pulse-rate  dropped  sud- 
denly to  100.  Later  an  aortic  stenosis  developed  gradually  and  the  patient  died  of  heart 
failure,  the  autopsy  showing  aortic  stenosis  and  sclerosis  and  marked  coronary  sclerosis. 
Dr.  Barker  informs  the  writer  that  he  also  has  seen  a  couple  of  cases  in  which  such 
attacks  were  associated  with  coronary  sclerosis. 

Quite  recently  similar  attacks  have  been  produced  by  T.  Lewis  upon  ligating  the 
coronary  arteries  in  cats  even  after  the  cardiac  nerves  had  been  sectioned. 

Painful  sensations  about  the  heart  are  particularly  common  in  asso- 
ciation with  coronary  sclerosis,  but  on  the  one  hand  they  are  by  no  means 
confined  to  this  condition,  and  on  the  other  hand  most  extensive  coronary 
sclerosis  may  be  present  without  the  occurrence  of  cardiac  pain.  The  most 
marked  form  of  cardiac  pain,  the  so-called  "angina  pectoris"  (pronounced 


382  DISEASES   OF   THE   HEART   AND   AORTA. 

an'gina,  not  angl'na)  to  be  discussed  below,  is  in  its  most  typical  form 
usually  associated  with  a  certain  degree  of  coronary  sclerosis. 

ANGINA1  PECTORIS. 

In  1768  both  Heberden  and  Rougnon  described  attacks  of  pain  in  the 
chest.  Tne  former  recognized  the  condition  the  more  clearly  and  described 
it  in  the  following  words: 

"But  there  is  a  disorder  of  the  breast  marked  with  strong  and  peculiar  symptoms, 
considerable  for  the  kind  of  danger  belonging  to  it,  and  not  extremely  rare,  which  deserves 
to  be  mentioned  here  at  length.  The  seat  of  it,  and  sense  of  strangling  and  anxiety  with 
which  it  is  attended,  may  make  it  not  improperly  be  called  angina   pectoris. 

"  They  who  are  afflicted  with  it  are  seized  while  they  are  walking  (more  espe- 
cially if  it  be  up-hill  and  soon  after  eating)  with  a  painful  and  most  disagreeable 
sensation  in  the  breast,  which  seems  as  if  it  would  extinguish  life  if  it  were  to  increase  or 
to  continue;   but  the  moment  they  stand  still  all  this  uneasiness  vanishes. 

"In  all  other  respects  the  patients  are,  at  the  beginning  of  the  disorder,  perfectly 
well,  and  in  particular  have  no  shortness  of  breath,  from  which  it  is  totally 
different.  The  pain  is  sometimes  situated  in  the  upper  part,  some- 
times in  the  middle,  sometimes  at  the  bottom  of  the  os  sterni, 
and  often  more  inclined  to  the  left  than  to  the  right  side.  It  like- 
wise very  frequently  extends  from  the  breast  to  the  middle  of  the  arm.  The  pulse  is, 
at  least  sometimes,  not  disturbed  by  this  pain,  as  I  have  had  opportunities  of 
observing  by  feeling  the  pulse  during  the  paroxysm.  Males  are  most  liable  to  this 
disease,  especially  such  as  have  passed  their  fiftieth  year.  After  it  has  con- 
tinued a  year  or  more,  it  will  not  cease  as  instantaneously  upon  standing  still,  and  it  will 
come  on  not  only  when  the  persons  are  walking  but  when  they  are  lying 
down,  especially  if  they  lie  on  the  left  side,  and  oblige  them  to  rise  out  of  their  beds. 
In  some  inveterate  cases  it  has  been  brought  on  by  the  motion  of  a  horse  or  a  carriage 
and  even  by  swallowing,  coughing,  going  to  stool,  speaking,  or 
any   disturbance   of   mind. 

"Such  is  the  usual  appearance  of  this  disease,  but  some  varieties  may  be  met  with. 
Some  have  been  seized  while  they  were  standing  still  or  sitting,  also  upon  first  waking  out 
of  sleep,  and  the  pain  sometimes  reaches  down  the  right  arm  as  well 
as  the  left  and  even  down  to  the  hands,  but  this  is  uncommon;  in  a 
very  few  persons  the  arm  has  at  the  same  time  been  numbed  and  swelled.  In  one  or  two 
persons  the  pain  has  lasted  some  hours  or  even  days,  but  this  has  happened  when  the  com- 
plaint has  been  of  long  standing  and  thoroughly  rooted  in  the  constitution;  once  only  the 
very  first  attack  continued  the  whole  night. 

" I  have  seen  nearly  a  hundred  people  under  this  disorder,  of  which  num- 
ber there  have  been  three  women  and  one  boy  two  years  old.  All  the  rest 
were  men  near  or  past  the  fiftieth  year  of  their  age. 

"  Persons  who  have  persevered  in  walking  till  the  pain  has  returned  four  or  five  times 

have  then  sometimes  vomited The  termination  of  angina  pectoris  is  remarkable. 

For  if  no  accident  intervene  but  the  disease  go  on  to  its  height,  the  patients  all 
suddenly  fall  down  and  perish  almost  immediately.  The  angina 
pectoris,  as  far  as  I  have  been  able  to  investigate,  belongs  to  the  class  of  spasmodics,  not 
of  inflammatory  complaints.     For, 

"  In  the  first  place,  the  access  and  the  recess  of  the  fit  is  sudden. 

"Secondly,  there  are  long  intervals  of  perfect  health. 

"Thirdly,  wine  and  spirituous  liquors  and  opium  afford  considerable  relief. 

"Fourthly,  it  is  increased  by  disturbance  of  mind: 

"Fifthly,  it  continues  many  years  without  any  other  injury  to  the  health. 

"Sixthly,  in  the  beginning  it  is  not  brought  on  by  riding  on  horseback  or  in  a  car- 
riage, as  is  usual  in  diseases  arising  from  scirrhus  or  inflammation. 

"  Seventhly,  during  the  fit  the  pulse  is  not  quickened. 

"Lastly,  its  attacks  are  often  after  the  first  sleep,  which  is  a  circumstance  common 
to  many  spasmodic  disorders. 

1  Pronounced  "angina";  e.g.,  "Insperato  abiit  quem  una  angina  sustulit  hora"  (Lucilius). 


ANGINA   PECTORIS.  383 

"With  respect  to  the  treatment  of  this  complaint,  I  have  little  or  nothing  to  advance, 
.  .  .  .  Quiet,  warmth,  and  spirituous  liquors  help  to  restore  patients 
who  are  nearly  exhausted  and  to  dispel  the  effects  of  a  fit  which  does  not  soon  go  off. 
Opium   taken  at  bedtime  will  prevent  the  attacks  at  night." 

Heberden's  contemporary,  the  great  John  Hunter,  suffered  from  this 
disease,  and  described  his  attacks  most  vividly. 

The  modern  aspects  of  the  whole  subject  have  been  discussed  in  a 
masterly  way  by  Sir  W.  Gairdner  as  well  as  in  the  more  recent  monographs 
of  W.  Osier  and  G.  A.  Gibson. 

CHARACTER    OF    THE    PRECORDIAL    PAIN    AND    CLINICAL    SUMMARY. 

In  Heberden's  description  we  have  epitomized  almost  all  the  clinical 
features.  (1)  The  sudden  attacks  of  oppression  in  the  chest,  with  a  feeling 
of  strangling,  and,  as  Hunter  puts  it,  "as  though  the  sternum  was  being 
drawn  back  to  the  spine,"  or,  in  the  words  of  Matthew  Arnold,  as  "though 
there  were  a  mountain  upon  my  chest."  (2)  The  mental  anguish  (termed 
by  Gairdner  angor  animi),  with  the  fear  of  impending  death,  especially  pro- 
nounced in  John  Hunter.  (3)  The  intense  pain,  situated  sometimes  in  the 
lower  sometimes  in  upper  part  of  the  sternum,  more  frequently  to  the  left 
than  to  the  right  (although  occasionally  to  the  latter),  and  very  often 
radiating  to  the  arm,  especially  the  left.  (4)  Some  of  the  disturbances 
of  sensation;  even  Heberden  speaks  of  numbness  of  the  arm.  (5)  Changes 
in  the  pulse  in  some  cases:  intermissions;  extrasystoles  in  some  cases 
(Hunter) ;  alternating  pulse  in  others  (Mackenzie) .  (6)  The  extreme  pallor 
and  constriction  of  peripheral  arteries  during  the  attack.  (7)  The  sudden 
death.  (8)  The  main  factors  in  bringing  on  attacks, — walking  up-hill, 
flatulence  and  digestive  disorders,  bending  down  in  undressing,  mental 
excitement  or  anxiety,  and  especially  anger;  but  none  of  the  more  gentle 
emotions,  such  as  pity,  sorrow,  etc.,  even  when  felt  intensely.  (The  effect 
of  exposure  to  cold  does  not  seem  to  be  mentioned  by  these  writers.)  (9) 
The  association  of  the  condition  with  sclerosis  of  the  coronary  arteries.  (10) 
Its  frequent  association  with  abnormal  fatty  deposits  about  the  heart 
(cf.  Jenner  and  also  page  306).  (11)  The  relief  of  symptoms  by  means  of 
opium,  warm  applications,  hot  drinks  (vasodilator  mechanisms),  and 
counter-irritation  (Heberden).  (12)  Its  incurability,  owing  to  the  seat  of 
the  trouble. 

To  these  points  clinical  observations  since  Jenner  have  added:  (1) 
The  existence  of  anginoid  attacks  with  several  conditions  other  than  those 
of  coronary  sclerosis,  particularly  with  over-indulgence  in  tobacco,  with 
hysteria,  with  hyperthyroidism,  and  with  other  purely  vasomotor  phe- 
nomena, as  well  as  with  practically  all  the  valvular  diseases  of  the  heart. 
(2)  The  frequent  association  of  angina  pectoris  with  certain  definite  areas 
of  tenderness  which  represent  spinal  segments  corresponding  to  the  referred 
pain.  (3)  The  occurrence  of  rise  in  blood-pressure  with  each  attack.  (4) 
The  relief  of  the  attacks  by  inhalations  of  amyl  nitrite  and  other  vasodilator 
drugs.    (5)  The  ending  of  the  attack  in  diaphoresis. 

Sir  William  Gairdner  has  called  attention  to  the  occurrence  of  certain 
cases  resembling  Heberden's  angina  pectoris  in  every  way  except  in  the 
absence  of  pain  as  a  symptom  (angina  sine  dolore). 


384 


DISEASES   OF   THE   HEART   AND    AORTA. 


Paths  Traversed  by  the  Pain  Sensations. — The  afferent  impulses  from 
the  heart  have  been  traced  by  Ludwig  and  Cyon  through  the  depressor 
fibres  of  the  vagus.  It  has  been  shown  by  Eyster  and  Hooker  that  the 
afferent  impulses  from  the  aorta  and  coronary  arteries  do  not  take  this 
same  path  but  pass  upward  in  the  main  bundle  of  the  vagus.  There  is  no 
evidence  from  animal  experiment  that  afferent  impulses  pass  in  any  other 
way;  but  Henry  Head,  as  a  result  of  his  most  extensive  studies  upon  pain 
in  visceral  disease,  states  that  this  "produces  impulses  which  pass  into 
the  spinal  cord  by  the  white  rami.  The  segment  on  which  they 
infringe  is  excited  and  pain  is  produced.  At  the  same  time  all  potentially 
painful  influences  passing  into  this  segment  from  the  afferent  nerves  are 
exaggerated,  and  ultimately  the  body  wall  may  become  tender." 

These  sensations  of  referred  pain  follow  the  same  path  as  has  been  described  by 
Bayliss  for  the  vasodilator  fibres  with  which  protopathic  sensation  seems  to  be  closely 
associated,  as  shown  in  herpes  zoster,  etc.  Protopathic  sensations  are  referred  back  to  the 
distribution  of  the  corresponding  nerve  segments  without  close  reference  to  the  points 
at  which  they  arise. 

Insensibility  of  the  Heart  to  Touch. — The  heart  itself  seems  to  be  devoid  of  tactile 
sensation,  for  Harvey  gives  the  following  description  of  the  condition  in  the  nineteen-year- 
old  son  of  Viscount  Montgomery,  who  had  a  fistulous  opening  in  the  chest  wall  over  the 
heart  following  fracture  of  the  rib  in  early  childhood.    The  youth  never  knew  when  we 

touched  his  heart  except  by  the  sight  or  the  sen- 
sation he  had  through  the  external  integument. 
The  writer  has  found  that  tapping  the  skin  over 
the  heart  of  a  patient  whose  chest  wall  had  been 
removed  for  empyema  caused  no  sensation,  while 
gripping  the  ventricles  caused  a  feeling  of  oppres- 
sion over  the  lower  end  of  the  sternum,  but  no 
extrasystoles  or  pain.1 

Palpitation  and  Anginal  Sensations 
Compared. — The  sensations  which  may  be 
felt  from  the  heart  itself  may  be  either 
rhythmic  and  felt  as  a  distinct  sensation 
accompanying  each  systole  of  the  heart, 
such  as  the  feeling  of  palpitation,  or  the 
pain  felt  at  each  beat  in  some  cases  of 
pericarditis,  especially  those  associated 
with  pneumonia.  The  sensation  in  the 
latter  condition  may,  however,  arise  in 
the  parietal  pericardium,  and  may  have 
nothing  to  do  with  the  heart  itself. 

Sensations  of  palpitation  may  be 
very  distressing,  partly  on  account  of  the 
feelings  of  suffocation  which  accompany 
them,  partly  on  account  of  the  mechan- 
ical shock  of  the  heart  beating  forcibly  against  the  chest  wall  like  a  bird 
in  a  cage.  But,  however  intense  and  distressing,  the  sensation  of  palpi- 
tation is  always  a  pressure  sensation  and  never  one  of  pain.  On  the  other 
hand,  the  real  cardiac  pain  is  never  intermittent,  never  felt  as  a  distinct 
sensation  with  each  beat  of  the  heart,  but,  whether  dull  and  aching  or 

1  Sano  (Arch.  f.  d.  ges.  Physiol.,  1909,  cxxix,  217)  states  that  touching  the  exposed 
heart  of  an  unanaesthetized  rabbit  does  not  even  frighten  the  animal. 


Fig.  167. — Distribution  of  pain  in  attacks 
of  angina  pectoris.  (Schematic,  after  Head 
and  Mackenzie.)  ASCAO,  area  correspond- 
ing to  the  ascending  aorta;  TR,AO,  area  cor- 
responding to  the  transverse  aorta;  L.A,R.A, 
area  corresponding  to  left  and  right  auricles 


ANGINA  PECTORIS. 


385 


sharp  and  stabbing,  it  has  no  throbbing  quality  about  it.  It  is,  therefore, 
to  a  quite  different  category.  Hirschfelder  has  added  some  evidence  for 
this  view  by  observing  that  in  some  cases  of  palpitation  the  sensation 
was  referred  definitely  to  the  root  of  the  aorta,  and  was  exactly  similar 
in  character  to  other  sensations  of  throbbing  in  the  radial  artery  alone, 
which  were  sharply  localized  along  its  course  and  not  spreading  like  a  pro- 
topathic  sensation. 

Referred  Pains  in  Angina  Pectoris. — James  Mackenzie  and  Henry 
Head  have  called  attention  to  the  commonness  of  referred  pain  and  tender- 
ness in  angina  pectoris.  Mackenzie  showed  that  there  is  often  tenderness 
in  the  areas  supplied  by  the  second 
and  third  cervical  segments,  whose 
fibres  along  with  some  from  the 
spinal  accessory  run  down  to  the 
heart  through  the  vagus.  This  would 
account  for  the  occipital  headaches 
and  tenderness  of  the  sternocleido- 
mastoid and  trapezius  muscles  which 
are  frequently  present.  The  muscu- 
lar tenderness  is  elicited  by  squeez- 
ing gently  between  the  thumb  and 
forefinger. 

The  distribution  of  the  pain  and 
hyperesthesia,  according  to    Head, 
bears  a  close  relation  to  the  chamber  most  affected,  and  particularly  to 
the  somatic  segment  of  the  embryo  to  which  it  corresponds. 


Fig.  168. — Distribution  of  attacks  of  pain  and 
sensory  disturbances  in  a  case  of  angina  pectoris. 
(After  Head,  with  permission  of  the  publishers  of 
Brain.) 


Correspond  embryo- 
logically  to 

Nerve  supply 

Associated  phenomena  and 
pain  referred  to 

5,  6,  7,  8  thoracic 

5,  6,  7,  8  segments 

Lower    axilla    and    shoulder- 

blades. 

2,3,4,5, 6  thoracic 

2-6  thoracic  seg- 

Chest  wall   from   2d-7th  rib, 

ments 

ulnar  surface  of  forearm 
to  wrist,  and  inner  aspect 
of  upper  arm. 

Ascending  aorta. . . 

3  and  4  cervical.  . 

3   and  4  cervical 

These  segments  also  to  3  and  4 

segments 

c.  and  1  thor.  Tenderness 
in  neck  of  sternomastoid  and 
trapezius  muscles.  Tender- 
ness and  pain  at  back  of 
neck.   (Dilatation  of  pupil?) 

CIV r... 

CIV 

Laryngeal  areas  of  neck  (4th 

branchial  bar). 

Descending  aorta.  . 

Thoracic  segments 

2-12,  esp.  4-12 . . . 

Back  or  front  of  chest,  espe- 

corresponding 

cially  below  nipple;    abdo- 

2-12 

men. 

Pulmonary  artery. 

c.  v-vm 

CV 

Outer  two-thirds  of  arm  and 
hand;    arm  muscles. 

Thus,  the  auricles  (atria),  which  are  the  hindmost  in  the  development  of  the  cardiac 
tube,  receive  their  innervation  from  and  refer  their  pain  to  the  fifth,  sixth,  seventh,  and 
eighth  thoracic  segments.     The  ventricles,  the  next  chambers  neadward,  correspond  to 

25 


386 


DISEASES  OF  THE  HEART  AND   AORTA. 


the  second  to  the  sixth  thoracic;  the  ascending  aorta  from  the  semilunar  valves  to  the 
origin  of  the  ductus  arteriosus  corresponds  to  the  primitive  aorta  with  the  third  and  fourth 
branchial  artery,  and  the  pain  is  referred  to  these  segments  (but  an  aneurism,  etc.,  involv- 
ing this  in  adult  life  will  also  involve  the  neighboring  nerves  and  the  pain  will  be  referred 
to  the  first,  second,  and  third  thoracic  segments  as  well).  The  fifth  to  the  eighth  cervical 
segments,  corresponding  to  the  pulmonary  artery,  will  be  involved,  and  pain  may  not 
be  referred  over  these  areas.1  (There  are  many  notable  exceptions  to  this  rule  even  among 
Head's  cases;  but  there  is  usually  overlapping  of  these  areas.) 

Blood=Pressure  Changes  During  Anginal  Attack. — During  the  attack  of  angina  the 
blood-pressure  is  often  high  (Fig.  169)  though  Mackenzie  finds  that  there  is  often  no  change. 
In  one  case,  under  the  writer's  care,  who  remained  free  from  pain  at  120  mm.  Hg,  a  rise 
to  130  mm.  was  accompanied  by  pain  from  cardiac  overwork,  while  a  fall  to  105  mm.  caused 
pain  because  too  little  blood  was  forced  through  the  coronary  vessels. 

Sudden  Death  and  Motor  Disturbances. — The  phenomena  thus  far 
considered  are  purely  sensory;  and  the  question  arises,  what  are,  if  any, 
the  motor  disturbances  connected  with  angina  pectoris?  It  is  evident  that 
the  cessation  of  the  heart-beat  in  sudden  death  that  occasionally  occurs 

may  be  due  either  to  the  occlusion 
of  the  artery  or  to  a  sudden  onset 
of  complete  heart-block  as  in  the 
Adams-Stokes  syndrome.  The  lat- 
ter condition  is  sometimes  associ- 
ated with  angina  pectoris  and  in 
some  cases  due  to  coronary  sclerosis 
(see  page  578),  though  this  is  rare. 
Much  more  frequently  the  pulse  be- 
comes regular  after  a  short  time,  or 
sudden  death  from  heart-failure  sets 
in  just  as  in  the  experiments  of  Cohn- 
heim  and  v.  Schulthess-Rechberg. 

During  the  attacks  of  angina 
pectoris  the  blood-pressure  is  often 
high,  though  Mackenzie  states  that  in  many  cases  there  is  no  change  what- 
ever. This  seems  to  be  due  to  a  true  pectoral  vasomotor  crisis  in  the  sense 
of  Pal,  rising  sharply  with,  and  falling  sharply  after,  the  attack,  as  shown  in 
Fig.  169. 

ETIOLOGY   AND   VARIETIES   OF  ANGINA    PECTORIS. 

The  idea  that  sclerosis  of  the  coronary  arteries  was  the  lesion  which 
caused  angina  pectoris  seems  to  have  originated  not  with  Heberden  but  with 
Edward  Jenner,  discoverer  of  vaccination,  who  was  so  certain  of  its 
pathology  that  before  doing  an  autopsy  upon  a  case  he  made  a  bet  with  a 
friend  that  he  would  find  thickening  of  the  coronary  arteries.     He  won. 

This  indeed  seems  to  be  correct  for  very  many  cases  of  fatal  angina, 
since  Huchard  found  coronary  sclerosis  present  in  128  out  of  145  autopsies 
recorded  in  the  literature,  and  most  of  the  others  were  in  cases  of  adherent 
pericardium  of  valvular  disease.  Vernon  (Brit.  M.  J.,  1911,  i,  613),  on  the 
other  hand,  finds  but  50.1  per  cent,  of  coronary  disease  in  a  series  of  283  cases 
collected  from  various  authors.  Osier  calls  attention  to  occasional  deaths 
from  tobacco  and  other  toxic  anginas. 

1His  own  cases  56,  57,  and  58,  as  well  as  cases  of  many  other  writers,  show  tenderness 
during  and  after  attacks  due  to  aneurism  involving  the  ascending  aorta. 


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Fig.    169. — Blood-pressure  curve   showing  crises  of 
hypertension  during  attacks  of  angina  pectoris. 


ANGINA   PECTORIS.  387 

Angina  Pectoris  Without  Coronary  Sclerosis. — In  1812,  J.  Latham  re- 
ported a  number  of  cases  which,  in  spite  of  the  occurrence  of  intense  anginal 
symptoms,  did  not  run  the  usual  course  ending  in  sudden  death,  and  to  these 
he  gave  the  name  of ''pseudo-angina''  (angina  notha). 

Bean,  Stokes,  and  Graves  also  described  reflex  and  toxic  forms  of  angina, 
but  a  much  clearer  light  was  thrown  upon  the  subject  by  Nothnagel's  article 
entitled  "Angina  pectoris  vasomotoria."  He  says,  "We  must  interpret  this 
symptom-complex  to  indicate  that  we  are  not  dealing  with  a  disease  which 
arises  primarily  in  the  heart,  but  that  the  symptoms  of  stenocardia  are  of 
secondary  origin  and  are  brought  on  by  a  very  general  spasm  of  the  arteries." 

The  term  "pseudo-angina"  has  been  severely  criticised  by  Balfour  and 
Gibson,  since  "angina"  is  a  symptom,  not  a  disease,  and  in  all  cases  it  is  a 
very  real  one.  Nothnagel's  term,  "vasomotor  angina,"  or  Huchard's  "  reflex 
angina,"  seems  preferable  to  the  writer  on  this  account,  in  contrast  to  "coro- 
nary angina"  as  synonymous  with  "true  angina." 

Theories  as  to  Causation  of  Anginal  Pain. — Many  theories  have  been 
advanced  to  explain  the  causation  of  pain  in  anginal  attacks.  These  may 
be  classified  as  follows: 

(1)  Ischaemia  from  Coronary  Stenosis. — The  original  view  of  Jenner  was  later  supple- 
mented by  Allan  Burns,  that  the  attack  may  be  brought  on  by  asphyxia  of  the  heart  muscle 
when  there  was  a  disproportion  between  the  amount  of  blood  flowing  to  it  and  the  amount 
of  blood  which  it  needed.  Potain,  in  1870,  was  the  first  to  introduce  the  theory  that 
angina  pectoris  is  due  to  "  the  intermittent  claudication  of  the  heart " ;  but  Allan  Burns 
had  already  completely  demonstrated  this  causal  factor  in  1809  and  had  described  bis 
observations  in  the  following  words :  "  If  we  call  into  vigorous  action  a  limb  round  which 
we  have  with  a  moderate  degree  of  tightness  applied  a  ligature,  we  find  that  the  member 
can  only  support  its  action  for  a  very  short  time,  for  now  its  supply  of  energy  and  its  expen- 
diture do  not  balance  each  other  .  .  .  wc  witness  an  induction  of  an  extreme  degree 
of  debility  and  we  have  the  patient  complaining  of  an  unusual  painful  feeling  in  the  limb, 
but  still  all  its  muscles  are  in  a  state  of  inactivity.  ...  If  a  person  with  the  arteries 
of  the  heart  diseased  in  such  a  way  as  to  impede  the  progress  of  the  blood  along  them 
attempt  to  do  the  same  (ascend  a  steep  or  mount  a  pair  of  stairs),  he  finds  that  the  heart 
is  sooner  fatigued  than  the  other  parts  are,"  and  the  same  pain  results. 

(2)  Ischaemia  from  vasoconstrictor  spasm  of  the  coronary  arteries,  which  reduces 
the  functional  condition  to  the  same  state  as  described  by  Allan  Burns  for  the  coronary 
sclerosis.  This  seems  to  apply  to  the  vasomotor  and  toxic  anginas  and  often  consti- 
tutes a  factor  superimposed  upon  the  coronary  sclerosis  in  the  angina  vera.  Such  an 
action  of  drugs  upon  the  coronary  vessels  has  been  demonstrated  on  the  excised  heart  by 
O.  Loeb,  Langendorff,  and  Wiggers  (see  page  379). 

(3)  Acute  dilatation  of  the  heart,  producing  a  pain  similar  to  that  of  in- 
testinal colic.  This  theory  particularly  has  been  adhered  to  by  many  writers.  The 
similarity  between  the  anginal  pain  and  that  of  renal,  biliary,  pancreatic,  and  intestinal 
colic  suggests  that  it  belongs  to  the  common  form  by  which  the  visceral  nerves  give 
expression  to  overdistention.  Some  dilatation  usually  accompanies  the  attack,  and 
seems  to  be  a  primary  cause  of  the  pain  in  cardiac  overstrain  and  in  many  cases  of  val- 
vular lesion. 

(4)  Neuritis. — It  may  at  times  be  due  to  neuritis  of  the  cardiac  nerves,  or,  on 
the  other  hand,  to  a  neuritis  primary  in  the  brachial  nerves  and  referred  to  the  heart. 
Lesions  of  the  cardiac  plexus  have  been  described  by  Lancereaux,  Grocco,  and  Benenati.  but 
Herard  and  others  have  failed  to  find  them.  Nevertheless  it  is  quite  possible  that  sub- 
stances like  tobacco  (nicotine) ,  which  stimulate  sensory  nerves  in  the  heart  and  which  have 
a  specially  toxic  action  upon  the  ganglion  cells,  may  produce  toxic  neuritis  of  these  nerves. 

(5)  Neuralgia   of  the  cardiac  nerves. 

(6)  Action  of  other  constitutional  diseases  like  gout,  diabetes,  and  chronic  nephritis. 


388  DISEASES   OF   THE   HEART   AND    AORTA. 

But  it  is  most  probable  that  the  effects  are  due  to  the  other  above-mentioned  factors  which 
accompany  these  diseases, — arteriosclerosis  and  the  presence  of  vasoconstrictor  substances 
either  as  retention  products  or  internal  secretions. 

ASSOCIATED    CLINICAL    CONDITIONS. 

The  various  conditions  with  which  angina  is  associated  most  commonly 
might  be  classified  as  follows: 

I.  Organic  Lesions. 

A.  Sclerosis  of  coronary  arteries. 

B.  Aneurism,  especially  of  first  part  of  ascending  aorta. 

C.  Valvular  lesions,  especially  aortic  insufficiency.    (This  constitutes  a  very 

common  group.) 

D.  Aortic  aneurism,  especially  of  the  sinuses  of  Valsalva  and  the  ascending 

arch. 

E.  Adherent  pericardium.      (The  most  frequent  form  which  is  seen  in 

children.) 
II.  Vasomotor  anginas. 

A.  Hysterical  type,  most  common  in  women,  associated  with  other  vaso- 

motor disturbances  and  stigmata  of  hysteria. 

B.  Toxic,  due  to  the  action  of  various  poisons,  especially  (a)  tobacco,  (6) 

caffeine,  taken  both  as  tea  and  as  coffee. 

C.  Associated  with  hyperthyrodism  and  exophthalmic  goitre. 

III.  Attacks  of  more  or  less  anginoid  pain  occur  in  the  cases  of  acute  dilatation  of 
healthy  hearts,  due  to  primary  cardiac  overstrain. 

Angina  Pectoris  in  Valvular  Diseases. — The  attacks  of  angina  pectoris 
associated  with  coronary  sclerosis,  which  represent  the  original  form  de- 
scribed by  Heberden,  are  usually  designated  as  angina  vera.  These  are 
very  often  associated  with  valvular  lesions,  especially  with  aortic  insuffi- 
ciency in  which  the  coronary  lesions  are  usually  continuous  with  those  of 
the  aorta,  but  they  are  also  common  in  association  with  other  valvular 
lesions,  since  it  is  rare  to  find  a  case  of  chronic  valvular  disease  without 
some  disease  of  the  coronary  arteries.  The  presence  of  valvular  disease, 
therefore,  rather  favors  than  excludes  the  diagnosis  of  coronary  sclerosis. 

In  spite  of  the  frequency  with  which  these  two  conditions  are  asso- 
ciated, occasionally  one  encounters  cases  of  angina  with  valvular  disease, 
especially  aortic  insufficiency,  without  any  disease  of  the  coronary  vessels 
whatever,  as  was  well  exemplified  by  a  patient  with  a  ruptured  aortic  valve 
who  was  for  five  years  under  observation  at  the  Johns  Hopkins  Hospital. 
During  this  time  he  suffered  from  very  frequent  attacks  of  typical  angina 
pectoris.  He  died  suddenly  while  at  stool.  Autopsy  showed  rupture  of 
aortic  leaflet.  The  coronary  arteries  were  soft  and  the  walls  were  not 
thickened  anywhere. 

Angina  Pectoris  in  Acute  Dilatation. — It  is  possible:  (1)  that  under 
these  conditions  acute  dilatations  of  the  heart,  due  to  momentary  diminu- 
tion in  tone  of  the  heart  muscle,  might  be  the  immediate  cause  of  the  pain, 
which  would  thus  be  of  primary  cardiac  rather  than  vascular  origin.  (2) 
That  in  such  dilatation,  etc.,  centripetal  stimuli  may  arise  in  the  heart 
which  may  cause  a  general  vasoconstriction.  (This  is  contrary  to  the  usual 
depressor  effect  of  stimuli  arising  in  the  heart,  but  it  is  not  at  all  certain 
that  in  the  presence  of  such  a  pathological  condition  as  angina  pectoris 
the  paths  of  least  resistance  in  the  central  nervous  system  may  not  be  quite 


ANGINA   PECTORIS.  389 

different  from  what  they  are  in  the  normal  individual.)  (3)  Miss  Hyde  in 
Porter's  laboratory  has  shown  that  dilatation  of  the  heart  in  itself  caused 
diminution  in  the  flow  through  the  coronary  arteries,  and  it  is  possible 
that  the  circulation  may  thus  be  diminished  to  a  point  at  which  relative 
ischsemia  of  the  heart  may  set  in  and  cardiac  pains  result. 

Angina  Pectoris  in  Aneurism. — Attacks  of  angina  pectoris  are  very 
common  in  cases  of  aneurism  involving  the  ascending  arch,  and  especially 
in  early  small  aneurisms  near  the  sinuses  of  Valsalva.  This  has  long  been 
known,  but  is  the  subject  of  an  especially  interesting  article  by  Dr.  Osier 
upon  "Angina  pectoris  as  an  early  symptom  of  aneurism." 

The  anginoid  pains  in  this  condition  are  probably  simply  reflex,  not  the  result  of 
primary  peripheral  vasoconstriction,  cardiac  ischaemia,  etc.,  but  simply  the  occurrence  of 
pain  sensation  arising  in  the  aortic  walls  from  overstretching  of  the  aorta  under  pressure 
heightened  from  any  cause  whatever,  or  from  increased  excursion  of  the  aortic  wall  as  a 
result  of  increased  systolic  output,  etc.,  as  is  so  frequently  seen  in  the  abdomen  in  nervous 
women  with  epigastric  pain  due  to  a  throbbing  of  the  abdominal  aorta.  In  the  later  stages 
of  the  aneurism,  the  symptoms  may  be  less  intense,  due  perhaps  to  the  fact  that  by  erosion, 
etc.,  pressure  upon  the  aneurism  has  diminished,  perhaps  to  the  fact  that  after  a  time 
endings  of  the  sensory  nerves  have  been  permanently  injured  or  rendered  less  sensitive 
by  the  progressive  change  in  the  aortic  wall. 

Anginal  Attacks  in  Children.— Angina  pectoris  also  occurs  in  children,  especially  in 
association  with  mitral  stenosis,  as  illustrated  by  the  following  case:  The  patient  was 
a  boy  aged  8  who  had  had  rheumatism  in  the  right  hip  two  years  previously,  and  since 
then  "had  attacks  of  pain  over  the  heart,  especially  after  exercise.  The  pain  was  so 
severe  that  it  compelled  him  to  stand  perfectly  still  until  it  passed  off;  his  cheeks  became 
blue  and  pale.  He  sometimes  felt  as  though  held  in  a  vise,  but  never  had  any  feeling  of 
fear.  He  also  had  at  times  pain  on  the  right  side  over  about  the  sixth  rib,  which  was 
sometimes  present  with  that  on  the  left  side,  but  often  present  without  it.  Exercise  seemed 
to  bring  on  both.  Examination  showed  a  very  slightly  enlarged  heart  with  systolic  retrac- 
tion over  the  fourth  left  interspace,  none  about  origin  of  diaphragm  (Broadbent's  sign 
absent).  Area  of  cardiac  flatness  changes  with  respiration.  The  first  sound  at  the  apex 
was  snapping  in  character  and  was  preceded  by  a  well-defined  rumble.  Second  sound  was 
clear,  accentuated  over  the  pulmonic  area.  Pulse  92  per  minute,  of  good  volume,  regular 
in  force  and  rhythm." 

Such  attacks  are  quite  definite  angina  vera  in  the  sense  of  Heberden,  and  indeed  the 
latter  includes  a  similar  case  in  his  list.  In  children  the  association  is,  however,  much 
more  commonly  with  valvular  lesions  than  with  coronary  sclerosis,  and  perhaps  most 
frequently  of  all  with 

Adherent  Pericardium. — This  is  an  extremely  common  concomitant  and  cause  of 
anginal  attacks,  especially  in  children  and  adolescents.  The  pains  are,  perhaps,  simply 
reflex  aches  from  the  ordinary  tugs  upon  the  pericardium,  perhaps  brought  about  by  the 
stretching  of  the  pericardial  fibres  which  occurs  when  the  heart  becomes  dilated. 

VASOMOTOR    ANGINA. 

The  second  great  group  of  cases  with  anginal  symptoms  are  those  in 
which  the  anginal  symptoms  are  of  purely  vasomotor  origin  (Raynaud's 
disease  of  the  heart)  and  are  not  associated  with  organic  lesions, — the 
angina  pectoris  vasomotoria  of  Nothnagel  (angina  pectoris  spuria  of  Latham, 
angines  de  poitrine  reflexes  of  Huchard).  The  characteristic  phenomenon 
in  this  group  is  the  occurrence  of  general  or  local  vasocon- 
striction ushering  in  the  attack;  that  is,  there  are  usually 
coldness,  numbness,  often  tingling,  weakness,  and  heaviness  in  the  left 
arm,  pallor  of  the  latter,  with  marked  diminution  in  size  and  caliber  of 
the  left  radial,  often  also  of  the  right  radial  artery,  sometimes  of  the  vessels 


390  DISEASES   OF   THE   HEART   AND    AORTA. 

of  the  leg,  trunk,  and  head.  The  patient  may  become  pale  and  blue  or  the 
lips  ashen,  and  the  course  of  the  attacks  may  exactly  simulate  those  of 
coronary  sclerosis.  Death  in  such  attacks  is,  however,  extremely  rare. 
It  has  occurred  in  several  cases  in  which  no  coronary  sclerosis  nor  other 
lesion  was  present  to  account  for  the  death.  However,  Dr.  Osier  suggests 
that  in  these  cases  there  may  have  been  myocardial  changes  demonstrable 
only  by  the  method  of  Krehl. 

Hysterical  Angina. — The  most  common  form  of  vasomotor  angina  is 
the  neurotic  or  hysterical  type,  which  is  most  common  in  young  women 
and  is  associated  with  the  other  stigmata  of  hysteria.  It  may  also  occur  in 
men.  For  example,  a  neurotic  young  physician  recently  under  the  writer's 
care  developed  anginal  symptoms  (fear,  precordial  constriction,  pain  down 
left  arm)  after  seeing  a  relative  die  of  angina  pectoris.  He  recovered  after 
being  assured  his  trouble  was  trivial. 

Clinical  Groups  with  Anginal  Symptoms  and  their  Characteristic  Features 

(modified  from  Huchard) . 

Coronary  Angina. — Site  of  disturbance. — Stenosis  or  obliteration  of  the 
coronary  arteries.  (In  some  cases  valvular  lesion  or  aneurism  only).  Age. 
— Age  of  arteriosclerosis  after  40.  Factors  bringing  on  attack. — Effort  of 
some  sort,  mental  or  physical.  Rarely  spontaneous,  sometimes  nocturnal. 
Not  associated  with  any  other  form  of  neurosis.  Nature  of  pain. — Ag- 
onizing sensation  of  pressure.  Usually  felt  most  acutely  behind  sternum. 
Referred  pain  down  arm,  especially  left  arm,  and  over  chest,  neck,  etc. 
Duration. — 2  to  15  minutes,  stopping  soon  after  standing  still.  Attitude. 
— Silent,  immobile.  Prognosis. — Grave;  almost  always  fatal.  Treatment. 
— Vasodilators. 

Hysterical  Angina. — Site  of  disturbance. — Central  nervous  system  acting 
through  the  vasomotor  nerve  and  cardiac  plexus.  Age. — At  all  ages,  even 
childhood;  sometimes  at  menopause.  Most  frequent  in  women.  Factors 
bringing  on  attack. — Usually  spontaneous  onset  without  effort,  often  recur- 
ring at  fixed  hours  and  associated  with  other  neurotic  symptoms.  Nature 
of  pain. — Pain  less  agonizing,  with,  feeling  that  the  heart  is  distended — felt 
most  intensely  at  the  apex.  Duration. — 1  to  2  hours,  not  diminished  by 
standing  still,  not  increased  by  walking.  Attitude. — Agitated;  walking  about. 
Prognosis. — Mild;  never  fatal.  Treatment. — Antineurotics  and  antineuralgics. 

Gastrointestinal. — Site  of  disturbance. — Distention  or  neuralgia  due  to 
gastric  troubles.  Age. — At  all  ages,  especially  among  women.  Factors 
bringing  on  attack. — Not.  brought  on  by  effort.  Nature  of  pain. — Precordial, 
not  substernal  pain;  with  fulness  of  chest  and  distention  of  heart  but  less 
radiation.  Signs  of  dilatation  of  right  heart;  increase  of  inverse  diameter 
to  right.  Duration. — 1  to  2  hours.  Prognosis. — Death  rare.  Treatment. — 
Antidyspeptic  remedies. 

Tobacco. — Site  of  disturbance. — Spasm  of  coronary  arteries.  Factors 
bringing  on  attack. — Angina  associated  with  toxic  disturbances,  vertigo, 
gastric  and  respiratory  troubles.  Onset  spontaneous.  Nature  of  pain. — 
Attacks  associated  with  bradycardia,  intermittent  pulse,  arrhythmia,  pal- 
pitations.    Attacks  longer  than  those  of  angina  vera.     Prognosis. — Death 


ANGINA   PECTORIS.  391 

rare.  Attacks  often  disappear  rapidly  on  giving  up  tobacco.  Treatment. — 
Stopping  tobacco,  tea,  and  coffee.  Rest  and  mental  quiet.  Light  diet. 
(Anginas  due  to  tea,  coffee,  etc.,  brought  about  by  the  same  cause.) 

Acute  Cardiac  Overstrain  (with  or  without  Valvular). — Site  of  disturbance. 
— Sudden  dilatation  of  the  heart.  Age. — At  any  age,  but  most  common  in 
young  athletes,  soldiers,  anaemic  girls.  Factors  bringing  on  attack. — Comes 
on  in  the  midst  of  some  unusual  effort,  such  as  a  mountain  climb,  boat  race, 
a  charge,  or  a  dance.  Nature  of  pain. — In  the  heart  itself,  usually  retro- 
sternal. Associated  with  signs  of  dilatation  to  right  and  left,  extreme 
dyspnoea,  often  systolic  murmur  and  arrhythmia.  Duration. — In  maxi- 
mum intensity  a  few  minutes,  after  cessation  of  attack,  the  pains  often 
continuing  or  recurring  as  less  intense  pain,  tachycardia  or  arrhythmia 
usually  persisting  some  time  after  attack.  Attitude. — Immobile.  May 
throw  himself  to  the  ground  in  the  midst  of  the  effort.  Prognosis. — Death 
rare.  Permanent  weakening  of  the  heart  if  the  over-exertion  is  soon  and 
frequently  repeated.  Treatment. — Prolonged  rest  and  general  cardiac 
therapy  until  cardiac  dilatation  has  passed  off;  gradual  resumption  of 
active  life. 

Angina  Pectoris  in  Hyperthyroidism.  —  Very  closely  resembling  the 
neurotic  group  are  the  cases  of  angina  associated  with  exophthalmic  goitre, 
in  which  the  attacks  are  sometimes  more  like  those  of  neurotic,  sometimes 
more  like  those  of  the  coronary  type.  The  crucial  point  in  the  diagnosis 
is  the  detection  of  hyperthyroidism  by  the  application  of  the  numerous 
tests  for  Graves's  disease,  etc. 

A  case  which  has  been  for  the  past  year  and  a  half  and  still  is  under 
the  writer's  care  will  serve  as  type  of  this  condition  (see  page  690). 

Treatment  is  the  same  as  for  the  Graves's  disease  which  is  the  primary 
condition  (see  Part  IV,  Chapter  II).  The  attacks  themselves  may  be 
treated  symptomatically  with  amyl  nitrite,  etc.,  but  the  important  factor 
is  the  treatment  of  the  underlying  disease. 

Tobacco  Angina. — Anginal  attacks  due  to  tobacco  are  not  uncommon, 
both  in  young  persons  beginning  their  first  excesses  in  tobacco  and  in  older 
persons  whose  over-indulgence  is  adding  itself  to  a  beginning  or  advancing 
coronary  sclerosis.  In  both  the  symptoms  disappear  soon  after  the  tobacco 
is  absolutely  given  up,  persistence  of  the  attacks  more  than  a  few  days 
after  this  being  evidence  that  some  damage  to  the  coronaries  has  occurred. 
The  attacks  themselves  may  very  closely  resemble  those  of  true  angina,  but 
very  frequently  precordial  pains  not  of  an  anginal  character  may  be  felt 
by  smokers  between  or  for  some  time  before  such  attacks. 

The  main  factor  in  the  effect  of  tobacco  smoke,  as  shown  by  Ratner  and  Lee,  is  the 
nicotine,  although  small  amounts  of  HCN,  CO,  and  pyridine  bases  are  present  in  the 
smoke.  Moreover,  it  is  probable  that  the  action  of  smoked  tobacco  is  exerted  especially 
upon  the  coronary  arteries,  because  it  enters  the  heart  directly  from  the  pulmonary  vein 
without  preliminary  dilution  in  the  peripheral  circulation. 

Nicotine  seems  to  have  the  effect  of  (1)  stimulating  the  vagus,  (2)  producing  vaso- 
constriction, (3)  thereby  of  raising  the  blood-pressure.  (4)  Kravkov  (Roussky  Vratch,  1914, 
xiii,  1)  found  that  nicotine  caused  constriction  of  the  coronary  arteries,  which  may  explain 
tobacco  angina  entirely.  Moreover,  Jackson  and  Matthews  have  recently  shown  for  aconite, 
which  in  many  ways  is  a  similar  drug,  that  much  of  its  action  is  exerted  through  stimulation 
of  the  sensory  endings  of  the  depressor  nerve.  It  is  possible  that  nicotine  angina  is  due  in 
part  to  similar  sensory  stimulation. 


392  DISEASES   OF  THE   HEART   AND    AORTA. 

Angina  in  Acute  Dilatation. — The  attacks  of  pain  and  precordial  dis- 
comfort during  acute  cardiac  overstrain  and  dilatation  may  reach  anginoid 
intensity,  as  was  noted  by  da  Costa  among  the  soldiers  of  the  Civil  War. 
He  not  infrequently  encountered  patients  who  had  suffered  so  intensely  in 
the  midst  of  a  charge  that  they  could  endure  it  no  longer  and  had  thrown 
themselves  to  the  ground,  exposed  to  almost  certain  death  from  the  point- 
blank  fire  of  the  enemy,  rather  than  continue  to  bear  the  torment  within 
(page  189).     These  pains  are  usually  retrosternal,  often  with  numbness  of 
the  arms  and  tingling  in  the  fingers,  and  associated  with  feeling  of  compres- 
sion and  with  palpitation.     These  pains  occur  in  otherwise  healthy  persons 
during  the  height  of  supreme  effort,  while  in  patients  with  myocardial  weakness 
or  coronary  sclerosis  only  a  slight  effort  or  indeed  even  emotional  excitement 
may  suffice  to  bring  them  on. 

DIAGNOSIS. 

The  actual  differentiation  of  the  various  groups  is  not  always  easy  in 
the  individual  cases,  as  one  frequently  has  a  coronary  sclerosis  with  a 
tobacco  angina  superinduced  upon  it,  a  gastric  etiology  where  there  are 
already  attacks  of  angina  vera,  etc.,  and  since  it  is  a  safe  rule  never  to  diag- 
nose the  milder  conditions  until  the  more  serious  can  be  ruled  out  with 
reasonable  probability.  These  cases  may  cause  the  physician  anxiety, 
since  he  remains  uncertain  whether  to  expect  sudden  death  or  whether 
he  is  dealing  with  a  comparatively  mild  condition. 

Case  Illustrating  Doubtful  Diagnosis. 

E.  W.,  widow,  aged  65,  has  had,  since  her  menopause  at  54,  occasional  attacks  of 
precordial  pain,  most  intense  just  behind  the  sternum  and  especially  about  the  level 
of  the  third  costal  cartilage.  She  feels  as  though  some  one  were  bor- 
ing through  from  sternum  to  spine  with  a  sharp  instrument.  The  pain  is 
also  felt  over  the  left  side  of  the  chest  and  down  the  left  arm,  which  sometimes 
becomes  numb,  cold,  weak,  and  heavy.  During  the  attack  she  feels  as  "though  the 
end  has  come."  These  attacks  come  on  apparently  spontaneously  without  definite  asso- 
ciation with  either  emotional  disturbance,  exposure  to  cold,  or  muscular  effort.  They 
last  an  hour  or  two  and  are  relieved  by  amyl  nitrite  or  nitroglycerin.  She  feels 
weak  for  a  day  or  so  after  an  attack,  but  at  other  times  is  extremely  active  for  her  age 
and  rarely  short  of  breath.  The  patient  is  not  at  all  neurotic.  She  has  used  coffee  and 
beer  in  moderation  all  her  life.  It  must  be  added  that  near  the  end  of  the  menopause 
and  before  the  first  cardiac  attack,  she  had  a  severe  spell  of  grippe  which  kept  her 
in  bed  for  four  weeks  and  left  her  very  much  prostrated. 

On  physical  examination  the  patient  is  well  nourished.  Slightly  emphysematous, 
but  lungs  otherwise  normal.  Heart  not  enlarged;  action  regular  in  force  and  rhythm; 
sounds  clear,  neither  second  sound  especially  accentuated.  Pulse  between  attacks  is  of 
good  large  volume  and  quality,  apparently  about  normal  tension;  vessel  wall  not  specially 
thickened.  No  ascites.  Liver  not  enlarged.  Feet  always  swollen  from  varicose  veins, 
not  especially  so  during  or  after  attacks. 

In  this  case  the  question  of  crucial  importance  is  whether 
the  angina  is  due  to  the  occurrence  of  the  menopause  and  is 
neurotic,  or  to  the  influenza  which  she  contracted  about  the 
same  time  and  which  may  have  brought  on  a  coronary  sclerosis. 
The  attacks  themselves  resemble  angina  vera,  although  their  duration  is  longer  than 
usual.  The  age  of  the  patient  and  the  history  of  severe  influenza  also  are  in  favor  of  coro- 
nary sclerosis.  On  the  other  hand,  the  fact  that  ordinary  exertion  does  not  seem  to  bring 
them  on,  but  that  they  occur  when  the  patient  is  moderately  quiet,  is  in  favor  of  the  neu- 
rotic.   It  must,  however,  be  borne  in  mind  that  the  patient's  statements  in  this  regard 


ANGINA  PECTORIS  393 

may  be  inaccurate,  and,  further,  that  in  occasional  cases,  where  the  diagnosis  of  functional 
angina  seemed  quite  well  established,  autopsy  has  shown  definite  coronary  sclerosis.  It 
seems  impossible  to  establish  a  definite  diagnosis  here,  and  the  management  of  the  case  is 
therefore  directed  toward  the  severer  form,  ordering  as  quiet  a  life  as  the  patient  will  carry 
out  (since  potassium  iodide  is  not  well  borne),  vigorous  use  of  amyl  nitrite  and  nitroglycerin 
at  the  time  of  the  attacks,  and  erythrol  tetranitrate  thereafter.  A  diet  of  small  quantities 
of  food  low  in  purin  bodies  and  salt  is  insisted  on. 

Since  these  measures  have  been  instituted  she  has  remained  entirely  free  from  angina 
attacks  for  two  years,  in  spite  of  another  attack  of  influenza.  These  facts  are  in  favor  of  a 
reflex  origin  of  the  condition. 

Differentiation  from  Abdominal  Diseases. — Angina  pectoris  is,  as  a 
rule,  easily  differentiated  from  other  diseases,  though  occasionally  an  attack 
of  biliary,  pancreatic,  or  left  renal  colic  referred  to  the  shoulders  or  even 
intestinal  colic  high  in  the  epigastrium  may  closely  simulate  it.  Careful 
physical  examination  and  location  of  the  areas  of  tenderness  over  the 
affected  viscus  should  rule  out  this  error. 


TREATMENT. 

The  treatment  of  angina  pectoris  can  be  divided  into  two  divisions :  Pro- 
phylaxis against  attacks,  and  treatment  during  the  attack. 

Since  the  anginal  attacks  are  brought  about  chiefly  by  anxiety,  exertion 
and  overeating,  effective  prophylaxis  should  be  directed  at  these  provocative 
factors. 

The  patient's  mode  of  life  and  habits  should  be  carefully  inquired  into 
in  every  detail  to  determine  all  the  sources  of  wasted  energy,  emotional  and 
physical,  and  an  attempt  should  be  made  to  readjust  his  habits  and  manner 
of  life  so  as  to  admit  of  the  greatest  conservation  of  energy.  Very  often  hurry 
and  worry,  and  not  the  effort  inherent  in  the  work  itself,  represent  the 
patient's  greatest  expenditures  of  energy,  and  if  the  patient  follows  advice  to 
cut  out  unessentials  and  to  perform  the  essential  work  and  movements  with 
great  deliberation  he  may  be  spared  many  anginal  attacks.  One  of  the  chief 
modes  of  wasting  energy  is  rapid  talking;  and  much  good  may  be  accom- 
plished by  drilling  the  patient  in  slow,  deliberate  speech. 

One  patient,  seventy-two  years  old,  under  the  writer's  care,  who  had  been 
suffering  daily  attacks  of  angina  vera,  remained  free  from  pain  for  several 
years  merely  by  changing  from  quick  and  nervous  to  slow  and  deliberate 
movements  and  observing  a  few  of  the  essential  precautions  discussed  on 
page  215.  It  was  shown  to  him  that  by  ascending  a  staircase  slowly  at  the 
cost  of  a  minute  or  two  extra  time,  he  saved  himself  several  hours  daily  that 
would  have  been  lost  in  recuperation  from  attacks;  that  rising  rapidly  from 
a  chair  or  suddenly  striding  across  a  room  cost  almost  in  hours  what  they  saved 
in  seconds,  and  that  in  every  way  for  the  anginal  patient  "Haste  makes 
waste,"  and  brings  pain  in  its  wake. 

He  should  be  taught  that  worry  has  the  same  effect  as  bodily  exertion  in 
bringing  on  attacks  and  that,  for  the  angina  patient,  it  is  better  meekly  to 
submit  to  any  condition  than  to  allow  himself  to  be  subject  to  worry  in 
striving  against  it. 

The  patient's  diet  should  be  carefully  investigated  and  any  articles  of  food 
which  seem  to  bring  on  attacks  should  be  carefully  avoided.  One  of  the  most 
important  factors  in  such  digestive  disturbance  is  rapid  eating.     Flatulence 


394  DISEASES  OF   THE  HEART  AND  AORTA. 

and  air  swallowing  contribute  largely  both  to  discomfort  and  pain  and  these 
may  sometimes  be  controlled  by  valerian. 

The  attacks  themselves,  once  precipitated,  demand  immediate  attention. 
Absolute  quiet  is  usually  assumed  spontaneously  by  the  patient  himself. 
The  condition  usually  demands  treatment  with  drugs. 

For  the  milder  attacks  the  milder  vasodilators,  such  as  a  little  brandy 
or  a  teaspoonful  of  spiritus  setheris  nitrosi,  often  accompanied  by  half  a  tea- 
spoonful  of  aromatic  spirit  of  ammonia,  usually  suffice,  but  the  more  severe 
ones  require  the  inhalation  of  a  few  minims  of  amyl  nitrite  or  the  adminis- 
tration of  one  or  two  drops  of  spirit  of  nitroglycerin. 

The  administration  of  the  nitrites  introduced  by  Sir  Lauder  Brunton  in 
1867  is  often  almost  specific  in  its  action,  but  in  other  cases  absolutely  fails. 
Both  the  success  and  failure  of  these  drugs  seem  to  depend  upon  the  condition 
of  the  coronary  circulation  as  was  well  illustrated  in  a  case  of  coronary  angina 
under  the  writer's  care  in  1912.  This  patient  was  free  from  pain  when  her 
blood-pressure  was  120  mm.  Hg,  but  suffered  pain  whenever  it  rose  to  130 
or  fell  to  110.  At  130  it  was  relieved  by  nitrites  because  the  blood-pressure 
was  returned  to  120,  the  overwork  of  the  heart  relieved  and  an  optimal 
coronary  circulation  re-established.  At  110  it  was  aggravated  by  nitrites, 
because  the  blood-pressure  was  brought  down  to  100  or  105,  and  this  was  too 
low  to  drive  enough  blood  through  the  coronaries  to  nourish  the  heart  muscle. 
The  low  pressures  require  heart  stimulants,  the  higher  pressures  require 
vasodilators. 

The  blood-pressure  may  be  kept  down  with  sodium  nitrite  (.06  to  0.12 
Gm.,  gr.  i  to  ii),  whose  action  lasts  one  or  two  hours,  or  with  erythrol  tetra- 
nitrate  (.03  to  .06  Gm.,  gr.ss  to  i)  whose  action  lasts  four  to  five  hours. 

When  the  blood-pressure  is  too  low  digitalis  or  strophanthin  should  be 
given  continuously  during  the  periods  when  attacks  are  frequent  and  for  a 
few  days  after  an  attack.  The  digitalis  may  well  be  administered  along  with 
nitrites  in  order  to  maintain  dilatation  of  the  peripheral  and  coronary  vessels 
throughout  the  period  of  its  action. 

In  severe  attacks,  the  pain  may  be  so  severe  that  it  may  require  mor- 
phine to  subdue  it,  and  the  most  severe  attacks  resist  even  the  action  of 
morphine.  If  morphine  is  used  with  frequency  it  should  be  accompanied  by 
small  doses  of  atropine  in  order  to  inhibit  the  effects  upon  the  respiratory 
centre  and  the  production  of  cardiac  asthma  during  the  stages  of  morphine 
habituation. 

Between  attacks,  bromides  in  large  doses  may  be  of  some  benefit  by 
quieting  the  anxious  mind  of  the  patient  and  thus  warding  off  the  attacks 
that  might  be  brought  on  through  mental  excitement. 

Potassium  Iodide. — Potassium  iodide  in  moderate  doses — 0.3  Gm.  (gr.  v) 
to  4  Gm.  (31)  t.i.d. — should  be  given,  as  it  sometimes  seems  to  diminish  the 
frequency  and  severity  of  attacks. 

Caffeine,  Theobromine,  and  Theophylline. — Caffeine  and  especially 
theobromine  and  theophylline  preparations — especially  acettheobromine 
sodium  ("agurin")  and  acettheophylline — have  been  highly  recommended, 
from  the  clinical  stand-point,  by  Askanazy,  Kaufmann  and  Pauli,  R.  Breuer, 
Buch,  Pineles,  v.  Leyden,  and  others,  to  relieve  and  to  ward  off  the  attacks 
of  stenocardia. 


ANGINA  PECTORIS.  395 

Oswald  Loeb  has  given  an  experimental  basis  to  these  observations  by  demonstrat- 
ing on  the  excised  heart  that  these  drugs  increase  the  blood  flow  through  the  coronary 
vessels  as  well  as  increase  the  systolic  output  and  the  force  of  the  heart-beat.1  Theobromine 
and  theophylline  are  to  be  preferred  to  caffeine,  since  they  do  not  increase  peripheral 
resistance  and  have  little  action  upon  the  higher  nervous  centres,  but,  on  the  other  hand, 
a  more  marked  action  on  the  coronary  arteries.  On  the  other  hand,  they  are  not  very 
certain  in  producing  their  effect.  They  may  be  helpful  in  some  cases  and  may  absolutely 
fail  in  others,  and,  while  they  are  worthy  of  a  trial  in  almost  every  case,  they  cannot  as 
yet  be  expected  to  supplant  the  nitrites  and  iodides. 

Diet. — rDiet  is  all-important.  It  should  be  chiefly  lactovege- 
tarian  in  character.  The  meals  should  be  small  in  amount,  to  pre- 
vent overloading  and  distention  of  the  stomach  and  hence  the  pushing  up 
of  the  diaphragm.  Gastric  fermentation  should  be  prevented 
by  removing  from  the  diet  any  articles,  such  as  soft  hot  breads,  heavy  and 
greasy  pastry,  etc.,  which  may  be  found  to  produce  flatulence,  and  by  general 
treatment  of  the  gastric  condition.  Air-swallowing  should  be  care- 
fully looked  for  and  treated  (see  page  705).  Meat  and  soups  should 
be  reduced  to  small  quantities,  since  they  contain  considerable  quantities 
of  purin  bodies  which  have  a  vasoconstrictor  action  and  which  also  act 
injuriously  upon  the  kidneys.  The  vegetable  and  cereal  foods  should  make 
up  the  bulk  of  the  diet.  Salt  should  be  reduced  for  the  same  reason.  Liquids 
should  be  restricted  to  about  1500  c.c.  a  day. 

Milk  may  be  a  staple  article  in  the  diet,  unless,  as  in  many  persons, 
it  tends  to  flatulence.  This  is  sometimes  obviated  by  adding  a  very  little 
weak  tea  or  coffee,  but  very  often  it  must  be  dispensed  with  altogether. 

Tobacco  should  be  absolutely  excluded  in  both  organic  and  func- 
tional cases. 

Tea  and  coffee  in  small  amounts  (one  cup  a  day,  very  weak)  probably 
have  very  little  effect  upon  the  average  individual  who  has  been  accustomed 
to  them,  but  may  be  quite  important  factors  in  bringing  on  the  attacks  in 
persons  whose  sensitiveness  is  a  little  above  normal  and  in  whom  there  is  a 
tendency  to  angina.    It  is  best  for  them  to  be  given  up. 

Local  Treatment  of  the  Chest  Wall. — Vigorous  counter-irritation  to 
the  chest  wall,  by  blistering,  etc.,  is  also  of  value,  and  Hasselbach  and 
Jacobaeus  report  very  marked  improvements,  lasting  a  year  or  so,  from 
exposure  of  the  precordium  to  the  Finsen  light  for  an  hour  a  day  until  a 
marked  cutaneous  reaction  or  even  blistering  has  set  in. 

Electrical  Treatment. — J.  O.  Hirschf elder  states  that  in  five  cases  he 
has  obtained  striking  relief  of  the  symptoms  by  treatment  with  the 
galvanic  current,  applying  the  anode  (a  pad  4  cm.  in  diameter) 
to  the  neck  over  the  course  of  the  vagus,  and  the  cathode  (6-12  cm. 
in  diameter)  to  the  precordium,  and  passing  a  current  of  2  0  m  i  1 1  i  a  m  - 
p  e  r  e  s  for  five  minutes  to  each  side  of  the  neck.  One  patient  remained 
free  from  attacks  until  his  death  two  years  after  the  treatment;  another  has 
remained  free  for  several  years.  In  the  other  three  the  relief  was  less  per- 
manent, but  still  very  gratifying. 

1  Dr.  G.  S.  Bond,  in  the  writer's  laboratory,  has  been  unable  to  produce  any  appre- 
ciable change  in  the  outflow  from  the  coronary  veins  of  the  dog's  heart  in  situ;  and  with 
the  amyl  nitrite  and  nitroglycerin  observed  a  marked  decrease  in  the  outflow,  even  when 
the  animal's  heart  was  dilated. 


396  DISEASES  OF  THE  HEART  AND  AORTA. 

In  other  cases  the  use  of  electric  baths,  and  especially  with  the 
si  nusoidal  current,  may  be  of  value  (Rumpf),  but  the  effect  is 
readily  overdone.  Sir  William  Ewart  recommends  inhalations  of  C02  (see 
page  234). 

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Physiol.,  Leipz.,  1908,  xxi. 
Mackenzie,  James:  Heart  Pain  and  Sensory  Disorders  Associated  with  Heart  Failure, 

Lancet,  Lond.,  1895,  i,  16. 
Head,  H.:  Pain  in  Visceral  Disease,  Brain,  Lond.,  1893,  xvi,  1;  1894,  xvii,  339;  1896, 

xix,  153. 


ANGINA  PECTORIS.  397 

Head,  H.,  Rives,  W.,  and  Sherren,  Jr. :  The  Afferent  Nervous  System  from  a  New  Aspect, 
ibid.,  1905,  xxviii,  99.  Sherren,  J.:  Some  Surgical  Observations  on  Referred  and 
Reflected  Pain,  Clin.  J.,  Lond.,  1905,  xxxvi,  168.  Abstracted  in  editorial,  J.  Am.  M. 
Assoc,  Chicago,  1909,  lii. 

Head,  H.,  and  Thompson,  Th.:  The  Grouping  of  Afferent  Impulses  within  the  Spinal  Cord 
ibid.,  1906,  xxix,  536. 

Harvey,  Wm. :  The  Works  of  Wm.  Harvey,  trans,  by  R.  Willis.  Printed  for  the  Sydenham 
Soc,  Lond.,  1847,  382. 

Hirschfelder,  A.  D.:  Observations  on  a  Case  of  Palpitation  of  the  Heart,  Bull.  Johns 
Hopkins  Hosp.,  Baltimore,  1906,  xvii,  299. 

Huchard,  H.:  Traite  clinique  des  maladies  du  cceur  et  de  l'aorte,  3d  edit.,  Paris,  1899, 
ii,  p.  1  et  seq. 

Ratner,  Lee.    Quoted  on  p.  717. 

Jackson,  D.  E.,  and  Matthews,  S.  A.:  The  Sensory  Nerves  of  the  Heart  and  Blood-vessels 
as  a  Factor  in  Determining  the  Action  of  Drugs,  Am.  J.  Physiol.,  Bost.,  1908,  xxv,  255. 

Lancereaux:  De  l'alteration  de  l'aorte  et  du  plexus  cardiaque  dans  l'angine  de  poitrine, 
Compt.  rend.  Soc.  de  biol.,  Par.,  1864,  4  s.,  i,  15. 

Grocco,  P.:  Sull  angina  di  petto,  Settimana  Med.  di  Sperimentale,  Firenze,  1896,  i,  1,  13, 
109,  169,  181. 

Benenati,  U.:  Sull'  origine  nevritica  dell'  angina  pectoris  da  aortite  sifilitica,  Riforma  Med. 
Roma,  1902,  xviii,  326,  339,  351. 

Mott,  F.  W.  Quoted  from  Oliver,  Th.:  A  Lecture  on  Angina  Pectoris  and  Allied  Con- 
ditions, Lancet,  Lond.,  1905,  ii,  812. 

Herard:  Angine  de  poitrine  caracterisee  anatomiquement  par  un  retrecissement  considera- 
ble des  deux  arteres  coronaires  a  leur  origine  sans  lesions  des  plexus  cardiaques,  Bull. 
Acad,  de  Med.,  Par.,  1883,  2  ser.,  xii,  1522. 

Latham,  J.:  Med.  Trans.  Roy.  Coll.  Phys.,  Lond.,  1812.    Quoted  from  Gibson. 

Nothnagel,  H.:  Angina  pectoris  vasomotoria,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1867, 
iii,  309. 

Osier,  W.:  Angina  Pectoris  as  an  Early  Sign  in  Aneurism  of  the  Aorta,  Med.  Chron.,  Man- 
chester, 1906,  lxiv,  69. 

Lauder-Brunton,  T.:  On  the  Use  of  Nitrite  of  Amyl  in  Angina  Pectoris,  Lancet,  Lond. 
1867,  ii,  97. 

Askanazy:  Klinisches  ueber  Diuretin,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  lvi,  209. 

Kaufmann  and  Pauli:  Zur  Symptomatologie  des  stenokardischen  Anfalles,  Wien.  klin. 
Wchnschr.,  1902,  xv,  1160. 

Breuer,  R.:  Zur  Therapie  und  Pathogense  der  Stenokardie  und  verwandter  Zustande, 
Munchen.  med.  Wchnschr.,  1902. 

Pineles,  Fr. :  Theocinbehandlung  stenokardischer  Anfalle,  Mitth.  d.  Gesellsch.  f .  inn.  Med., 
Wien,  1903-1904.     (Quoted  from  Pal.) 

v.  Leyden,  E.:  Funfzig  Jahre  innerer  Therapie,  Therap.  d.  Gegenw.,  Berl.,  1909,  1,  1. 

Hasselbach,  H.  A.,  and  Jacobaeus,  H.:  Ueber  die  Behandlung  von  Angina  Pectoris  mittelst 
starken  Kohlbogenlichtbadern,  Berl.  klin.  Wchnschr.,  Berl.,  1907,  xliv,  1247. 

Hirschfelder,  J.  O.:  Personal  communication. 

Rumpf:  Zur  Einwirkung  oszillierender  Strome  auf  das  Herz,  Zentralbl.  f.  innere  Med., 
Leipz.,  1907,  xxviii,  441. 


PART  III. 


i. 

ENDOCARDITIS. 

In  spite  of  the  greater  frequency  of  arteriosclerosis  and  myocarditis, 
the  clinical  pictures  of  valvular  diseases  are  so  much  more  definite  as  to 
render  them  the  most  striking  of  all  diseases  of  the  heart.  They  constitute 
indeed  a  large  percentage  of  all  diseases  seen  by  the  physician,  numbering 
1781  (7.6  per  cent.)  of  the  23,200  cases  admitted  to  the  medical  service 
of  the  Johns  Hopkins  Hospital  from  1889  to  1908. 


HISTORICAL. 

Vieussens  in  1715  described  lesions  of  the  valves  occurring  in  the  form  of  warty  or 
cauliflower  excrescences  or  vegetations,  which  prevented  the  closure  of  the  valves.  Vir- 
chow  called  attention  to  the  fact  that  as  a  rule  these  vegetations  were  not  situated  at  the 
margins  of  the  cusps,  but  at  a  little  distance  from  the  margin,  at  the  line  of  closure  where 
the  cusps  struck  together,  at  the  point  where  injury  to  the  endothelial  cells  was  most  likely 
to  occur.  That  this  injury  was  usually  due  to  the  action  of  bacteria  was  shown  when  Winge 
and  Heiberg  and  Virchow  in  1869  demonstrated  microscopically  the  presence  of  minute 
granules  within  the  vegetations.  In  1883  Weichselbaum 
cultivated  staphylococci  and  streptococci  from  endocardial 
vegetations,  and  his  pupil  Wyssoko witch,  as  well  as  Orth 
and  Ribbert,  produced  them  experimentally  in  animals  by 
the  injection  of  bacteria  into  the  blood. 

PATHOLOGICAL    ANATOMY. 

Development  of  the  Lesions. — Mechanical  or 
toxic  injury  is  an  important  factor  in  bringing 
about  these  lesions  upon  the  valves.  Indeed 
Wyssokowitch  found  that  his  experiments  suc- 
ceeded only  after  he  had  punctured  or  injured 
the  valves  with  probes;  while  Ribbert  supplied 
the  mechanical  factor  by  injecting  emulsions 
of  potato  cultures  which  contained  small  masses 
of  potato  that  hurled  themselves  against  the 
valves.  E.  C.  Rosenow  has  shown  that  vege- 
tations are  due  to  the  lodging  of  emboli  of  ag- 
glutinated cocci  within  the  valves  and  are  best  produced  when  the  valves 
are  vascular.  The  fibrinous  exudate  is  poured  out  rapidly  after  the  injury, 
and  is  whipped  into  strands  by  the  action  of  the  current,  so  that  within 
one  hour  after  mechanical  injury  of  the  aortic  valve  a  mass  of  fibrin  having 
the  cauliflower  shape  of  a  vegetation  may  be  found  filling  the  hole  in  the 
valve  (Hirschf elder). 
398 


Fig.  170.  —  Fibrinous  deposit 
upon  an  aortic  cusp  one  hour  after 
mechanically  injuring  the  valve, 
showing  how  the  cauliflower- 
shaped  mass  of  fibrin  tends  to  plug 
the  hole  in  the  valve.  (Kindness 
of  the  Johns  Hopkins  Hospital 
Bulletin.) 


ENDOCARDITIS. 


399 


Ulcerative  Endocarditis. — The  fate  of  this  fibrinous  exudate  and  the 
type  of  the  lesion  varies  with  the  virulence  of  the  germ.  If  the  virulence 
is  high  the  lesion  is  often  large  and  may  involve  the  walls  of  the  auricle 
or  ventricle  (mural  endocarditis)  as  well  as  the  cusps  of  the  valve  (valvu- 
litis) .  The  necrosis  spreads  into  the  deeper  tissues  of  the  valve  or  even 
penetrates  through  it,  and  the  vegetation  consists  of  a  mass  of  degenerated 
fibrin,  clumps  of  bacteria,  and  necrotic  tissue  (Fig.  174)  rich  in  polymor- 
phonuclear leucocytes.  Under  the  influence  of  the  ferments  which  these 
secrete,  the  masses  become  partly  liquefied,  so  that  their  attachment  to 
the  cusps  is  loosened  and  they  may  be  readily  swept  off  as  emboli  by  the 
force  of  the  blood  stream  only  to  cause  infarction  and  abscesses  in  dis- 
f  ant  tissues.  Such  emboli  naturally 
vary  in  size  from  a  small  bit  of  fibrin 
barely  capable  of  plugging  a  capillary 
to   a   mass   almost  the  size   of  the  I 


Fig.  171.  —  Mitral  endocarditis  showing  large 
vegetations.  A,  mural  portion  of  the  vegetations; 
B,  vegetations  along  line  of  closure. 


Fig.  172. 


-Injection  of  chronically  inflamed  valves. 
(After  v.  Langer.) 


valve  itself.  However,  they  rarely  reach  the  tremendous  size  attained  by 
the  non-septic  emboli  which  arise  from  intra-vitam  thrombi  in  the  auricles. 
Chronic  Endocarditis. — When  the  bacteria  upon  the  valves  are  less 
virulent  or  the  immunity  of  the  patient  develops,  a  different  process  occurs. 
The  areas  of  necrosis  are  smaller  and  are  walled  off  with  leucocytes.  Later 
these  give  place  to  the  fibroblasts  and  plasma  cells  of  chronic  inflammation, 
which  in  turn  are  replaced  by  strands  of  newly  formed  connective  tissue, 
which  push  out  into  the  exudate  and  finally  replace  it  altogether,  leaving 
a  solid  vegetation  composed  entirely  of  fibrous  tissue.  With  the  ingrowth 
of  connective  tissue  blood-vessels  penetrate  into  the  vegetation,  entering 
it  from  the  subendocardial  layers  of  myocardium  just  as  they  enter  scle- 
rotic patches  in  arteriosclerosis  (Koester,  v.  Langer,  Darier,  Ribbert),  Fig. 
172.  As  healing  becomes  complete  the  endothelial  layer  of  the  intima 
slowly  grows  in  from  the  periphery  and  gradually  covers  the  entire  vegeta- 


400 


DISEASES  OF  THE  HEART  AND  AORTA. 


Muscular  tissue 


tion.  This  relining  of  the  vegetation  with  endothelium  is,  from  a  prog- 
nostic stand-point,  a  most  important  step  in  the  healing,  for,  as  Wyssoko- 
witch  has  shown,  infection  occurs  most  readily  when  the  surface  of  the 
valve  is  injured,  and  clinical  experience  shows  that  a  valve  once  injured 
is  particularly  liable  to  rein- 
fection. Thus,  it  is  common  to 
find  a  fresh  ulcerative  endo- 
carditis occurring  upon  a  valve 
which  is  already  the  subject  of 
a  chronic  endocarditis,  several 
different  stages  appearing  upon 
the  same  specimen. 

INFECTIVE    AGENTS. 

The  most  important  infec- 
tive agents  in  the  causation  of 
endocarditis  are  the  micro- 
coccus of  rheumatic  fever, 
the  pyogenic  cocci,  the 
pneumococcus.  the  gono- 
coccus,  the  bacillus  influ- 
enza?, and  the  spirochaete 
pallida  (triponema  pallidum) 
of  syphilis. 

Rheumatism. — By  far  the  teadlnese 
most  frequent  cause  of  heart 
disease  is  rheumatism,  which 
gave  rise  to  62.6  per  cent,  of 
Horder's  cases  of  malignant 
endocarditis,  and  occurs  in 
about  the  same  percentage  in 
the  milder  forms.  However, 
the  exact  causal  factor  of  rheu- 
matism itself  is  not  yet  settled. 
Sahli  in  1893  isolated  what  he 
thought  to  be  a  staphylococcus 
from  joints,  endocardium,  and 
the  heart's  blood   of  patients 

dying  of  acute  non-suppurative  arthritis,  and  then  stated  that  he 
garded    acute    articular   rheumatism   as    an    infectious 
ease   due  to  the   action  of   attenuated   pyogenic   cocci. 

Recently  Menzer  and  Rufus  Cole  have  revived  this  view,  and  the  latter  has  produced 
non-suppurative  arthritis  and  endocarditis  in  rabbits  by  the  injection  of  streptococci  from 
various  sources,  showing  also  that  in  the  joints  these  assume  the  diplococcus  arrangement. 

Triboulet,  Wassermann,  Westphal  and  Malkoff,  and  Poynton  and  Paine,  however, 
regard  the  micrococcus  (diplococcus)  which  they  have  obtained  in  cases  of  the  rheumatic 
cycle  as  a  specific  organism  or  at  least  a  specific  strain,  though  Walker  has  shown  that  its 
cultural  characteristics  are  by  no  means  sharply  defined.  The  micrococcus  (rheumaticus) 
of  Poynton  and  Paine  assumes  the  diplococcus  form  in  the  joints  but  becomes  a  strep- 


Chord  ?e 


Fig. 


Papillary  muscle 


173. — Structure   of   the   normal    auriculoventricular 
valve.     (After  Piersol.) 


"  re- 

dis- 

j  >  i 


ENDOCARDITIS. 


401 


tococcus  in  culture  media,  just  as  Cole  found  for  many  ordinary  streptococci.  Beattie  and 
Longcope  also  have  isolated  what  they  believe  to  be  the  micrococcus  of  Poynton  and  Paine 
from  cases  of  arthritis  with  endocarditis,  and  have  produced  both  conditions  in  animals. 
Poynton  has  obtained  the  same  germ  from  the  cerebral  cortex  in  simple  chorea  and  from 
the  tonsils.  Rosenow  (Jour.  Infect.  Dis.,  1912,  xi,  210;  Jour.  Am.  Med.  Assoc,  1915,  lxv, 
1687)  has  been  able,  by  injection  of  cultures  of  streptococci  freshly  obtained  from  the  peri- 
articular tissues  of  patients  with  rheumatic  fever,  to  produce  arthritis  in  66  per  cent.,  en- 


Fig.  174. — Photomicrograph  of  a  specimen  showing  acute  and  subacute  endocarditic  lesions  upon 
the  mitral  valve.  A.  Entire  specimen  (low  power).  B.  Outline  sketch  showing  the  portions  from  which 
C,  D,  and  E  are  taken.  C.  Margin  of  the  area  of  acute  endocarditis  (high  power).  D.  Ulcerating  area, 
showing  masses  of  necrotic  tissue  and  exudate.  E.  Area  where  the  process  is  more  chronic,  showing 
strands  of  newly-formed  fibrous  tissue  entering  the  vegetation. 

docarditis  in  46  per  cent,  and  myocarditis  in  44  per  cent,  of  the  71  animal  injections,  while 
older  cultures  of  the  same  germs  yielded  only  21  per  cent,  of  positive  results.  No  other 
strains  of  streptococci  from  various  sources  yielded  such  a  high  percentage,  except  those 
from  endocarditis  which  yielded  84  per  cent,  of  endocarditis  lesions  in  44  rabbits,  but  only 
15  per  cent,  of  them  developed  arthritis. 


The  Pyogenic  Cocci. — The  pyogenic  cocci  of  puerperal  fever,  abscess, 
and  septicaemia  are  also  very  common  causes  of  endocarditis.  They  are 
identified  with  special  frequency  in  the  malignant  forms,  owing  to  the  readi- 
ness with  which  they  are  then  cultivated,  but  there  seems  little  doubt  that 

less  virulent  strains  are  responsible  for  cases  of  chronic  endocarditis  as  well. 
26 


402 


DISEASES  OF  THE  HEART  AND  AORTA. 


Pneumococcus. — Wells  found  that  the  pneumococcus  caused  endo- 
carditis in  4  per  cent,  of  his  517  autopsies  upon  cases  dying  of  pneumonia, 
and  hence  the  latter  disease  is  a  relatively  frequent  cause  of  endocarditis. 
Lenhartz  states  that  the  endocarditis  often  arises  as  a  recrudescence  after 
the  fever  from  the  original  pneumonia  has  subsided  (13th  to  15th  day),  and 
that  it  is  often  malignant  and  accompanied  by  meningitis. 

Gonococcus. — The  importance  of  the  gonococcus  in  producing  endo- 
carditis as  well  as  rheumatism  is  growing  from  year  to  year. 

The  clinical  association  of  endocarditis  and  urethritis  was  recognized  by  Ricord  in 
1847  and  by  Brandes  in  1854.  V.  Leyden  in  1893  demonstrated  upon  the  valves  cocci 
which  decolorized  by  Gram's  methods,  but  the  first  positive   cultures  of  the 

B 


Fig.  175. 


-Endocarditic  lesions.    A,  ulcerative  endocarditis  with  perforation  of  one  of  the  aortic  cusps. 
B,  healed  chronic  endocarditis  of  the  mitral  valve. 


gonococcus  from  the  blood  during  life  were  made  at  the  Johns  Hopkins  Hospital  by  Thayer 
and  Blumer  in  1895.  Since  then  the  condition  has  been  found  frequently,  and  should 
always  be  sought  for  in  cases  of  gonorrhceal  rheumatism. 

Miscellaneous  Infections. — Occasionally  endocarditis  arises  during  or 
after  diphtheria,  scarlet  fever,  and  smallpox,  though  in  these  cases,  as  in 
tuberculosis,  the  lesion  is  probably  most  frequently  produced  by  streptococci 
which  are  present  as  a  mixed  infection.  True  tuberculous  endocarditis  is  rare 
(Marshall),  though  it  has  been  produced  experimentally  in  animals  (Michaelis 
and  Blum).  Cecil  and  Soper  (Arch.  Int.  Med.,  1911,  viii,  1)  reported  meningo- 
coccus endocarditis. 

The  bacillus  of  influenza  is  also  an  important  factor  (Austin),  though 
it  has  been  encountered  far  less  frequently  in  endocarditis  than  in  myocar- 
ditis; but  this  germ  must  always  be  reckoned  with,  especially  in  bringing 
on  additional  changes  in  valves  which  have  been  subject  to  previous  infec- 
tion by  other  organisms. 

1  The  term  micrococcus  rheumaticus  is  used  for  convenience,  but  with  all  reservations 
as  to  possible  specificity. 


ENDOCARDITIS.  403 

Syphilis. — Whether  true  valvular  lesions  are  produced  by  the  spiro- 
chete pallida  of  syphilis  has  not  been  absolutely  proved,  but  recently 
Collins  and  Sachs  and  Longcope  have  obtained  a  positive  Wassermann 
reaction  in  a  large  percentage  of  cases  of  aortic  insufficiency  in  which  the 
valves  were  puckered,  shrunken,  and  calcified.  In  these  cases  it  is  not  the 
intima  but  the  middle  fibro-elastic  layer  of  the  valves  in  which  the  change 
goes  on,  exactly  analogous  and  usually  coincident  with  similar  changes  in 
the  deeper  layers  of  the  intima  and  media  of  the  aorta. 

Sclerotic  and  Atheromatous  Lesions  of  the  Endocardium.  —  Besides 
these  forms  of  endocarditis  there  seems  to  be  a  certain  number  of  cases, 
especially  of  lesions  about  the  aorta,  in  which  sclerosis  and  calcification 
take  place  in  the  fibro-elastic  layer  of  the  valves  exactly  as  in  the  luetic 
lesion,  but  in  which  the  patient  has  never  had  a  luetic  infection  (as  in  the 
case  of  J.  L.,  page  573).  The  similarity  here  is  exactly  like  that  between 
luetic  and  non-luetic  arteritis,  as  shown  by  Ophuls,  and  needs  no  further 
comment.  ! 

PATHOLOGICAL    PHYSIOLOGY. 

The  disturbances  in  heart  action  due  to  endocarditis  may  depend 
upon  three  immediate  causes: 

(1)  The  mechanical  effects  due  to  leaks  or  obstructions  at  any  of  the  valvular  orifices. 
(This  will  be  discussed  in  detail  in  connection  with  each  of  the  chronic  valvular  lesions.) 

(2)  The  weakening  of  the  heart  muscle  due  to  the  acute  myocarditis  and  the  fatty 
and  parenchymatous  changes  in  the  muscle  cells,  resulting  from  the  direct  invasion  of  the 
muscle  by  the  cocci,  from  effect  of  their  toxins  upon  it,  and  from  the  anaemia  which  fre- 
quently accompanies  the  infection. 

(3)  The  weakening  of  the  heart  which,  as  in  other  febrile  and  infectious  diseases, 
results  from  lowering  of  vasomotor  tone,  and  which  is  brought  about  by  a  relative  empti- 
ness of  the  blood-vessels.    This  is  accompanied  by  low  blood-pressure  and  rapid  pulse. 

In  the  chronic  forms  of  carditis  the  first  is  the  most  important  factor; 
while  in  the  simple  acute  and  the  malignant  forms  the  two  latter  frequently 
outweigh  it,  so  that  there  may  be  few  symptoms  referable  to  the  local 
mechanical  effects  upon  the  circulation. 

Effects  on  the  Circulation. — The  physical  signs  will  be  discussed  par- 
ticularly in  the  case  of  individual  valvular  lesions;  but  in  general  it  may 
be  said  that  a  leak  at  an  orifice  necessitates  an  increase  in 
the  output  of  the  chamber  in  order  to  compensate  for  the 
amount  regurgitating  or  an  increase  in  force  of  contraction  of  the  cham- 
ber behind  it.    Thus,  in  mitral  insufficiency, 

Ventricular    systolic    output  =  Output    into    aorta  +  Backflow 
into  auricle; 

while  in  aortic  insufficiency 

Ventricular    systolic     output  =  Output    into     aorta  =  Outflow 
through  peripheral  vessels  +  Backflow  into  ventricle. 

In  either  of  these  cases  the  circulation  may  be  maintained  either  by  increasing  this  output 
per  beat  or  by  increasing  the  heart-rate;  and  in  neither  of  these  cases  is  the  pulse-pressure 
proportional  to  the  systolic  output  of  the  ventricle. 

On  the  other  hand,  when  a  valvular  orifice  is  narrowed  it  may  have  little  or  no  effect 
until  the  narrowing  reaches  a  certain  point;  for,  though  it  slows  the  inflow  or  the  outflow, 
as  the  case  may  be,  yet  the  duration  of  systole  or  of  diastole  may  be  sufficiently  great  to 


404 


DISEASES  OF  THE  HEART  AND  AORTA. 


permit  of  complete  filling  or  emptying  during  the  time  available;  but  beyond  this  greater 
driving  power  is  needed  and  the  chamber  behind  the  stenosis  must  undergo  hypertrophy. 
Regurgitations  usually  cause  dilatation  of  the  chambers  into  which  the 
leak  occurs,  unless  a  great  increase  in  tonicity  of  the  muscle  has  caused  the  cavity 
actually  to  decrease  in  size  (Stewart,  Cameron,  Hirschf elder,  Cloetta). 

CLINICAL    GROUPING. 

Clinically,  endocarditis  (or  carditis1)  has  been  divided  by  Osier  into 
three  groups: 

(1)  The  malignant  type,  in  which  septic  and  highly  febrile  symp- 
toms, with  symptoms  also  due  to  septic  embolism  in  various  parts  of  the 
body,  dominate  the  clinical  picture,  and  in  which  the  cardiac  lesions  may 
spread  rapidly  and  involve  almost  all  the  valves.  This  is  usually  fatal 
during  the  acute  attack. 


Fig.  176. — Temperature  curve  from  a  case  of  malignant  endocarditis. 


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Fig.  177. — Temperature  curve  from  a  case  of  simple  acute  endocarditis. 

(2)  The  simple  acute  type,  in  which  one  or  two  valves  (the 
mitral  and  aortic)  are  affected,  but  where  the  lesions  remain  confined  to 
them.  The  salient  features  of  the  disease  are  not  those  due  to  high  fever 
and  embolism,  although  these  may  at  times  be  present,  but  those  usually 
produced  by  the  infective  agent ;  and  in  addition  there  are  weakness,  an- 
orexia, and  anemia,  some  respiratory  distress,  and  syncope  on  exertion. 

1  Carditis  =  inflammation  affecting  endocardium,  myocardium,  and  pericardium 
simultaneously. 


ENDOCARDITIS.  405 

Occasionally  there  are  cedema,  enlargement  of  the  liver,  ascites,  precordial 
pain,  and  palpitation,  but  these  are  often  absent. 

(3)  Chronic  endocarditis  usually  follows  after  an  attack  of 
simple  acute  endocarditis,  although  it  may  set  in  insidiously  as  a  result  of 
progressive  sclerotic  changes  in  the  valves,  especially  in  association  with 
arteriosclerosis,  syphilis,  and  chronic  anaemias.  The  original  characteristics 
of  an  infectious  disease  have  subsided,  and  the  picture  is  entirely  due 
to  the  mechanical  effects  of  leaking  valves  and  weakened  heart  muscle; 
in  short,  to  slowing  of  the  circulation,  dyspnoea,  cough,  cedema,  digestive 
disturbances,  palpitation,  precordial  and  referred  pains. 

MALIGNANT    ENDOCARDITIS. 

PATHOGENESIS. 

Most  commonly  an  attack  of  malignant  carditis  is  not  the  first  heart 
disease  from  which  the  patient  has  suffered,  but  it  is  found  that  the  acute 
process  involves  a  valve  which  already  shows  marks  of  a  chronic  endocardi- 
tis. This  is  not  at  all  surprising,  since  Rosenbach,  Wyssokowitsch,  Hasen- 
feld,  and  others  have  shown  that  valves  once  injured  become  the  seat  of 
inflammatory  processes  much  more  readily  than  when  intact.  If  the 
original  lesion  is  a  very  chronic  one  and  the  vegetation  well  supplied  with 
blood-vessels  (Ribbert),  organization  of  the  exudate  may  go  on  even  more 
readily  than  in  an  intact  valve;  but  if  the  older  exudate  is  still  fibrinous 
or  fresh,  the  tendency  to  soften  and  ulcerate  is  greater  than  if  it  were  rest- 
ing upon  a  base  of  relatively  healthy  tissue. 

Often  the  second  and  malignant  infection  may  be  due  to  an  organism 
quite  different  from  that  producing  the  first,  so  that  one  frequently  finds 
a  malignant  endocarditis,  due  to  the  streptococcus,  the  pneumococcus,  or 
the  gonococcus,  attacking  vegetations  originally  of  rheumatic  origin. 

In  the  chronic  forms  of  valvular  lesion  the  symptoms  of  an  acute 
febrile  disease  have  disappeared,  and  are  replaced  by  clinical  pictures  with 
characteristic  forms  of  hypertrophy,  stasis,  and  murmurs. 

Occurrence  and  Distribution. — The  relative  rarity  of  malignant  endocarditis  is  shown 
by  the  fact  that  only  45  cases  have  occurred  among  23,200  admitted  to  the  Johns  Hopkins 
Hospital  (0.19  per  cent.),  as  compared  with  1781  (7.6  per  cent.)  of  chronic  valvular  disease; 
also  by  the  statistics  of  Horder,  who  encountered  150  cases  among  19,904  patients  admitted 
to  St.  Bartholomew's  Hospital  (0.75  per  cent.).  The  occurrence  of  Horder's  150  cases  as 
regards  age  was  as  follows:  Under  5,  2  cases;  5  to  10  years,  5;  10-15  years,  9;  1.5-20 
years,  29;   20-30  years,  39;  30-40  years,  31;  40-50  years,  23;   50-60  years,  8;   over  60,  4. 

The  involvement  of  the  valves  was:  Mitral,  38;  aortic,  22;  mitral  and  aortic,  63; 
tricuspid  and  mitral,  14;  pulmonary  and  mitral,  7.  There  were  mural  auricular  lesions 
in  43;   mural  ventricular  in  8;   congenital  heart  lesions  in  8. 

Other  signs  and  complications  were:  Enlarged  spleen,  47;  heart  failure,  66;  haema- 
turia  (sometimes  only  microscopic),  46;  petechia?,  43  (on  legs  only  in  10);  brain  symp- 
toms in  22  (choreiform  movements  in  7;  retinal  hemorrhages  noted  in  5,  though  certainly 
more  frequent);    embolic  aneurisms,  20. 

TYPES    OF    MALIGNANT    ENDOCARDITIS. 

Osier  in  his  masterly  lectures  has  divided  the  cases  of  malignant 
endocarditis  into  three  clinical  groups,  which  may  present  both  acute 
and  chronic  forms. 


406  DISEASES  OF  THE  HEART  AND  AORTA. 

1.  The   septicaemic,   in  which  the  symptoms  are  primarily  those  of  septicaemia. 

2.  The  typhoidal  type,  which  closely  resembles  severe  typhoid  fever  or  acute 
miliary  tuberculosis, — continuous  high  fever,  enlarged  spleen,  and  absence  of  other  local- 
ized symptoms. 

3.  The  cerebral  type,  dominated  by  embolism  of  the  brain,  coma,  meningitis, 
paralyses. 

Septicaemic  Type. — The  septicaemic  type  is  the  most  common  and 
typical,  usually  following  abscess,  puerperal  fever,  operation,  wounds, 
occasionally  tonsillitis  or  quinsy,  or  some  other  definite  infection,  and  is 
characterized  by  prostration,  anorexia,  malaise,  frequently  headaches,  and 
shaking  chills.  In  Horder's  150  cases  the  fever  was  continued  in 
12,  irregular  and  intermittent  in  37,  quotidian  in  40,  absent  in  5.  The 
temperature  sometimes  fell  for  a  period  before  death.  The  complexion 
has  the  sallow  yellowish  color  of  hsematogenous  jaundice,  there  is  rapidly 
progressing  increasing  anaemia,  and  the  eyes  are  dull.  There  is  sometimes 
acute  purulent  conjunctivitis,  sometimes  disturbances  of  vision  or  even 
blindness  due  to  the  presence  of  minute  emboli  or  hemorrhages  upon  the 
retina.  The  cheeks  are  sunken;  the  skin  is  usually  dry  except  during  the 
rigor  (in  contrast  to  the  drenching  sweats  of  rheumatic  fever) ;  the  tongue 
is  dry  and  furred;  the  lungs  may  be  clear  or  septic  bronchopneumonia  may 
be  present.  Respiration  is  usually  rapid.  The  signs  over  the  heart  are 
variable.  In  some  cases  there  are  no  abnormalities  in  heart  sounds,  cardiac 
area,  or  in  pulsations,  except  for  a  rapid  pulse-rate,  and  then  the  diagnosis 
may  long  remain  obscure;  or,  on  the  other  hand,  the  loudest  murmurs  may 
be  present  both  in  systole  and  in  diastole,  and  these  have  a  distribution 
corresponding  to  almost  any  of  the  valvular  lesions,  or  more  usually  to 
several  lesions  combined.  These  signs  often  change  markedly 
from  day  to  day,  corresponding  to  the  progression  of  the  lesion 
from  valve  to  valve,  the  growth  of  the  individual  vegetations,  or  the  dis- 
appearance of  the  latter  as  they  slough  off  into  the  blood  stream.  The 
pulse  is  small  and  collapsing,  but  usually  too  rapid  for  dicrotism,  and  the 
blood-pressure  is  low  (maximal  85  to  110  mm.,  minimal  60  to  90).  It 
becomes  larger  and  more  typically  water-hammer  in  character,  and  the 
diastolic  pressure  falls  to  40-50  mm.  if  a  leak  sets  in  at  the  aortic  valve. 
The  loud  systolic  murmur  over  the  tricuspid  area,  corresponding  to  tricuspid 
insufficiency  either  functional  or  organic,  is  among  the  most  common  in 
malignant  endocarditis,  for  this  valve  bears  the  brunt  of  both  the  increasing 
organic  lesions  and  the  progressive  weakening  of  the  heart  muscle.  Accom- 
panying this  there  is  also  systolic  pulsation  in  the  jugular  vein.  A  diastolic 
murmur  may  be  present  to  either  left  or  right  of  the  sternum,  and  may 
correspond  to  either  aortic  or  pulmonic  insufficiency,  the  distribution  in. 
the  latter  case  being  somewhat  different  from  the  former.  A  pericardial 
friction,  associated  with  the  onset  of  fibrinous  or  purulent  pericarditis,  is 
not  uncommon. 

The  liver  is  frequently  enlarged,  either  from  cardiac  weakness  or 
from  a  definite  suppurative  hepatitis  and  cholangitis.  When  associated 
with  tricuspid  insufficiency  it  may  pulsate  with  systole. 

The  spleen  is  often  enlarged,  from  the  presence  of  infarctions  of 
greater  or  less  extent.  The  abdomen  may  be  otherwise  normal  or  may 
be   tense,   and  there   may  be  local  tenderness  and   muscle   spasm  from 


ENDOCARDITIS.  407 

localized  infection  or  general  peritonitis;  not  infrequently  these  areas 
correspond  to  the  uterus  (especially  in  puerperal  endocarditis)  or  to 
the  kidney,  owing  to  infarction,  in  which  case  there  are  also  albuminuria 
and  haematuria. 

There  is  sometimes  oedema  of  the  extremities.  Arthritis  is 
frequent,  often  accompanied  by  injury  to  the  epiphyses  as  well  as 
the  joints,  and  occasionally  by  spontaneous  fractures.  The  skin  may  show 
very  numerous  small  purple  petechiae  or  large  areas  of  ecchymosis; 
or,  on  the  other  hand,  there  may  be  numerous  subcutaneous  abscesses  of 
varying  size. 

The  blood  count  is  usually  low,  especially  the  haemoglobin,  cor- 
responding to  the  type  of  a  secondary  anaemia.  Sometimes  500,000  ery- 
throcytes are  destroyed  each  day.  There  is  almost  always  a  polymorpho- 
nuclear leucocytosis  (20,000-30,000).  As  has  been  seen  blood  cultures  are 
positive  in  about  90  per  cent,  of  the  cases, — colonies  of  the  infective  agent, 
usually  20-40  per  cubic  centimetre  of  blood. 

The  urine  is  of  variable  amount,  and  specific  gravity  usually 
high.  It  generally  contains  albumen  and  casts,  and  often  there  is  definite 
haematuria  due  to  infarction  of  the  kidney.  Sometimes  the  blood  can  be 
seen  only  with  the  microscope.  Not  infrequently  there  is  cystitis  with 
cocci  in  the  urine  in  considerable  quantities. 

Typhoidal  Type. — The  cases  of  the  typhoidal  type  are  characterized 
also  by  asthenia,  by  high  fever  (103°  to  106°),  which  is  more  or  less  continu- 
ous, frequently  flushed  face,  dry  tongue,  sometimes  coma  vigil  and  picking 
at  bedclothes,  enlarged  spleen,  but  otherwise  no  definite  localizing  symp- 
toms. There  may  be  a  slight  bronchitis  or  small  foci  of  bronchopneumonia. 
The  cardiac  signs  may  be  indefinite,  or  may  be -thought  to  be  remnants  of 
old  valvular  lesions.  The  differentiation  from  typhoid  fever  on  the  one 
hand  and  acute  miliary  tuberculosis  on  the  other  may  be  impossible  by 
the  simple  methods  of  physical  diagnosis,  and  the  diagnosis  must  rest  with 
the  blood  culture.  Occasionally  the  presence  of  petechia?  in  the  skin  may 
suggest  typhus  fever.  Examination  of  the  eye-grounds  may  show  small 
white  spots  of  retinal  exudation  and  occasional  hemorrhages,  but  the  pic- 
ture may  be  difficult  to  distinguish  from  typhoid  lymphomata  or  miliary 
tubercles.  The  presence  of  leucocytosis  is  suggestive,  but  not  decisive, 
while  the  absence  of  Widal  reaction  is  of  value  only  as  negative  evidence. 
The  only  decisive  evidence  is  given  by  the  blood  culture. 

Cerebral  Type. — In  the  third  or  cerebral  type  the  symptoms  due  to 
embolism  of  the  brain  and  usually  of  the  left  middle  cerebral  artery  domi- 
nate the  picture.  There  is  a  history  of  onset  with  fever,  weakness,  and 
perhaps  chills,  perhaps  a  shower  of  petechia?  over  the  body,  and  haematuria, 
and  then  a  sudden  onset  of  hemiplegia,  with,  or  more  usually  without,  con- 
vulsions, and  perhaps  relapse  into  unconsciousness.  The  patient  is  then 
left  with  unconsciousness,  hemiplegia  (usually  right-sided),  and  usually 
aphasia,  more  or  less  disturbance  of  vision,  and  choked  disk.  The  septic 
infarct  may  also  give  rise  to  purulent  meningitis,  so  that  there  may  be 
unconsciousness,  rigidity  of  the  neck,  and  Kernig's  sign  as  well,  and  the 
cerebrospinal  fluid  obtained  from  lumbar  puncture  may  be  under  high 
tension,  cloudy,  rich  in  albumen  and  in  cocci. 


408  DISEASES  OF  THE  HEART  AND  AORTA. 

These  lesions  are  produced  by  septic  emboli  of  varying  sizes  carried 
off  the  necrotic  surfaces  of  the  infected  valves.  In  Horder's  series  they 
occurred  in  14.6  per  cent,  of  the  cases.  The  symptoms  vary  in  character 
and  severity,  according  to  the  location  and  extent  of  the  lesion,  from  a  few 
choreiform  movements  to  paralyses,  convulsions,  and  coma.  Aphasia  is, 
of  course,  relatively  common. 

The  diagnosis  of  the  primary  condition  may  depend  upon  the  varying 
heart  signs  and  the  positive  blood  culture. 

CHRONIC    INFECTIVE    ENDOCARDITIS    (OSLER). 

Osier  has  called  attention  to  the  existence  of  a  chronic  form  of 
malignant  endocarditis,  which  may  last  from  four  to  fourteen 
months.  It  is  characterized  by  an  asthenic  condition,  with  remittent  or 
intermittent  fever  rising  to  a  maximum  of  102°-103°,  chills  and  sweats,  in 
about  60  per  cent,  of  the  cases,  petechia?,  especially  upon  the  shins,  enlarged 
spleen,  and  heart  signs,  which  vary  as  the  process  extends  from  valve  to 
valve,  or  the  valve  substance  sloughs.  There  is  usually  a  progressive  anaemia. 
Painful  petechiae  ,  erythematous  cutaneous  nodules  (Osier),  and  tender- 
ness of  the  lower  part  of  the  sternum  (Libman  and  Celler,  Am.  J.  M.  Sc,  1910, 
cxl,  516)  are  pathognomonic  features.  The  blood  culture  is  usually  positive, 
but  the  cocci  often  circulate  in  showers,  absent  from  the  blood  one  day,  present 
on  another.  Repeated  cultures  must  be  made.  The  characteristic  cocci 
("streptococcus  viridans,"  Schottmueller,  Muench.  Med.  Wchnschr., 
1903, 1, 849;  1909, 1, 617)  are  always  free  from  capsules  by  which  they  are  differ- 
entiated from  the  pneumococcus,  but  like  pneumococci  they  are  soluble  in  bile. 
The  colonies  in  blood  agar  are  surrounded  by  a  green  zone.  The  cocci  may  or 
may  not  ferment  inulin.  They  are  always  Gram-positive.  However,  both 
Libman  and  Celler  and  A.  Kinsella  (Arch.  Int.  Med.,  1917,  xix,  367)  agree  that 
the  colonies  are  not  always  surrounded  by  a  green  zone,  but,  on  the  other  hand, 
though  white  or  grayish,  they  are  never  surrounded  by  a  clear  white  zone  of 
complete  haemolysis.  This  differentiates  them  from  the  hsemolytic  streptococcus. 

Diagnosis. — The  diagnosis  of  chronic  infection  endocarditis  usually 
depends  upon  the  blood  culture,  for  the  clinical  picture  may  be  so  pleomorphic 
as  to  simulate  many  other  diseases. 

Thompson  has  also  called  attention  to  the  fact  that  acute  hyperthyroidism  (Base- 
dow's disease,  exophthalmic  goitre)  may  present  a  clinical  picture  of  fever,  chills,  sweats, 
tachycardia,  dilated  heart  with  systolic  murmurs,  which  closely  simulates  that  of  malig- 
nant endocarditis.  The  thyroid  in  these  cases  is  enlarged  and  tender  and  the  ocular  signs 
are  usually  pronounced. 

The  crucial  points  in  the  differential  diagnosis  of  malignant  endocarditis 
are,  therefore,  given  in  the  following  table: 

From  pneumonia — petechia?,  signs  of  valvular  lesions. 

From  typhoid  fever — by  leucocytosis,  absence  of  Widal  reaction,  blood  culture. 

From  rheumatic  fever — by  enlarged  spleen,  petechia;,  chills,  blood  culture. 

From  malaria — by  absence  of  plasmodia,  leucocytosis,  heart  signs,  positive  blood 
culture. 

From  miliary  tuberculosis — by  leucocytosis,  heart  signs,  absence  of  tubercle  bacilli, 
positive  blood  culture. 

From  cerebrospinal  meningitis — by  absence  of  intracellular  diplococci  in  cerebro- 
spinal fluid,  positive  blood  culture  yielding  other  germs. 

From  acute  Basedow's  disease — by  positive  blood  culture,  absence  of  oculomotor 
signs  of  Basedow's  disease,  polymorphonuclear  leucocytosis. 


ENDOCARDITIS.  409 

Case  of  Streptococcus  Viridans  Endocarditis. 

John  P.  (No.  8806),  an  American  railroad  laborer,  single,  aged  25,  was  admitted  to  the 
University  of  Minnesota  Hospital  on  May  30,  1916,  complaining  of  weakness,  pain  in  the 
abdomen  and  back,  nose  bleed  and  cough.  Family  and  personal  history  negative,  except 
for  pneumonia  five  years  previously.     No  venereal  infections. 

The  present  illness  began  with  rheumatism  two  months  previously.  In  spite 
of  this  he  continued  with  his  work  on  bridge  building  until  he  gradually  grew  weaker  and 
was  compelled  to  quit  work  a  few  weeks  later,  about  six  weeks  before  his  admission.  About 
two  weeks  before  admission  he  was  suddenly  seized  with  a  sharp  pain  in  the  left  side  of  the 
abdomen  and  back,  better  the  next  day,  but  followed  a  week  later  by  a  similar  pain  on  the 
right  side.  A  week  later  he  had  a  profuse  nose  bleed.  He  has  had  cough  and  expectoration 
for  a  week  but  no  night  sweats,  and  has  voided  small  amounts  of  urine  three  or  four  times 
a  night. 

Physical  examination  by  Dr.  Rowntree.  The  patient  is  very  pale  and 
anaemic,  with  pearly  conjunctivas.  The  lips  are  pale.  There  is  considerable  pyorrhoea  and 
caries,  tonsils  are  small,  throat  is  clean.  Pupils  are  unequal  and  do  not  respond  to  light. 
Skin  is  dry,  with  marked  pigmentation  in  the  axilla.  The  point  of  maximal  impulse  is  at 
least  12  cm.  to  the  left  in  the  fifth  interspace  and  cardiac  dulness  extends  16  cm. 
to  the  left  and  5  cm.  to  the  right.  Both  sounds  can  be  heard  at  the  apex.  The  first 
sound  is  snappy;  second  sounds  are  equal  over  aortic  and  pulmonary  areas.  Pulse  is 
greatly  accelerated.  There  is  a  systolic  whiff  in  the  neck.  Lungs  show  a  few  rales  in 
left  lower  chest.  Liver  and  spleen  not  felt.  Joints  :  Both  knees  and  right  ankle 
are  swollen  and  larger  than  surrounding  skin,  but  not  reddened,  and  not  particularly  tender 
to  touch.  Skin:  There  are  no  evidences  of  petechial  hemorrhages,  no  subcutaneous 
hemorrhages,  no  oedema.  Glands  :  Epitrochlears  are  definitely  enlarged.  There  is  a 
small  mass  palpable  under  the  skin  of  the  upper  right  arm  and  two  masses  palpable  under 
the  skin  of  the  left  forearm.  Urine  :  1050  to  1800  cubic  centimetres  in  amount,  straw- 
colored,  acid,  specific  gravity  1010  and  contained  a  large  amount  of  albumen,  a  small 
amount  of  pus,  many  hyaline  and  a  few  granular  casts  on  admission,  but  on  June  6,  a  few 
red  blood  corpuscles  were  present.  Phenolsulphonphthalein  excretion  42  per  cent.  Spu- 
tum contained  no  tubercle  bacilli.  Fasces  contained  occult  blood  by  benzidin  test  on 
August  2nd.  The  blood  showed  4,100,000  red  corpuscles,  48  per  cent,  hemoglobin,  14,400 
leucocytes,  of  which  67  per  cent,  were  polymorphonuclear,  29  per  cent,  lymphocytes,  two 
per  cent,  transitionals,  two  per  cent,  eosinophiles.  Blood  :  Wassermann  negative. 
Blood  culture  taken  July  7,  1916,  showed  the  streptococcus  viridans  about 
43  colonies  per  plate  containing  1  cubic  centimetre  of  blood.  Temperature  :  The 
temperature  usually  ranged  from  98.5°  to  101.5°,  on  many  days  never  rising  above  100°, 
on  others  reaching  as  high  as  103°.    The  pulse  rate  ranged  from  80  to  130  per  minute. 

He  became  steadily  worse  in  spite  of  general  treatment  with  Blaud's  pills,  elixir  of 
iron,  quinine  and  strychnine,  calcium  lactate  gr.  xv,  and  tincture  of  digitalis  minims  xx. 

Transfusion  of  human  blood  was  without  avail  as  was  repeated  infusion  of  Dakin's 
hypochlorite  solution  which  was  followed  by  thrombosis  of  median  basilic  vein.  Patient 
died  on  August  23,  1916.  The  heart  showed  large  thrombi  about  1  cm.  in  diameter  adherent 
to  all  the  valves,  none  of  which  were  ulcerated.  There  were  old  vegetations  on  the  mitral 
valve;  marked  dilation  and  hypertrophy  of  heart.     No  abscesses  in  the  heart  waH 

TREATMENT. 

The  treatment  of  malignant  endocarditis  is  the  treatment  of 
any  form  of  general  septicaemia — absolute  rest,  very  light,  soft  or  milk 
diet  amounting  to  as  near  3000  calories  per  day  as  possible,  and  avoidance 
of  excitement.  Drugs  are  of  little  value.  Strychnine  may  be  given  in  doses 
of  2-3  mg.  Q-$  to  -jV  gr.)  every  four  hours,  or  digitalis  also,  with  a  view 
of  increasing  the  activity  of  the  vasomotor  centre  and  the  tonicity  of  the 
heart;  but  little  is  accomplished  by  their  use,  and  in  some  cases  the  heart 
muscle  is  already  so  much  injured  by  the  infection  that  further  stimu- 
lation is  actually  harmful.     Salt  infusions  may  be  given,  but  they  serve  to 


410  DISEASES  OF  THE  HEART  AND  AORTA. 

swell  the  volume  of  blood,  to  dilate  the  heart,  and  to  increase  its  work, 
and,  although  they  may  perhaps  "wash  out  the  toxic  substances  through 
the  kidneys/'  it  is  doubtful  whether  they  are  at  all  effectual. 

Intravenous  Injections. — Intravenous  infusions  of  collargol  and  other  metallic  com- 
pounds have  been  tried  and  some  apparently  favorable  results  reported,  but  these  have 
invariably  been  shown  to  be  overestimated  when  the  work  was  repeated  by  more  careful 
observers.  The  antistreptococcus  serum  of  Marmorek  has  been  used  in  cases  of  malignant 
streptococcic  endocarditis,  but  this  also  has  no  value. 

Inoculations  with  Bacterial  Vaccines. — More  recently  A.  E.  Wright  has  instituted 
the  method  of  inoculating  the  patient  with  small  doses  of  killed  cultures  of  the  germ,  caus- 
ing the  infection  in  the  hope  of  thereby  increasing  the  production  of  protective  substances. 
Though  this  is  the  most  promising  of  all  the  methods,  it  has  failed  to  give  satisfactory 
results  in  the  hands  of  careful  observers  such  as  Rosenow  and  Horder. 

SIMPLE   ACUTE   ENDOCARDITIS. 

The  malignant  forms  of  carditis  described  in  the  foregoing  chapter 
are  relatively  infrequent  (0.19  per  cent,  of  admissions  to  the  Johns  Hopkins 
Hospital).  Much  more  common  are  the  milder  infections  which  assume 
the  form  of  simple  acute  or  subacute  endocarditis,  and  in  which  the  symp- 
toms are  often  referable  mainly  to  a  mild  subacute  fever  and  anaemia,  and 
with  comparatively  less  frequency  stamped  with  the  typical  features  of  heart 
disease,  so  that  the  latter  may  become  evident  only  on  physical  examination. 

Rheumatism. — Unlike  the  malignant  form,  which  is  usually  of  pyogenic 
origin,  the  simple  endocarditis  is  far  more  frequently  rheumatic  (Bouillaud, 
1835),  manifesting  itself  in  association  with  other  manifestations  of  the 
"rheumatic  cycle," — tonsillitis,  rheumatic  arthritis,  chorea,  pleurisy,  or 
the  rheumatic  erythemata;  rheumatism  being  the  etiological  factor  in  65.6 
per  cent,  of  all  cases  of  endocarditis  in  the  Medical  Clinic  at  Zurich,  in  36.7 
per  cent,  at  Jena,  and  in  58  per  cent,  at  Leipzig. 

Similar  figures  appear  from  the  clinics  of  Great  Britain  and  America,  the  statistics 
of  the  Johns  Hopkins  Hospital  being  quite  according  to  the  rule. 

A  much  higher  percentage  of  the  cases  of  rheumatism  acquire  endocarditis  than  is 
true  of  any  other  disease.  It  was  present  in  61.3  per  cent,  of  all  cases  of  this  disease  in 
children  in  West's  series,  in  66  per  cent,  of  Fuller's  cases  and  in  80  per  cent,  of  the  cases 
reported  by  Cadet  de  Gassicourt. 

Gibson  states  that  the  likelihood  of  endocardial  infec- 
tion is  proportional  to  the  severity  of  the  rheuma- 
ti  c    af  f  e  c  tion. 

The  same  relative  frequency  applies  also  to  chorea,  the  other  important  member  of 
the  rheumatic  cycle.  Stephen  Mackenzie  finds  60.6  per  cent.,  Donkin  40  per  cent.,  Osier 
51.4  per  cent.,  affected  with  carditis,  although  the  arthritic  history  is  often  absent. 

Other  Infections. — Other  diseases,  though  occasional  causes,  are  much  less  frequently 
followed  by  endocarditis.  Thus,  Osier  found  it  twelve  times  in  216  autopsies  upon  cases 
of  phthisis,  five  times  in  100  pneumonia  cases,  twice  in  80  autopsies  upon 
typhoid  fever;  and  he  states  that  it  is  not  uncommon  in  scarlet  fever. 
In  most  of  these  cases  the  secondary  infection  with  streptococcus  is  probably  responsible 
for  the  condition.  Influenza,  smallpox,  measles,  and  diphtheria  also 
are  occasional  etiological  factors.  In  all  these  diseases  any  overwork  or 
other  overstrain  upon  the  heart  during  the  course  of  the  in- 
fection increases  its  susceptibility  and  enhances  the  liability  to  affection 
of  the  endocardium,  just  as,  according  to  Poynton,  fright  (or  hard  study  at  school)  pre- 
disposes to  affection  of  the  brain,  namely  chorea. 


ENDOCARDITIS. 


411 


Age. — As  to  age  it  may  be  said,  that,  in  contrast  to  both  the  malignant 
and  the  chronic  forms  of  endocarditis,  the  simple  acute  carditis  which  repre- 
sents the  usual  beginning  of  the  process  presents  itself  most  frequently  in 
children,  especially  in  the  second  decade  of  life,  and  that  the  age  of  maxi- 
mum frequency  is  the  age  of  the  greatest  expo- 
sure, the  second  and  third  decades. 

The  frequency  is  due  merely  to  the  fact  that  rheu- 
matism is  then  more  frequent,  although  when  contracted 
in  childhood  it  appears  to  be  followed  by  a  greater  per- 
centage of  cardiac  complications  than  in  older  persons, 
and  pericarditis  (especially  adherent  pericardium)  and 
myocarditis  are  more  severe.  Of  145  cases  under  15 
years  of  age  Holt  and  Crondall  found  under  5  years  14 
cases,  5-10  years  71  cases,  and  10-14  years  60  cases, 
38  per  cent,  being  males  and  52  per  cent,  females.  It 
is  especially  noteworthy  that  of  these  145  cases  almost 
90  per  cent,  were  brought  about  by  diseases  of  the  rheu- 
matic cycle,  in  contrast  to  60-65  per  cent,  in  older  persons. 
Indeed,  the  earlier  in  life  the  rheumatic  infection  is  con- 
tracted, the  more  it  assumes  the  type  of  a  general  carditis 
and  the  less  severely  are  the  joints  involved.  As  many 
writers  have  stated,  rheumatic  fever  in  children  usually  assumes  the  form  of  a  tonsillitis, 
with  carditis  and  chorea,  and  is  frequently  devoid  of  any  arthritic  symptoms  whatever. 
The  myocarditis  has  been  discussed  in  Part  II,  Chapter  IX,  and  is  an  important  fea- 
ture. The  weakness  of  the  heart  muscle  which  results  leads  to  dilatation  and  overfilling 
of  the  chambers,  and  this  in  turn  increases  the  leaks  due  to  the  lesions  upon  the  valves. 


AGE 

-9 

-19 

-29 

-39 

-A3 

-59 

-69 

BsrMille 
40 

30 

A 

20 

Mi}* 

% 

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10 

/ 

'mi 

/ 

"Tv 

--\ 

"A 

o 

1/ 

■'k\ 

Fig.  178.  —  Diagram  showing 
relative  frequency  of  the  most  im- 
portant valvular  lesions  at  various 
ages.  (Modified  from  Gillespie.) 
Solid  line,  mitralinsufficiency;  bro- 
ken line,  mitral  stenosis;  dotted  line, 
aortic  insufficiency.  The  figures  in- 
dicate the  decades.  Under  9  years, 
—9;  10-19,-19;  20-29,-29;  etc. 


Per  MITRAL 

tent    INSUFFICIENCY 
100 


MITRAL 
STENOSIS 


AORTIC  INSUFFICIENCY ^q!i5 


r  .  i  i  i  m.  1 

i 

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i 

i      i  -1  Ma  1  i 

1  -Ji  !  !  IB     ! 

i  6j  i       jKi   !   l 

i 

i   10-!  I  1  lOi  j  j 

[)i 

i'  "tf 

1  'r\\  l  T\ 

s. 

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t\ 

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y 

IE 

Th 

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Zm 

M-\ 

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HBl  CASES     JH.H 

I         I  AUTOPSIES  -BERL. 
Fig.  179. — Diagram  showing  the  relative  frequency  of  the  various  valvular  lesions  in  1781  cases  of 
valvular  heart  disease  admitted   to  the  Medical  Service  of  the  Johns  Hopkins   Hospital  from   1889  to 
1908,  as  well  as  those  found  by  Sperling  in  300  autopsies  in  Berlin.     Small  space,  5  per  cent.;  Berl.,  Berlin; 
J.  H.  H.,  Johns  Hopkins  Hospital. 

Sex. — Many  authors,  among  them  Osier,  state  that  men  are  more  fre- 
quently affected  than  women;  though  v.  Jurgensen  states  that  valvular 
disease  occurs  with  practically  the  same  frequency  in  both  sexes. 


INVOLVEMENT    OF    INDIVIDUAL    VALVES. 

The  relative  frequency  with  which  the  valves  are  involved  is  shown 
by  the  analysis  of  1781  cases  of  endocarditis  admitted  in  the  Johns  Hopkins 
Hospital  from  1889  to  1908,  represented  diagrammatically  in  Fig.  179. 
The  figures  show  a  general  correspondence  to  those  of  v.  Jurgensen  in  2470 
cases  in  the  German  clinics. 


412  DISEASES  OF  THE  HEART  AND  AORTA. 


PATHOLOGICAL    PHYSIOLOGY. 

The  pathological  physiology  of  simple  acute  endocarditis  presents  the 
condition  due  to  the  individual  valvular  lesion  (to  be  considered  in  detail 
in  the  appropriate  chapters  dealing  with  the  chronic  endocarditis),  modi- 
fied or  added  to  by  an  element  of  diminished  vasomotor  tone  due  to  the 
acute  febrile  condition.  As  the  result  of  this  vasodilatation,  especially  in 
the  abdominal  area,  the  blood  collects  in  the  dilated  veins  and  capillaries, 
the  blood-pressure  may  be  low,  and  the  symptom  complex  of  arterial 
ansemia  or  low  blood-pressure  sets  in.  Moreover,  there  is  usually  a  certain 
degree  of  actual  ansemia  added  to  the  lesion,  and  this  often  increases  the 
difficulty  in  breathing;  although  it  does  not,  as  a  rule,  bring  on  the  red  and 
purple  hue  of  chronic  cyanosis.  Still  further  the  increase  in  the  leakage 
causes  damming  back  and  secondary  dilatation  of  the  chambers  behind 
it,  cedema  in  the  walls  of  the  ventricles  and  in  the  valve  cusps,  and 
increased  susceptibility  to  infection. 

PATHOLOGICAL    ANATOMY. 

The  endocarditis  itself  is  less  severe  than  in  the  malignant  form.  Fewer 
bacteria  are  deposited  upon  the  valves,  and  these  show  less  tendency  to 
multiply,  so  that  the  process  of  organization,  as  a  rule,  outraces  necrosis, 
and  consequently  the  separation  of  emboli  is  rare.  The  valves  thus  show 
an  injured  surface  covered  by  a  more  or  less  thick  or  exuberant  layer  of 
fibrin,  with  active  organization  proceeding  upward  from  its  base.  This 
may  be  seen  in  any  stage  of  advancement,  from  fresh  fibrin  in  the  early 
stage  to  completely  organized  firm  young  connective  tissue,  covered  by 
intact  endothelium,  when  healing  has  become  complete. 

Pathologically,  the  difference  between  the  malignant  and  the  simple 
endocarditis  is  merely  the  usual  difference  between  a  mild  and  a  virulent 
infection  of  any  tissue.  There  may  be  no  actual  difference  in  etiology,  and 
the  malignant  form  may  represent  only  a  very  virulent  strain  of  the  same 
organism  which  would  ordinarily  produce  a  milder  infection;  or,  on  the 
other  hand,  micro-organisms  of  the  same  virulence  may  produce  different 
types  of  lesion  in  persons  with  different  powers  of  resistance. 

SYMPTOMS. 

It  is  particularly  noticeable  that_in  these  cases  during  the  first  attack 
the  symptoms  due  to  distinct  heart  failure  are  largely  absent,  and  the 
main  symptoms  are  those  of  accompanying  rheu- 
matic disease,  along  with  the  weakness,  pallor,  and  ansemia  (usually  about 
60  per  cent,  haemoglobin) ,  such  as  might  be  due  to  any  mild  fever,  though 
occasionally,  as  in  the  case  of  J.  A.  (page  415),  the  onset  of  aortic  insuffi- 
ciency is  attended  by  pain  and  sudden  collapse.  The  temperature  rarely 
attains  101°  unless  an  acute  arthritis  or  acute  pneumonia  is  present.  The 
pulse  is  usually  rapid  and  regular.  Its  quality  depends  upon  the  nature 
of  the  lesion,  being  large  and  collapsing  in  the  presence  of  aortic  insuffi- 
ciency, small  in  mitral  stenosis,  and  of  moderate  size  in  mitral  insufficiency. 
The  blood-pressure  is  sometimes  above,  sometimes  below  normal. 


ENDOCARDITIS.  413 


PHYSICAL   SIGNS. 

As  a  rule,  the  patient  does  not  seem  very  ill,  he  has  sometimes  an 
anxious  expression,  is  usually  pale  and  sallow,  in  contrast  to  the 
older  cases  of  mitral  disease,  who  usually  show  a  flushed  and  cyanotic  hue. 
Occasionally  choreic  movements  are  present.  It  is  very  common  for  the 
tonsils  to  be  enlarged,  since  these  are  the  usual  portals  of  entry  for  the 
rheumatic  infection,  and  there  is  frequently  a  yellow  exudate  in  the  crypts 
or  a  membrane  over  their  surfaces.  In  almost  all  rheumatic  cases  there 
are  foci  of  cocci  (streptococcus  or  micrococcus  rheumaticus?)  in  the  deeper 
tissue  of  the  tonsil.  Along  with  this  infection  the  so-called  tonsillar  lymph 
gland  just  below  the  angle  of  the  jaw  and  often  the  submaxillary  and 
anterior  cervical  lymph  glands  are  enlarged.  The  chest  shows  no  special 
peculiarity  except  that  precordial  bulging  is  often  present,  espe- 
cially marked  in  children  (see  page  152),  even  in  the  first  attack  of  endo- 
carditis. The  cardiac  signs  are  the  same  as  for  the  chronic  valvular  lesions, 
though  usually  less  marked.  They  will  be  discussed  in  detail  under  the 
special  chapters. 

The  liver  is  usually  not  enlarged  unless  there  is  marked  heart  fail- 
ure. Occasionally  the  spleen  is  palpable  and  even  hard,  tender,  and 
painful,  as  a  result  of  a  fresh  or  old  infarct,  and  this  condition  may  persist 
unchanged  for  years. 

A  few  months  ago  the  writer  saw  in  the  Johns  Hopkins  Dispensary  a  young  girl  in 
whom  a  large,  very  hard  spleen  had  been  present  for  several  years,  first  appearing  during 
a  rather  severe  attack  of  simple  acute  mitral  endocarditis. 

There  is  often  slight  oedema  of  feet  and  ankles,  though  very  many 
cases  come  to  treatment  before  this  has  set  in.  The  presence  of  oedema 
in  an  early  acute  endocarditis  is  a  rather  grave  sign,  since  it  indicates  the 
failure  of  the  heart  to  respond  promptly  to  the  added  load. 

The  urine  is  usually  of  high  specific  gravity  and  contains  a  small 
amount  of  albumen  and  a  few  coarsely  or  finely  granular  casts, — a  typical 
febrile  albuminuria. 

The  blood  examination  usually  shows  a  slight  grade  of  secondary 
anaemia. 

SUBSEQUENT    COURSE. 

As  in  the  cases  cited  on  page  415,  there  is  usually  gradual  improve- 
ment under  any  treatment  in  which  the  main  factor  is  sufficient  rest, 
during  which  the  infection  subsides  (the  bacteria  dying,  or  more  commonly 
becoming  latent),  the  vegetations  undergo  gradual  organization  and  more 
or  less  thickening  or  shrinkage,  and  fever  passes  off/  as  does  the  acute  myo- 
cardial weakness.  The  patients  almost  always  recover  from  the  first  attack. 
Recurrence  is  especially  common,  and  is  the  danger  against  which  especial 
precaution  must  be  taken,  the  more  so  as  the  second  attack  often  spreads 
to  another  valve  or  even  to  two  more.  It  is  the  liability  to  repeated  attacks 
which  keeps  the  pathological  process  ever  fresh  and  increasing.  There  is 
then  usually  a  little  area  of  incompletely  organized  fibrin  always  present 
to  give  soil  to  any  stray  micrococcus  that  may  be  carried  by  the  blood 
stream,  and  thus  produce  a  new  outbreak  of  fresh  endocarditis  with  exacer- 
bation and  perpetuation  of  the  old  symptoms.     After  a  single  attack, 


414  DISEASES  OF  THE  HEART  AND  AORTA. 

especially  when  one  only  is  involved,  complete  organization  of  the  vegeta- 
tion may  set  in,  the  acute  myocardial  changes  subside,  and  the  heart  muscle 
may  soon  regain  its  normal  function. 

Compensation. — A  slight  leak  (see  page  420)  may  remain  at  the  site 
of  the  vegetation,  just  enough  to  produce  a  murmur  and  perhaps  even 
bring  about  slight  hypertrophy,  but  without  really  impairing  the  function 
of  the  heart;  and  the  individual  who  suffers  from  no  further  acute  endo- 
cardial changes  may  go  on  for  thirty  or  forty  years,  until  the  age  of  sclerosis 
sets  in  and  the  leak  is  widened  by  sclerotic  shrinkage,  without  the  appear- 
ance of  any  further  symptoms.  On  the  other  hand,  as  da  Costa  has  shown, 
persons  with  old  perfectly  compensated  valvular  lesions  are  much  more 
susceptible  to  cardiac  overstrain  and  acute  dilatation  than  are  normal 
individuals.  With  the  dilatation  there  comes  a  functional  insufficiency 
of  the  valves,  which  adds  its  effect  to  that  of  the  organic  lesion;  and  finally, 
as  Roy  and  Adami  have  shown,  stasis  brings  about  oedema  and  cellular 
infiltration  in  the  cusps.  This  infiltration  is  followed  by  further  valvular 
sclerosis  and  shrinking,  and  thus  the  cardiac  overstrain  in  itself  tends  to 
increase  permanently  the  original  lesion. 

When  hypertrophy  and  compensation  are  good  and  the  individual 
either  lives  a  quiet  life  or  has  developed  his  muscles  gradually  to  meet  the 
strain  of  his  surroundings,  he  may  escape  overstrains  entirely,  and  the 
lesion  may  either  be  stationary  or  may  shrink  by  gradual  sclerosis.  It  is 
a  rather  common  occurrence  to  find  perfectly  healthy  young  adults  or  even 
active  men  in  middle  age  who  have  had  well-compensated  mitral  insuffi- 
ciency persistent  since  childhood.  The  same  is  also  true  of  aortic  insuffi- 
ciency except  that  this  usually  again  makes  itself  felt  about  the  age  of  arterio- 
sclerosis, i.e.  about  the  age  of  forty.  Even  then,  with  good  care,  general 
hygiene,  avoidance  of  muscular  overstrain,  nervous  excitement,  and  over- 
eating, great  moderation  in  the  use  of  alcohol  and  tobacco,  and  especially 
personal  prophylactic  measures  against  infectious  diseases,  a  long  life 
may  be  attained  by  the  patient. 

Reinfection. — On  the  other  hand,  when  the  patient  is  still  subject  to 
recurrence  of  his  rheumatism  or  tonsillitis,  or  to  repeated  attacks  of  pneu- 
monia, bronchitis,  or  influenza,  the  probability  that  the  cardiac  lesion  will 
remain  quiescent  is  a  small  one,  and  it  becomes  more  likely  that  both  valve 
and  muscle  will  suffer  further  changes  whose  limit  it  is  impossible  to  pre- 
dict. It  is  therefore  most  important  not  to  give  a  definite  prognosis  to  the 
family  or  friends  of  the  patient  until  he  has  been  under  observation  for  about 
a  year  after  the  attack  of  endocarditis  has  subsided,  so  that  all  these  factors 
may  be  carefully  watched  and  taken  into  account,  prophylactic  measures 
be  instituted,  and  the  recuperative  power  of  the  heart  muscle  be  gauged. 

Complications. — Another  factor  even  more  important  than  the  endo- 
cardial lesion  is  the  involvement  of  the  pericardium  and 
especially  the  production  of  adherent  pericardium,  so  common 
in  the  first  and  second  decades.  This  condition  perhaps  more  than  any 
other  leads  to  early  heart  failure,  since  it  imposes  the  greatest  strain  of  all 
upon  the  heart;  and,  as  it  develops  insidiously  and  frequently  reaches  its 
maximum  only  after  the  first  acute  attack  has  passed  off,  it  should  be 
watched  for  with  great  care. 


ENDOCARDITIS.  415 


SIMPLE    ACUTE    ENDOCARDITIS. 

J.  A.,  male,  cannery  worker,  aged  15,  entered  the  hospital  complaining  of  rheu- 
matism. He  has  been  a  rather  delicate  boy,  having  had  erysipelas,  measles,  whooping- 
cough,  and  chicken-pox  when  a  child,  and  attacks  of  definite  articular  rheumatism  at  nine 
and  ten  years.    He  has  done  soldering  in  a  cannery  for  the  past  two  years. 

About  five  weeks  before  admission  he  began  to  complain  of  pain  in  his 
ankles  and  knees,  for  which  he  was  put  to  bed.  At  this  time  his  physician  found 
a  temperature  of  104°,  and  he  had  chilly  sensations,  but  no  shaking  chills. 
About  two  weeks  later  while  lying  down  he  felt  an  intense  pain  in  his  heart  and  be- 
gan to  get  white  in  the  face  and  blue  at  the  lips.  Since  then,  though  he  has  been 
losing  weight  and  strength,  he  has  had  no  more  pain.  He  has  had  occasional  headaches 
during  the  illness. 

Examination  shows  a  well-nourished  boy  of  sallow  color,  with  injected  pharynx, 
enlarged  tonsils,  and  enlarged  posterior  cervical  and  axillary  lymph-glands.  Chest 
is  well  formed  and  lungs  are  negative  but  for  a  few  moist  rales  over  the  left  apex. 

Heart . — There  is  marked  precordial  bulging.  The  apex  beat  is  seen  in 
the  4th  left  interspace  9  cm.  from  the  midline.  Dulness  extends  4  cm.  to  the 
right  of  the  midline  and  above  to  the  second  rib.  There  are  no  thrills.  The  first 
sound  at  the  apex  is  preceded  by  a  short  rumble  (Flint  murmur)  and  replaced 
by  a  soft  blowing  systolic  murmur.  The  second  sound  is  clear  at  the  apex, 
but  at  and  near  the  sternum  is  followed  by  a  blowing  diastolic  murmur, 
maximum  over  the  insertion  of  the  third  right  rib.  The  pulse  is  124  per  minute, 
small  but  definitely  collapsing,  and  there  are  well-marked  capillary 
pulsation  and  throbbing  of  the  carotids.     Blood-pressure:  maximal  115-125  mm.  Hg. 

Joints.  — There  are  swelling  of  right  elbow  and  left  ankle  and 
soreness  of  elbows,  knees,  and  right  hip;  slight  wasting  of  interossei  of  hands  and  feet. 
Genitalia  and  reflexes  are  normal. 

There  is  no  cedema.  Red  blood-corpuscles  5,000,000;  haemoglobin  75  per  cent.; 
leucocytes  11,000.  Urine. — Lemon  yellow.  Specific  gravity  1015;  alkaline;  no 
sugar;  a  trace  of  albumen;  a  considerable  number  of  coarsely  granular  casts. 

Oct.  31.  Dulness  extends  7.5  cm.  to  the  left  of  the  midline  and  2.5  cm.  to 
the  right.  Nov.  13.  Red  blood-corpuscles  5,000,000;  haemoglobin  80  per  cent.;  leuco- 
cytes 6,600.  General  condition  is  excellent.  Pulse  continues  rapid.  The  joints  are  clear. 
Jan.  5.  There  has  been  gradual  progressive  improvement.  Red  blood-corpuscles  4,700,000; 
haemoglobin  90  per  cent.;  leucocytes  11,000.  There  has  been  a  gradual  rise  in  the  maximal 
pressure  to  150-160  mm.  Hg,  as  the  patient's  improvement  has  continued  in  spite  of  the 
rapid  pulse.  The  patient  was  discharged  quite  well  on  Jan.  17,  but  had  a  second  more 
severe  attack  several  years  later. 

TREATMENT. 

The  treatment  of  the  acute  attack  of  endocarditis  partakes  in  general 
of  the  treatment  of  a  mild  febrile  disease  or  a  secondary  anaemia  on  the 
one  hand,  and  of  the  particular  valvular  disease  on  the  other.  Rest  in 
bed  until  a  couple  of  weeks  after  the  subsidence  of  all  febrile  symptoms 
is  therefore  an  absolute  necessity,  also  light  and  easily  digestible  diet,  at 
first  of  800-1000  calories,  later  2500. 

Digitalis  and  Strychnine. — As  a  rule,  digitalis  is  not  absolutely 
necessary,  and  is  dispensed  with  by  most  Anglo-American  practitioners. 

However,  Cloetta  has  shown  that  the  hearts  of  animals  in  which  aortic  insufficiency 
has  been  produced  experimentally  recover  much  better,  undergo  much  less  dilatation,  and 
acquire  much  greater  strength  if  digitalis  treatment  is  begun  at  once  and  is  continued  over 
long  periods  (about  a  year)  than  if  this  treatment  is  omitted.  Cloetta  claims  equally  good 
results  in  man,  but  his  cases  are  too  few  to  warrant  conclusions.  Nevertheless,  the  results 
are  sufficiently  definite  to  warrant  the  prolonged  use  of  digitalis  in  small  doses  (0.3  to  0.6 
c.c;  Tt^v  to  x  of  the  tincture)  in  cases  of  acute  endocarditis  with  cardiac  dilatation. 


416  DISEASES  OF  THE  HEART  AND  AORTA. 

In  cases  in  which  digitalis  is  not  used  strychnine  should  be  given 
in  doses  of  2  to  3  mg.  (^-0  to  to  gr-)  three  or  four  times  a  day. 

The  salicylate  preparations,  sodium  salicylate,  salol,  salipy- 
rin,  aspirin,  etc.,  should  be  given  for  the  rheumatism;  but,  although  they 
certainly  relieve  the  pain,  and  it  has  been  shown  that  they  are  excreted 
into  the  joint  cavity,  the  duration  of  the  fever  and  arthritis  does  not  seem 
to  be  much  affected  by  them,  and  certainly  the  frequency  of  cardiac 
involvement  is  unchanged.  On  the  other  hand,  the  salicylates,  especially 
in  large  doses,  have  a  depressant  effect  upon  the  heart,  and  the  use  of 
these  drugs  should  therefore  be  as  restricted  as  is  consistent  with  relief  of 
arthritic  pain. 

According  to  many  authorities,  the  salicylates  seem  to  be  more  effective  when  in- 
jected directly  into  the  joint  or  into  the  tissues  immediately  surrounding  it.  The  writer's 
experience  with  this  method  is  limited  and  in  the  cases  tried  its  results  were  not  striking, 
but  it  is  sometimes  worthy  of  trial.  Oil  of  wintergreen  (Oleum  gaultheriae,  methyl  sali- 
cylate) applied  to  the  skin  over  the  joint  also  seems  to  cause  great  relief  of  pain,  but  it  is 
possible  that  the  rubbing  may  also  cause  more  of  the  micrococci  to  be  thrown  out  in  the 
blood  stream  than  might  otherwise  be  the  case.  Hot  compresses  of  saturated  aqueous 
solutions  of  oil  of  wintergreen  to  the  joint  may  suffice  to  allay  pain. 

Other  Therapeutic  Measures. — It  is  most  important  to  relieve  anaemia, 
which  is  usually  present  and  which  is  always  a  contributing  factor  to  the 
fatty  degeneration  and  weakness  of  the  myocardium.  Rest,  full  diet 
especially  rich  in  eggs,  milk,  and  green  vegetables,  and  administration  of 
iron  usually  relieve  this  symptom. 

The  iron  may  be  administered  as  Pil.  ferri  carbonatis  (Blaud's  pills),  0.2  to  0.3  G. 
(gr.  iii  to  gr.  v)  t.i.d.,  p.c;  or  Massa  ferri  carbonatis  (Vallet's  mass,  a  more  stable  prepa- 
ration containing  honey  instead  of  sugar);  Elixir  ferri,  quininae  et  strychninse,  8  c.c.  (oii) 
t.i.d.,  a.c;   or  as  Syrup,  ferri  iodid.,  1  c.c.  (rc\,  xv)  t.i.d.,  p.c. 

If  the  anaemia  is  severe  or  does  not  yield  to  iron  alone,  arsenic  should 
be  given  as  well,  since  it  has  been  shown  that  iron  and  arsenic  together 
accelerate  formation  of  red  corpuscles  and  haemoglobin  more  than  does 
either  drug  alone. 

Arsenic  is  usually  given  in  the  form  of  Liquor  potassii  arsenitis  (Fowler's  solution), 
beginning  in  doses  of  0.2  c.c.  (Tt\,iii)  t.i.d.,  p.c,  and  increasing  one  drop  at  each  dose  until 
1  c.c.  (V(\,  xv)  is  reached  or  puffy  eyelids  and  albuminous  urine  show  that  the  physiological 
limit  has  been  reached. 

Prophylactic  Treatment. — One  of  the  most  important  factors  in  hasten- 
ing the  healing  of  a  fresh  vegetation  is  to  keep  it  from  being  reinfected  by 
bacteria  floating  in  the  blood  stream.  Every  focus  of  infection  is  a  store- 
house from  which  a  few  bacteria  are  given  off  from  time  to  time,  and  hence 
is  a  source  of  danger.  Accordingly  in  a  number  of  clinics,  and  particularly 
in  the  medical  clinic  of  the  Johns  Hopkins  Hospital,  under  Prof.  Barker's 
direction,  an  effort  is  being  made  to  stamp  out  every  focus  of  infection  to  be 
found  anywhere  in  the  body.  Carious  teeth,  paronychias,  and  ischiorectal 
abscesses  are  removed.  Particular  attention  is  given  to  the  tonsils.  These 
organs  are  the  main  portals  of  entry  for  the  rheumatic  infection.  In  persons 
who  are  subject  to  recurrent  tonsillitis  there  are  almost  always  small  ab- 
scesses containing  cocci  persisting  in  the  depths  of  the  tonsillar  tissue,  even 
when  there  is  no  inflammation  visible  upon  the  surface.    These  are  perma- 


ENDOCARDITIS.  417 

nent  portals  of  infection.  Dr.  Barker  therefore  insists  upon  the  removal 
of  enlarged  tonsils  in  most  cases  of  rheumatic  heart  disease.  This 
should  be  done  between  but  not  during  the  attacks,  since 
there  is  danger  of  throwing  more  cocci  into  the  blood.  The  improvement 
which  follows  removal  is  sometimes  immediate  and  striking.  The  patient's 
color  improves  within  a  few  days.  He  feels  better.  His  expression  is 
brighter,  and  he  appears  more  robust.  Improvement  is  more  rapid  and, 
since  reinfection  is  less  frequent,  it  is  more  permanent. 

It  is  naturally  of  great  importance  that  all  the  tonsillar  tissue  should  be  removed, 
since  a  small  amount  left  in  place  may  again  undergo  hypertrophy  and  become  reinfected. 
Such  complete  removal  is  impossible  with  the  guillotine,  the  snare,  and  the  electro-cautery, 
and  is  extremely  difficult  by  even  the  ordinary  intracapsular  dissection.  The  most  satis- 
factory method  known  to  the  writer  is  the  extracapsular  dissection. 

Palliative  Treatment  of  the  Tonsils.— By  way  of  palliative  or  prophylactic 
treatment  various  antiseptic  gargles  may  be  used.  Gargles  which  contain 
hydrogen  peroxide  are  to  be  preferred,  because  the  pus-cells  contain  a  catalase 
which  sets  free  the  oxygen.  The  nascent  oxygen  is  a  powerful  antiseptic,  and 
the  excess  collects  in  bubbles  which  mechanically  loosen  and  sweep  off  the 
exudate.  The  hydrogen  peroxide  should  not  be  stronger  than  2  volume  per 
cent,  (one  part  commercial  hydrogen  peroxide  to  four  parts  of  water). 

Other  gargles  that  may  be  used  are  Dobell's  solution,  dilute  Lugol's 
solution,  and  dilute  potassium  chlorate  solution  (especially  with  equal  parts 
of  dilute  hydrogen  peroxide). 

Prym's  suction  cups  may  also  be  applied  to  the  tonsils. 

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27 


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ENDOCARDITIS.  419 

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Lond.,  1903-04,  ix,  158. 
Beattie,  J.  M.:  Acute  Rheumatism  caused  by  the  Diplococcus  Rheumaticus,  ibid.,  1904,' 

ix,  272. 
Menzer:  Die  iEtiologie  des  akuten  Gelenkrheumatismus,  Berk,  1902. 
Cole,  Rufus  I.:  Experimental  Streptococcus  Arthritis  in  Relation  to  the  Etiology  of  Acute 

Articular  Rheumatism,  J.  Infect.  Dis.,  Chicago,  1904,  i,  714.    The  Etiology  of  Acute 

Articular  Rheumatism,  N.  York  and  Phila.  M.  J.,  N.  York,  1906,  lxxxiii,  534. 
Longcope,  W.  T.:  Experimental  Arthritis  and  Endocarditis  produced  by  a  Streptococcus; 

Isolated  from  the  Blood  of  a  Case  of  Rheumatism,  Endocarditis,  and  Chorea,  Am. 

J.  M.  So.,  Phila.,  1904,  cxxviii,  601. 
Austin,  Mabel  F.:  Endocarditis  due  to  a  Minute  Organism,  probably  the  Bacillus  Influenzae, 

Johns  Hopkins  Hosp.  Bull.,  Bait.,  1899,  x,  194. 
Marshall,  H.  T.:  Endocarditis  in  Tuberculosis,  Johns  Hopkins  Hosp.  Bull.,  1905,  xvi,  303. 
Michaelis,  L.,  and  Blum,  S.:  Ueber  experimentelle  Erzeugung  von  Endocarditis  tuber- 
culosa, Deutsch.  med.  Wchnschr.,  Leipz.,  1898,  xxiv,  550. 
Stewart,  H.  A.:  Experimental  and  Clinical  Investigations  of  the  Blood-pressure  Changes, 

in  Aortic  Insufficiency,  Arch.  Int.  Med.,  Chicago,  1907,  i,  102. 
Cameron,  P.  D.:    Physiological  and  Pharmacological  Studies  upon  Cardiac  Tonicity  in 

Mammals,  Thesis,  Edinb.,  1908. 
Hirschf elder,  A.  D.:  Recent  Studies  upon  the  Circulation  and  their  Importance  to  the 

Practice  of  Medicine,  J.  Am.  M.  Ass.,  Chicago,  1908,  li,  473. 
Hasenfeld,    A.:  Ueber   die    Entwicklung   einer   Herzhypertrophie   bei    der   Pyocyaneus- 

Endocarditis  und  der  dadurch  verursachten  Allgemeininfection,  Deutsches  Arch.  f. 

klin.  Med.,  Leipz.,  1899,  Ixiv,  763. 
Osier,  W.:  Chronic  Infective  Endocarditis,  Quart.  J.  M.,  1909,  ii,  219. 
Rosenow,  E.  O:  Phagocytic  Immunity  and  the  Therapeutic  Injection  of  Dead  Bacteria 

in  Endocarditis,  J.  Am.  M.  Ass.,  Chicago,  1908,  li,  1571. 
Holt  and  Crondall.     Quoted  from  Horder. 
Barker,  L.  F.:  Clinical  Lectures  at  the  Johns  Hopkins  Hospital.     (Unpublished.) 


II. 

MITRAL  INSUFFICIENCY. 

OCCURRENCE. 

Of  all  the  valvular  lesions  those  involving  the  mitral  valve  are  the 
most  common,  especially  those  which  lead  to  the  production  of  a  leak  at 
that  orifice  (mitral  insufficiency,  mitral  regurgitation,  incompetency  of  the 
mitral  valve). 

Involvement  of  the  mitral  valve  alone  was  found  to  be  present  in  51  per  cent,  of  1781 
cases  of  valvular  disease  admitted  to  the  Johns  Hopkins  Hospital  between  1889  and  1908, 
and  in  54  per  cent,  of  Sperling's  300  autopsies  on  similar  cases  in  Virchow's  Pathological 
Institute  in  Berlin.  (Fig.  179.)  Mitral  insufficiency,  both  alone  and  in  association  with 
other  lesions,  was  present  in  64  per  cent,  of  the  Johns  Hopkins  cases,  occurring  alone  in 
29  per  cent,  (see  the  Table,  Fig.  179). 

As  regards  age,  Gillespie  (Fig.  178)  has  found  from  a  study  of  816 
cases  that  its  frequency  is  about  uniform  between  ten  and  fifty  years,  after 
which  it  diminishes.  This  is  in  sharp  contrast  to  the  cases  of  mitral  ste- 
nosis, which  are  most  frequent  before  the  age  of  thirty  and  become  much 
rarer  after  thirty.  In  youth  women  are  slightly  more  often  affected;  in  old 
age  the  affection  is  a  little  more  common  among  men.  The  mortality  from 
mitral  insufficiency  becomes  greater  as  age  progresses. 

PATHOLOGICAL    ANATOMY. 

Pathologically,  cases  of  mitral  insufficiency  may  be  divided  into  two 
groups: 

1.  Organic,  due  to  vegetations,  cicatrizations,  or  atheromatous  plaques, 
thickening  of  the  edges  of  the  valves,  or  ulceration  upon  the  valve  itself. 

2.  Functional  (or  relative),  in  which  the  valves  are  intact,  but  closure 
becomes  imperfect  through  relaxation  of  the  muscle  into  which  the  cusps 
are  inserted,  or  through  stretching  of  the  chordse  tendinese. 

Organic  Mitral  Insufficiency.  —  The  pathogenesis  of  organic  insuffi- 
ciency is  simple.  The  lesions  arise  during  the  course  of  an  acute  or 
subacute  endocarditis,  and  frequently  result  from  the  accumulation  of 
inflammatory  exudates  from  several  successive  infections.  These  are 
cemented  into  permanent  structures  by  organization  and  calcification. 
Occasionally  a  perforation  of  the  valve  occurs  from  ulceration.  As  in 
acute  endocarditis,  infection  in  the  rheumatic  cycle  is  the  most  common 
cause  of  chronic  mitral  disease,  though  other  infections  may  represent  not 
only  primary  but  exacerbating  factors. 

The  vegetation,  once  formed,  gives  rise  to  the  leak  by  holding  apart 
the  neighboring  portions  of  the  cusps  so  that  regurgitant  streams  occur 
about  its  serrations  (Fig.  180,  a,  A). 

420 


MITRAL  INSUFFICIENCY. 


421 


Tests  for  Sufficiency  of  .Mitral  Valve. — It  is  easy  to  demonstrate  by  the  method  of 
Gad  (see  page  13)  and  Meigs  that  when  the  vegetation  is  not  extensive  the  mitral  cusps 
may  adapt  themselves  perfectly  to  its  contour  and  prevent  a  leak  altogether;  but  when, 
as  is  usually  the  case,  their  flexibility  is  altered  by  a  line  of  vegetation,  atheroma,  or  infil- 
tration, this  apposition  is  prevented.  The  amount  of  blood  actually  regurgitating,  and 
hence  the  functional  importance  of  the  lesion,  depends  largely  upon  these  factors,  as  well 
as  upon  the  concomitant  affection  of  the  cardiac  muscle. 

The  normal  mitral  valve  will  hold  without  leakage  against  a  column  of  water  forced 
into  the  ventricle  through  the  aorta  from  the  faucet  (T.  W.  King,  1837;  Gibson,  Meigs), 
poured  into  it  through  a  slit  near  the  apex  with  the  heart  inverted  (Bleichroeder),  or  forced 
into  it  through  an  infusion  needle  attached  to  a  Davidson  syringe  (Lauder  Bruntonj.  It 
will  close  tightly  about  a  rod,  clamp,  or  even  an  irregular  mass  of  knotted  string  shaped 
like  a  vegetation  (de  Sautelle  and  Grey,  Arch.  Int.  Med.,  1911,  viii,  734),  but  when  the 
heart  muscle  is  relaxed  or  the  valve  is  thickened  and  rigid  either  of  these  things  brings  on 
a  leak. 

B  C 


Fig.  180.  —Regurgitant  streams  in  organic  and  functional  mitral  insufficiencies.  A,  organic  mitral 
insufficiency;  B,  functional  insufficiency  of  the  papillary  type;  C,  relative  mitral  insufficiency;  a,  view 
from  above  the  valves  ;  b,  coronary  section  through  the  heart.  The  arrows  indicate  the  points  and  direc- 
tion of  regurgitations. 


Coexistence  of  Organic  and  Functional   Insufficiency. — As  has  been 

stated  above  (page  304),  Koester,  Krehl,  Geipel,  and  others  have  shown  that 
the  occurrence  of  vegetations  upon  the  valves  is  often,  perhaps  usually, 
accompanied  by  foci  of  myocarditis  in  the  papillary  mus- 
cles and  in  the  ring  of  musculature  about  the  mitral  orifice.  It  is  the 
weakening  of  these  muscle-fibres  especially  which  gives  rise  to  the  func- 
tional insufficiencies,  and  it  is  therefore  probable  that  in 
many  cases  of  organic  mitral  insufficiency  the  ele- 
ment of  superadded  muscular  insufficiency  is  a  very 
important  one.  Indeed  one  often  meets  with  persons  who,  in  spite 
of  medium-sized  vegetations,  suffer  little  or  no  discomfort  as  long  as  the 
heart  muscle  is  in  good  condition,  but  in  whom  cardiac  symptoms 
occur  as  soon  as  overstrain,  anaemia,  or  febrile  disease  weakens  the  mvo- 


422  DISEASES  OF  THE  HEART  AND  AORTA. 

cardium.  In  the  periods  of  apparent  health,  the  leak  is  confined  to  the 
streams  about  the  edges  of  the  vegetation.  In  the  added  functional  insuf- 
ficiency it  also  takes  place  at  other  points  along  the  line  of  closure.  How- 
ever, it  is  impossible  to  differentiate  clinically  between  the  organic  and  the 
functional  elements,  and  their  relative  importance  in  a  given  case  cannot 
be  accurately  estimated. 

Atheroma  of  the  Mitral  Valve. — Atheromatous  and  calcined  patches  along  the  face 
and  edges  of  the  cusps  of  the  valves  are  also  not  uncommon  (see  Fig.  275,  page  575) . 
These  changes  are  particularly  frequent  along  the  line  of  closure,  where,  as  shown  by  Roy 
and  Adami,  mechanical  injury,  hemorrhages,  and  exudates  are  most  frequent.  Patho- 
logically, they  are  brought  about  by  processes  similar  to  those  occurring  in  the  walls  of  the 
arteries  during  arteriosclerosis,  and  the  condition  is  frequently  associated  with  extensive 
sclerosis  of  the  coronary  arteries.  Calcified  plaques  may  also  be  present  in  the  myocardium 
(case  of  J.  L.,  Fig.  275).  The  mechanical  effect  of  such  thickenings  and  areas  of  rigidity 
is  to  prevent  the  cusps  from  accommodating  themselves  to  one  another,  giving  rise  to  leaks 
which  are  undistinguishable  clinically  from  those  due  to  vegetations. 

Hemorrhage  in  the  Mitral  Valve. — Occasionally  hemorrhages  occur  in  the  cusps  of 
the  mitral  valve,  especially  after  trauma  to  the  chest  (Kiilbs)  or  labor  (Weber  and 
Deguy),  and  in  new-born  infants  (Fahr).  It  is  probable  that  the  organization  of  the  clot 
initiates  a  fibrosis  which  leads  to  mitral  stenosis. 

Functional  Mitral  Insufficiency. — When  the  heart  muscle  attains  a 
certain  degree  of  weakness,  leaks  at  the  mitral  orifice  may  take  place. 
They  may  occur  as  the  direct  result  of  acute  cardiac  dilatation  from  a  pri- 
mary cardiac  overstrain,  though  they  arise  more  frequently  in  hearts  whose 
myocardium  has  already  undergone  degenerative  or  fibrous  changes  but 
whose  valves  are  still  intact.  This  functional  insufficiency  is  often  seen  in 
cases  of  myocarditis.  On  the  other  hand,  functional  insufficiency  of  the 
mitral  valve  may  arise  as  a  secondary  manifestation  in  organic  disease  of  the 
aortievalves.  This  occurs  especially  when  the  leak  attains  a  severe  grade  or 
the  work  of  the  heart  is  too  much  increased,  the  walls  of  the  ventricle  and 
the  papillary  muscles  becoming  overstretched  during  diastole.  This  phe- 
nomenon will  be  further  discussed  in  the  chapter  upon  aortic  insufficiency. 

Types  of  Functional  Insufficiency. — The  leaks  occurring  at  the  mitral 
valve  as  the  result  of  muscular  weakness  may  be  divided  into  two  groups : 

1.  Papillary  Insufficiency^ — Leaks  occurring  at  one  or  more  points  along  the 
valve  (Fig.  180,  B,  b)  when  the  weakness  of  a  papillary  muscle  or  stretching  of  a  chorda 
tendinea  allows  the  corresponding  portion  of  the  valve  to  be  lifted  a  little,  and  a  small 
regurgitant  stream  to  emerge  at  one  of  the  points  of  pouting  and  puckering  along  the  line 
of  closure.  This  may  be  termed  the  type  of  papillary  insufficiency,  and 
like  many  cases  of  uncomplicated  organic  insufficiency  may  correspond  to  the  escape  of 
only  a  small  quantity  of  blood.  This  papillary  insufficiency  represents  the  mildest  form  of 
functional  regurgitation.  The  mitral  valve  is  pushed  upward  during  systole,  like  a  sail, 
impelled  by  the  full  force  of  the  entire  ventricular  wall.  This  is  antagonized  by  the  pull 
of  the  relatively  small  papillary  muscles.  It  is  evident  that  fibre  for  fibre  the  papillary 
muscles  incur  a  much  greater  strain  than  the  fibres  in  the  ventricular  wall,  and  consequently 
they  are  often  the  first  to  weaken.  When  they  weaken  apposition  of  the  cusps  is  impaired 
and  regurgitation  sets  in.  Moreover,  since  T.  W.  King  and  Gibson  have  shown  that  the 
normal  mitral  valve  usually  holds  unless  dilatation  sets  in,  it  is  evident  that  the  papillary 
type  of  insufficiency  is  the  only  form  of  functional  insufficiency  that  can  occur  in  a  heart 
that  is  not  greatly  dilated, ^ 

2.  Relative  Insufficiency.— The  second  type  of  functional  insufficiency  is  met  with 
when  the  left  ventricle  is  dilated  to  such  an  extent  that  the  mitral 
orifice  becomes  larger  than  the  available  area  of  valve  surface, 
and  what  may  be    correctly  termed   a    relative   insufficiency    results.      Under 


MITRAL  INSUFFICIENCY. 


423 


these  conditions  the  leak  occurs  not  at  a  single  point  but  all  along  the  line  of  closure  (Fig. 
180,  C).  The  amount  of  blood  which  regurgitates  under  these  conditions  may  be  very  large. 
Pathogenesis  op  these  Types. — The  mode  of  occurrence  of  these  types  of  in- 
sufficiency may  be  readily  demonstrated  by  the  method  of  Gad  and  Meigs,  though  care 
must  be  taken  that  the  heart  used  for  the  experiment  is  not  in  a  condition  of  rigor  mortis. 
If  water  is  forced  into  the  ventricles  at  various  pressures,  it  will  be  seen  that,  as  shown  by  G. 
A.  Gibson,  leakage  will  occur  at  a  relatively  slight  pressure.  This  regurgitation  will  be 
small  in  amount,  and  will  be  seen  to  be  of  the  papillary  type;  but  if  the  pressure  is  suffi- 
ciently increased  and  the  ventricle  dilated,  the  cusps  of  the  valve  stand  apart,  the  true 
relative  insufficiency  (type  2)  is  produced,  and  a  large  amount  of  fluid  regurgitates.  The 
role  which  stretching  of  the  muscle  plays  in  this  regurgitation  may  be  shown  by  boiling  the 
heart  and  thereby  shortening  the  fibres  in  heat  rigor,  after  which  the  leak  that  was  present 
disappears  and  does  not  recur  until  much  greater  pressures  are  resorted  to.  Gibson  has 
caused  the  leak  to  disappear  by  tightening  a  ligature  about  the  mitral  muscular  ring.  It  is 
therefore  evident  that  the  tonicity  of  the  cardiac  muscle  is  an  important  element  in  deter- 
mining the  occurrence  and  the  degree  of  leak  both  in  functional  and  in  organic  mitral  insuffi- 
ciency. This  point  is  of  the  greatest  importance  in  therapeutic  considerations,  and  will  be 
referred  to  later. 

Occurrence  of  Functional  Insufficiency. — Functional  insufficiency  of 
the  mitral  valve  occurs  in  primary  cardiac  overstrain,  in  anaemias,  during 
the  course  of  and  convalescence  from  infectious  diseases,  and  in  many 
cases  of  aortic  disease.  A  certain  percentage  of  the  cases  in  which  aortic 
and  mitral  insufficiencies  are  found  simultaneously  belongs  to  this  group. 

Lian,  in  Frangois-Franck's  laboratory,  has  shown  that  the  contraction 
of  the  ring  of  muscle  about  the  mitral  valve  (mitro-aortic  ring)  narrows 
the  diameter  of  the  orifice  during  systole.  He  demonstrated  that  when 
contraction  is  weakened  the  valves  may  not  remain  in  perfect  apposition. 

MECHANICS    OF    THE    CIRCULATION    IN    MITRAL   INSUFFICIENCY. 

It  is  almost  axiomatic  to  state  that  the  systolic  regurgitation  of  blood 
from  left  ventricle  to  left  auricle  in  mitral  insufficiency  is  accompanied  by 
a  fall  of  pressure  in  the  former  and  a  rise  of  pressure  in  the  latter. 


COMPENSATED 


BROKEN  PULMONARY  COMPENSATION 


Fig.  181. — Diagram  showing  the  volume  and  pressure  curves  under  these  conditions.  (Schematic.) 
Upper  curve  (A),  interauricular  pressure;  solid  black  line,  volume  curve  of  the  left  auricle;  lower  curve 
(V),  intraventricular  pressure.  In  broken  pulmonary  compensation  the  left  auricle  is  dilated. 


The  regurgitation  of  blood  into  the  left  auricle  causes  a  systolic  rise  of 
pressure  to  take  place  in  this  chamber,  replacing  the  systolic  fall  of  pressure 
which  is  present  under  normal  conditions  (Fig.  181).  The  pressure  curve 
within  this  chamber  in  mitral  insufficiency  thus  resembles  that  seen  in  the 
right  auricle  in  tricuspid  insufficiency — a  rise  throughout  ventricular  systole 
with  a  fall  during  diastole,  and  a  small  rise  when  systole  of  the  auricle 
takes  place. 


424  DISEASES  OF  THE  HEART  AND  AORTA. 

The  pressure  conditions  within  the  pulmonary  circulation  are  of  the 
greatest  importance,  and  in  this  both  the  force-pump  and  the  suction- 
pump  actions  of  the  ventricle  show  themselves. 

Effect  of  Mitral  Insufficiency  without  Increase  in  the  Strength  of  the 
Ventricle. — If  the  force  of  the  left  ventricle  remains  unaltered  after  the 
production  of  the  insufficiency,  it  stands  to  reason  that  less  blood  will  reach 
the  arteries  and  pass  on  to  the  capillaries  and  systemic  veins  than  did  so 
before.  The  arterial  blood-pressure  will  fall.  Consequently  less  blood  will 
enter  the  right  side  of  the  heart  from  the  venae  cavae,  and  the  pressure  in  the 
latter  will  be  lowered.  The  systolic  output  of  the  right  ventricle  will  thus 
be  diminished  and  the  pressure  in  the  pulmonary  artery  will  fall.  On  the 
other  hand,  the  regurgitated  blood  in  the  left  auricle  and  pulmonary  veins 
added  to  that  coming  on  from  the  pulmonary  artery  will  cause  the  pres- 
sure in  the  left  auricle,  the  pulmonary  veins,  and  the  capillaries  of  the  lungs 
to  rise  (Fig.  183,  III). 


Fig.  182. — Curve  of  intraventricular  pressure  in  mitral  insufficiency  produced  on  a  mechanical 
model.  (After  Marey.)  P.  V.,  intraventricular  pressure;  P.  R.,  arterial  pressure.  The  horizontal  line 
denotes  the  production  of  insufficiency.  O,  notch  due  to  the  auricular  systole;  e,  summit  of  the  curve 
during  systole  of  the  ventricle. 

Pulmonary  Stasis. — As  v.  Basch  and  his  pupils  have  shown,  conges- 
tion of  the  pulmonary  capillaries  is  the  most  important  cause  of  cardiac 
dyspncea  (broken  pulmonary  compensation).  Hence  it  will  not  be  sur- 
prising that  dyspncea  from  this  cause  is  an  early  and  important  symptom 
of  mitral  insufficiency,  and  that  its  disappearance  depends  upon  other 
factors  which  tend  to  deplete  the  pulmonary  capillaries.  (Diminution  in 
the  amount  of  blood  entering  right  ventricle,  or  weakened  suction-pump 
action  of  left.)  The  capillary  area  is  sufficiently  elastic  to  accommodate  a 
considerable  amount  of  regurgitant  blood  before  this  furnishes  an  obstruc- 
tion to  the  pulmonary  artery,  just  as  is  the  case  with  the  capillaries  of  the 
splanchnic  area,  but  after  a  time  or  in  severe  lesions  the  intrapulmonary  stasis 
finally  makes  its  effect  felt  in  the  pulmonary  artery.  The  pressure  there  rises 
(Gerhardt) .  When  the  pulmonary  stasis  becomes  extreme  the  right  ventricle, 
too,  becomes  overloaded  and  dilated.  Broken  systemic  compen- 
sation sets  in  (Fig.  183,  IV).  Stasis  occurs  in  the  systemic  veins, 
oedema  and  ascites  take  place,  and  a  secondary  functional  insufficiency  of 
the  tricuspid  valve  may  usually  be  demonstrated.  With  the  occurrence  of 
this  secondary  leak  at  the  tricuspid  orifice,  less  blood  is  pumped  into  the 
pulmonary  circulation,  the  congestion  here  diminishes,  the  dyspncea  dimin- 


MITRAL  INSUFFICIENCY. 


425 


ishes  also,  and  in  spite  of  the  increased  gravity  of  the  condition  the  patient 
may  experience  some  temporary  relief  from  his  symptoms.  This  phenom- 
enon was  noted  by  T.  W.  King  in  1837,  and  was  designated  by  him  "the 
safety-valve  action  of  the  tricuspid  valve."  The  relief  is,  however,  only 
transitory,  as  the  accumulation  of  C02  in  the  blood  soon  gives  rise  to 
dyspnoea  from  stimulation  of  the  respiratory  centre  in  the  medulla,  and  the 
real  state  of  cardiac  failure  manifests  itself.  If  the  condition  is  allowed  to 
continue,  the  outcome  is  death. 


Fig.  183. — Diagram  showing  the  effects  of  mitral  insufficiency  upon  the  circulation.  I.  Normal. 
II.  Compensation  through  filling  of  the  auricle  in  systole  but  complete  emptying  in  diastole.  III.  Broken 
pulmonary  compensation.     IV.  Broken  systemic  compensation.  (Compare  with  Fig.  26.) 

Effect  of  Increase  in  the  Strength  of  the  Left  Ventricle. — If,  on  the 

other  hand,  the  force  of  the  left  ventricle  increases,  it  can  throw  more 
blood  out  into  the  aorta  and  arteries;  and  this  blood  must  first  be  drawn 
from  the  left  auricle  and  pulmonary  circulation.  So  that  if  the  output 
from  the  ventricle  increase,  it  will  soon  be  pumping  more  blood  into 
the  aorta  than  the  right  ventricle  (whose  force  has  remained  practically 
unchanged)  pumps  into  the  pulmonary  artery.  Accordingly  more  blood 
leaves  the  lungs  than  enters  them,  and  the  engorgement  passes  off.  The 
whole  condition  may  be  summed  up  by  the  statement  that  a  weakly 
acting  left  ventricle  overfills  the  lungs  with  blood, 
while  a  strongly  acting  left  ventricle  bails  them  out. 
The  whole  of  pulmonary  engorgement  is,  as  rightly 
claimed  by  v.  Basch,  a  problem  not  of  the  right  ventri- 
cle,  but   of  the  left. 


CLINICAL   MANIFESTATIONS. 
MITRAL   INSUFFICIENCY    WITHOUT    SYMPTOMS. 

The  earliest  circulatory  disturbance  in  mitral  insufficiency  is  stasis  in 
the  pulmonary  capillaries,  which,  as  v.  Basch  and  his  pupils  have  shown, 
leads  to  cardiac  dyspnoea.  Accordingly,  it  is  not  surprising  that  dyspnoea 
should  be  one  of  the  earliest  symptoms  of  mitral  insufficiency.     But  the 


426  DISEASES  OF  THE  HEART  AND  AORTA. 

pulmonary  stasis  does  not  occur  or  does  not  persist  when  the  action  of  the 
left  ventricle  is  sufficiently  vigorous,  and  hence  in  the  milder  cases  shortness 
■of  breath  may  be  absent  for  a  long  time  after  the  actual  formation  of  the 
lesion  and  may  make  itself  evident  only  upon  exertion. 

Thus,  a  young  friend  of  the  writer,  a  boy  of  eleven,  in  1907  contracted  tonsillitis  accom- 
panied by  the  typical  signs  of  mitral  insufficiency.  He  was  kept  moderately  quiet  on  account 
of  the  throat  lesion  and  had  apparently  recovered  completely,  so  that  the  family  did  not 
notice  any  abnormality  until  a  year  afterward,  when  he  became  somewhat  short  of  breath 
upon  walking  uphill.  Since  a  little  caution  has  been  exercised  against  fast  walking  he  no 
longer  becomes  short  of  breath  and  remains  perfectly  free  from  symptoms.  The  prognosis 
is  very  favorable.  In  some  more  vigorous  individuals  the  lesion  does  not  manifest  itself 
■at  all.  The  writer  has  in  mind  a  young  man  of  twenty-one  who  has  shown  signs  of  mitral 
insufficiency  for  eight  years,  but  during  that  period  has  excelled  at  football,  wrestling,  and 
all  the  severe  forms  of  sport;  also  a  professor  of  forty  who  has  had  a  mitral  lesion  of  rheumatic 
origin  for  some  time  without  the  slightest  physical  inconvenience.  These  cases,  though 
scarcely  to  be  regarded  as  the  rule,  are  encountered  with  great  frequency  in  patients  who 
.are  examined  for  some  other  cause.  Occasionally  such  persons  have  been  informed  of  their 
trouble,  sometimes  given  a  grave  prognosis,  and  come  to  the  physician  in  great  mental 
distress  because  they  have  been  told  that  they  have  "organic  heart  trouble,"  and  yet 
they  may  reach  middle  or  even  old  age  without  serious  inconvenience.  It  is  not  extremely 
uncommon  to  find  cases  in  whom  a  mitral  lesion  has  been  present  thirty  or  forty  years  with- 
out greatly  affecting  the  patient's  activity  or  enjoyment  of  life. 

Pulmonary  Complications  of  Mitral  Disease. — The  prolonged  stasis  and  high  pres- 
sure in  the  pulmonary  capillaries  may,  however,  give  rise  to  permanent  changes  in  their 
walls  and  in  the  tissues  about  them  and  facilitate  the  occurrence  of  a  chronic  bronchitis. 
This  bronchitis  resulting  from  stasis  may  be  considered  analogous  in  origin  to  the  ulcerations 
and  weeping  eczema  found  upon  the  legs  in  association  with  varicose  veins  or  cardiac  oedema. 
The  presence  of  this  chronic  bronchitis  is  liable  to  arouse  a  suspicion  of  tubercu- 
losis when  the  trouble  is  really  cardiac.  The  suspicion  is  sometimes  still  further  aroused 
in  the  cases  in  which  the  walls  of  the  capillaries  in  some  area  of  the  lungs  have  become 
eroded  and  occasional  pulmonary  hemorrhages  take  place.  Thus,  Osier  and  A.  G.  Gibson 
mention  the  case  of  a  physician  who  suffered  from  occasional  haemoptysis  due  to 
mitral  insufficiency  over  a  period  of  twenty-five  years,  each  attack  giving  rise  to  great  relief 
-of  his  cardiac  symptoms  by  relieving  the  engorgement  of  the  left  auricle.  The  diagnosis  in 
such  cases  is  often  difficult,  but  may  be  made  when  there«is  continued  absence  of  tubercle 
bacilli  from  the  sputum,  and  especially  from  the  ejected  blood,  associated  with  the  signs  of 
a  definite  mitral  insufficiency.  Further  confirmation  may  be  gained  by  a  negative  cuta- 
neous or  ophthalmic  reaction  with  tuberculin,  or  if  necessary  by  a  negative  subcutaneous 
injection  of  the  latter. 

MITRAL  INSUFFICIENCY    WITH    SYMPTOMS. 

Second  Stage  of  Mitral  Insufficiency  (Broken  Pulmonary  Compensa= 
tion). — A  more  severe  stage  with  less  favorable  prognosis  is  that  in  which  the 
lesion  manifests  itself  by  subjective  symptoms.  As  in  most  other  cardiac 
disturbances,  palpitation  occurs  early  in  the  disease.  Palpitation  is,  how- 
ever, common  in  healthy  persons,  and,  as  shown  by  Hirschfelder  (see  page 
213),  cannot  as  yet  be  regarded  as  signifying  functional  weakness,  so  that 
its  presence  scarcely  suffices  to  direct  suspicion  to  the  cardiac  valves. 

The  earliest  symptom  of  real  importance  is  shortness  of  breath. 
This  occurs  at  an  earlier  stage  in  affections  of  the  mitral  than  of  the  aortic 
valves,  but  is  more  marked  in  early  mitral  stenosis  than  in  early  mitral 
insufficiency.  Nevertheless,  it  may  be  quite  severe  in  compara- 
tively mild  grades  of  the  latter,  especially  on  exertion.  As  has 
been  stated  above,  the  dyspnoea  is  due  to  the  pulmonary  engorgement,  as 


MITRAL  INSUFFICIENCY.  427 

shown  by  v.  Basch.  It  is  therefore  liable  to  pass  off  when  the  left  ventricle 
hypertrophies  and  the  systolic  output  is  increased  and  the  suction-pump 
action  is  increased.  For  practical  purposes,  therefore,  such  persons  whose 
cardiac  function  has  been  restored  by  the  hypertrophy  of  the  left  ventricle 
may  be  said  to  have  passed  from  the  second  stage  insufficiency  back  into 
the  first.  They  often  remain  in  this  excellent  condition  for  a  number  of 
years,  and  sometimes  oscillate  between  the  first  and  the  second  stages  for 
a  number  of  years  more. 

Tonicity  of  the  Heart  as  a  Factor  Governing  the  Leak. — A  most 
important  factor  in  preserving  this  balance  is  the  tonicity  of  the  car- 
diac muscle;  for  when  the  tonus  is  maintained  the  cusps  of  the  valve 
are  approximated  as  tightly  as  possible  about  the  thickening,  and  the 
amount  of  leak  is  reduced  to  minimal,  whereas  when  the  tonicity  is  low 
the  organic  leak  is  further  supplemented  by  a  papillary  or  a  relative  insuf- 
ficiency. A  small  leak  is  thus,  if  only  for  a  time,  transformed 
into  a  large  one.  When  tonicity  is  low  it  is  harder  for  the  heart  to 
recover  from  such  an  additional  strain  than  if  the  latter  occur  at  a  time 
when  the  tonus  is  increased.  The  added  functional  insufficiency  may  thus 
become  permanent.    We  have  here  another  example  of  the  vicious  circle: 

Leak  at  mitral  valve 
Leak  increased  . 

A  I 

Papillary  or  Heart  strain 

relative  insufficiency  Diminished  tonicity 

It  is  evident,  therefore,  that  in  spite  of  the  comparative  ease  with 
which  patients  may  recover  from  the  symptoms  of  mitral  insufficiency 
when  the  case  is  placed  under  favorable  conditions  as  soon  as  possible,  yet 
the  case  may  rapidly  become  a  grave  one  if  these  precautions  are  neglected, 
so  that,  in  the  words  of  Osier,  mitral  insufficiency  may  be  either  the  mildest 
or  the  gravest  of  valvular  lesions. 

Third  Stage  of  Mitral  Insufficiency  (Broken  Systemic  Compensa= 
tion). — The  second  stage  of  mitral  insufficiency  represents  the  physiological 
conditions  shown  in  Fig.  183,  IV,  when  the  stasis  is  in  the  lungs  and  the 
work  of  the  right  ventricle  is  gradually  increasing.  The  third  stage  repre- 
sents that  in  which  the  right  ventricle  also  has  begun  to  fail, 
and  blood  begins  to  stagnate  in  the  systemic  veins  as  well.  The  pressure 
in  these  veins  increases  two-  to  threefold  (from  5-8  cm.  H20  to  20-30  cm.) 
as  can  be  shown  by  the  method  of  Eyster  and  Hooker.  As  a  result  they 
dilate  and  the  flow  through  them  is  slowed,  changes  occur  in  the  capillary 
walls,  and  cedema  soon  takes  place — first  in  the  feet,  later  in  the  shins, 
thighs,  genitalia,  and  back.  With  the  onset  of  these  manifestations  the 
shortness  of  breath  becomes  extreme,  a  dyspnoea  of  medullary  origin  adding 
its  effect  to  the  pulmonary  engorgement.  The  patient  is  compelled  to  sit  up 
all  the  time,  gasping  for  breath,  occasionally  with  paroxysms  of  real  cardiac 
asthma  and  palpitation,  sometimes  with  pains  in  the  heart,  severe  cough, 
and  expectoration  of  considerable  amounts  of  sputum  which  often  contains 
cells  loaded  with  blood  pigment  (Herzfehlerzellen) .  The  urine  becomes 
scant  and  loaded  with  albumin  and  casts.     Ascites  may  set  in  and  may 


428 


DISEASES  OF  THE  HEART  AND  AORTA 


even  become  so  great  as  to  require  repeated  tapping.  The  same  is  true  of 
hydrothorax.  On  this  account  it  is  more  common  upon  the  right  side. 
Unless  the  course  of  the  disease  is  checked,  death  may  follow  after  this 
stage  has  set  in;  but  if  the  work  of  the  heart  can  be  diminished  and  its  action 
strengthened  it  may  soon  pump  out  the  stagnating  blood  and  lower  the 
venous  pressure.  From  this  cause,  and  owing  to  the  concomitant  increase 
in  cardiac  tonicity,  the  dilatation  diminishes.  The  element  of  regurgitation 
which  is  of  functional  origin  disappears  and  the  amount  of  blood  regurgi- 
tating is  once  more  reduced  to  that  which  flows  past  the  vegetations.  The 
work  of  the  heart  is  again  brought  to  its  minimum,  and  thus  it  is  that 
almost  unhoped-for  recoveries  may  occur  in  mitral  insufficiency 
when  properly  treated. 

PHYSICAL    EXAMINATION. 

Inspection. — The  typical  picture  of  mitral  disease  is  seen  in  the  flushed 
pink  cheeks  with  slight  tinge  of  purple,  slightly  dilated  venules,  and  bright 
watery  eyes,  giving  on  superficial  inspection  the  appearance  of  superabundant 
health — the  so-called  mitral  facies.  This  is  in  sharp  contrast  to  the  pale, 
pasty,  or  sallow  color  of  aortic  insufficiency,  or  the  livid  purple  of  emphysema. 
The  lips  show  a  moderate  cyanosis.  There  is,  as  a  rule,  no  special  throbbing 
seen  in  the  carotids.  The  venous  pulse  is  usually  well  seen  and  is  of  the 
normal  "double"  type.  Since 
the  disturbance  of  function  in 
the  first  two  stages  is  in  the  pul- 
monary circulation  and  not  in 
the  systemic,  no  change  in  the 
jugular  pulsation  is  to  be  found 
nor  would  be  expected  until  the 
third  stage,  when  the  onset  of 
tricuspid  insufficiency  causes  it 
to  assume  the  "  single "  or  ven- 
tricular form. 

The  chest  may  show  pre- 
cordial bulging,  especially  in 
children  and  in  cases  of  long 
standing.  The  apex  impulse  if 
visible  is  displaced  out- 
wards toward  the  axilla 
rather  than  downwards. 
It  is  frequently  of  a  slow  heav- 
ing character,  while  in  cases  of 

long-standing  pulmonary  stasis  there  may  be  also  a  wavy  systolic  retrac- 
tion of  the  interspaces  which  mark  the  hypertrophy  of  the  right  ventricle. 
Occasionally  a  systolic  impulse  in  the  second  left  interspace  shows  the 
vigorous  pulsation  of  the  pulmonary  artery.  In  very  large  hearts  it  is  not 
uncommon  to  find  a  systolic  retraction  present  along  the  outer  border  of 
dulness,  even  when  adherent  pericardium  is  absent. 

In   long-standing    cases  changes  in  the  extremities  also  take  place, 
especially  slight  clubbing  of  the  fingers. 


Fig.  184. — Distribution  of  the  murmur  in  mitral  in- 
sufficiency. Distribution  upon  the  chest  wall.  Light 
line,  outline  of  cardiac  dulness;  heavy  line,  outline  of 
cardiac  flatness.  Shaded  area  shows  distribution  of  the 
murmur.  The  diagram  at  the  right  indicates  the  relation 
of  the  murmur  to  the  cardiac  cycle. 


MITRAL  INSUFFICIENCY. 


429 


Fig.  185. — Cross  section  of  the  body  show- 
ing how  the  thrill  and  murmur  reach  the  chest 
wall.  The  heavily  stippled  areas  indicate  the  areas 
over  which  the  murmur  is  heard. 


Palpation  usually  reveals  a  strong,  slow,  heaving  impulse  with  a  more 
or  less  intense  thrill  lasting  throughout  the  period  of  systole.  This  thrill 
is  probably  due  to  the  impact  of  eddy  currents  passing  by  the  vegetation 
and  striking  the  heart  wall,  whose  impact  sets  the  valve  into  vibrations 
that  are  communicated  along  the  chordse  tendinese  to  the  walls  of  the 

heart  and  then  to  the  chest.  It  is  most 
intense  at  the  apex,  but  is  often  pal- 
pable over  the  entire  precordium,  oc- 
casionally in  the  axilla,  and  sometimes 
at  the  back  in  the  left  interscapular 
region.  The  thrill  at  the  back  is  rarely 
felt  except  in  children  and  thin- 
chested  persons,  but  as  it  represents 
the  direct  impact  of  regurgitation 
it  is  very  characteristic.  In  a  few 
cases  the  thrill  from  a  mitral  lesion 
can  be  felt  in  the  vessels  of  the 
neck,  and  sometimes  also  over  the 
entire  chest. 

The  shock  accompanying  the  second  heart  sound  is  practically  un- 
changed, though  it  is  often  more  distinct,  especially  over  the  pulmonary  area. 
Percussion. — The  characteristic  cardiac  outline  in  mitral  insufficiency 
shows  an  increase  in  area  horizontally  (M  L)  towards  the  left,  which  is  some- 
times enormous  and  may  reach  well  into  the  axilla  and  as  much  as  22  cm. 
from  the  midline  by  percussion.  When  the  apex  approaches  the  axillary 
convexit3>-,  as  shown  by  Moritz, 
the  area  of  dulness  usually 
extends  somewhat  beyond  the 
actual  outline  of  the  heart;  but 
with  the  lightest  possible  percus 
sion  (the  threshold  percussion) 
this  error  may  often  be  reduced  to 
a  centimetre  or  less.  In  contrast 
to  the  cardiac  outline  in  aortic 
insufficiency,  the  left  border 
of  dulness  or  of  the 
shadow  seen  with  the 
X-ray  is  increased  diag- 
onally upwards  and  out- 
wards, as  well  as  outwards  in 
the  horizontal  diameter  (Fig. 
186).      The    upward    extension 

may  reach  the  second  rib  and  pass  outward  into  the  second  left  inter- 
space. According  to  the  autopsy  findings  of  Harris,  this  is  not  due  to  the 
dilatation  of  the  left  auricle,  but  to  the  increase  in  size  of  the  conus  arte- 
riosus of  the  right  ventricle  and  to  some  dilatation  of  the  pulmonary  artery. 

Harris  has  shown  that  even  an  extremely  dilated  left  auricle  is  not  visible  from 
the  front  of  the  chest  under  these  circumstances.  As  is  therefore  to  be  expected,  such  dila- 
tions correspond  to  the  later  rather  than  to  the  earlier  stages  of  the  disease,  and  are  also 


Fig.  186. — Radiograph  of  a  patient  with  mitral  in- 
sufficiency, showing  horizontal  enlargement  of  the  heart 
to  the  left.     (After  Bougsch  and  Schittenhelm.) 


430 


DISEASES  OF  THE  HEART  AND  AORTA. 


more  common  in  mitral  stenosis  than  insufficiency.    The  cardiac  dulness  is  not  increased 
to  the  right  until  the  third  stage  of  the  disease. 

The  Systolic  Murmur. — The  data  obtained  from  auscultation  usually 
furnish  the  basis  for  the  diagnosis  of  mitral  insufficiency.  The  character- 
istic sign  is  the  presence  of  a  murmur  heard  at  the  apex  and  in  the 
left  axilla  throughout  systole, — i.e.,  last- 
ing up  to  the  second  sound.  The  sounds 
of  different  systolic  murmurs  are  described 
by  the  French  writers  as  resembling  the 
rasping  of  a  file,  the  sawing  of  wood,  the 
hissing  of  a  jet  of  steam,  the  cooing  of  a 
dove !  These  variations  depend  upon  many 
sound-producing  factors  so  complex  that  it 
is  impossible  to  predict  the  characteristics 
of  the  lesion  upon  the  valve  by  the  murmur 
to  which  it  gives  rise.  In  general,  rough, 
roaring,  sawing,  and  purring  murmurs  are 
very  often  produced  by  thickened  or  calcified 
vegetations,  which  act  more  or  less  as  sound- 
ing-boards, while  whispering  or  blowing  mur- 
murs are  produced  by  regurgitant  streams 
passing  over  smooth-walled  valves,  and 
occur  especially  in  functional  insufficiencies. 
However,  exceptions  to  this  are  frequent. 

Digital  Imitation  of  the  Mitral  Systolic  Murmur. — The  mitral  systolic  murmur  can  be 
reproduced  by  Lamed's  or  Smith's  methods  by  a  stroke  across  the  elbow  or  across  the 
back  of  the  hand.  To  imitate  a  murmur  accompanying  the  first  sound  the  latter  should 
be  produced  by  a  slow  flexion  of  the  finger,  which  combines  the  blow  and  the  strok- 
ing. For  demonstrations  to  a  group  of  students  these  manoeuvres  may  be  carried  out 
upon  a  derby  hat.  The  stroke  should  be  of  long  duration  and  should  be  followed 
immediately  by  the  tap  which  represents  the  second  sound. 

Excellent  phonographic  tracings  of 
this  murmur  have  been  made  by  Eint- 
hoven  as  well  as  by  Weiss  and  Joachim. 
These  observers  have  shown  that  in  con- 
trast to  the  murmur  of  aortic  stenosis  the 
murmur  of  mitral  insufficiency  always 
begins  synchronously  with  the  first  sound. 
It  is  loudest  at  the  time  of  the 
first  sound,  which  it  may  entirely  re- 
place and  may  then  be  uniform  through- 
out the  period  of  systole  or  take 
on  a  decrescendo  character,  in 
murmur  which  folio ws  the  f i r st 
in  character. 


Fig.  187.  — Diagram  of  Fig.  186, 
showing  the  directions  in  which  car- 
diac enlargement  has  taken  place.  The 
broken  line  represents  the  outline  of  the 
normal  heart.  The  arrows  indicate  the 
conjugates  (ML  and  L)  which  are  most 
enlarged. 


MURMUR 


Fig.  188. — Graphic  records  of  the  heart 
sounds,  showing  the  systolic  murmur. 
(Kindness  of  Prof.  Einthoven.)  1,  2,  heart 
sounds.  The  vibrations  between  1  and  2 
and  some  of  those  composing  1  are  due  to 
the  murmur. 


contrast    to    the    aortic 
sound  and  is  crescendo 


They  have  shown  further  that  in  some  cases  the  first  sound  and  murmur  precede 
the  carotid  wave  by  a  greater  interval  than  normally  (lengthening  of  the  presphygmic 
period  from  .08-.09  sec.  to  .12-15  sec).  At  the  very  beginning  of  systole  blood  rushes 
back  into  the  auricle.  This  escape  causes  the  pressure  in  the  ventricle  to  rise  more  slowly 
than  usual  and  hence  aortic  valves  open  a  little  later.     Hence  the  presphygmic  period  is 


MITRAL  INSUFFICIENCY.  431 

later.  It  is  possible  that  the  duration  of  the  presphygmic  period  may  serve  as  a  guide 
to  indicate  the  degree  of  leakage, — shortening  indicating  an  improvement,  lengthening 
an  increase  in  leakage.  However,  other  observers  find  lengthened  presphygmic  periods 
from  different  causes. 

In  the  accidental  murmurs  of  ana?mia  Weiss  and  Joachim  have  found  a  normal 
presphygmic  period. 

It  is  stated  by  some  writers  that  functional  murmurs  occur  late  in  systole,  mesosystolic 
or  telesystolic,  because  comparatively  little  regurgitation  occurs  until  the  intraventricular 
pressure  has  reached  its  maximum  and  the  papillary  muscles  begin  to  weaken.  There  are 
no  graphic  records  supporting  this  claim,  and  the  subject  demands  experimental  investiga- 
tion rather  than  clinical  speculation. 

As  regards  distribution,  the  murmur  of  mitral  insufficiency  is  heard 
over  those  areas  of  chest  wall  which  are  nearest  to  the  left  ventricle  and 
left  auricle,  namely,  the  apex  and  the  neighboring  areas  to  the  left  (Fig.  184). 

The  reason  why  the  murmur  of  mitral  insufficiency  is  heard  so  loudly  at  the  apex  is 
not  perfectly  clear,  since  this  propagation  is  opposite  to  the  direction  of  the  regurgitant 
stream.  It  is  possible,  however,  that  the  vibrations  of  the  mitral  valve  may  be  transmitted 
to  the  anterior  papillary  muscle  and  apex  by  the  papillary  muscles  which  act  like  violin 
strings.  This  would  also  explain  why  the  murmur  is  so  loud  in  the  anterior  part  of  the  left 
axilla  at  a  considerable  distance  from  the  left  auricle  but  near  the  anterior  papillary  muscle 
(Fig.  185).  De  Sautelle  and  Grey  (Arch.  Int.  Med.,  1911,  viii,  734)  have  shown  on  the 
excised  pig's  heart  that  this  is  probably  the  true  explanation,  for  not  only  is  the  murmur 
loudest  over  the  insertion  of  the  papillary  muscles,  but  if  the  latter  are  cut  off  and  sewed 
to  another  part  of  the  wall  it  then  becomes  loudest  over  that  area. 

In  children  and  in  many  persons  with  small,  thin-walled  chests  the 
murmur  is  also  heard  over  the  left  interscapular  region  to  which  it  is  trans- 
mitted directly  from  the  left  auricle.  In  children  and  thin-walled  chests  the 
murmur  may  also  be  transmitted  directly  backward  from  the  left  auricle  to 
the  left  intrascapular  region;  but,  though  some  German  observers  will  not 
diagnose  mitral  insufficiency  without  it,  it  is  by  no  means  always  present. 

In  order  to  obviate  these  disturbing  factors,  August  Hoffmann  and  later  Gerhartz  have 
attempted  to  use  the  oesophageal  auscultation  described  on  page  170,  but  it  is  un- 
pleasant to  the  patient,  and,  besides,  the  murmur  may  be  no  more  distinct  than  at  the  apex. 

Another  rarer  site  for  the  systolic  murmur  of  mitral  insufficiency,  as  shown  by  Naunyn, 
is  the  pulmonary  area — the  second  and  third  left  interspaces  at  the  sternal  margin  and  as 
far  out  as  the  parasternal  line.  Naunyn  thinks  that  in  this  region  the  vibrations  are  com- 
municated by  the  hypertrophied  and  dilated  left  auricle  to  the  pulmonary  artery.  This 
murmur  must  always  be  carefully  differentiated  from  the  accidental  pulmonary  murmur 
heard  in  this  region  and  from  that  due  to  pulmonary  stenosis  and  sclerosis. 

Over  the  right  ventricle,  that  is  from  the  left  parasternal  line  to  the 
left  sternal  margin,  the  murmur  of  mitral  insufficiency  is  usually  heard,  and 
it  is  sometimes  transmitted  with  great  intensity  along  the  fifth  rib. 

Differentiation  from  Accidental  and  Tricuspid  Murmurs. — This  is  in 
sharp  contrast  to  the  accidental  or  "haemic"  murmurs  which  are 
loudest  over  the  right  ventricle  and  especially  over  its  upper  portion  (in  the 
second  and  third  left  interspaces) .  These  murmurs  diminish  over  the  apex 
while  the  mitral  murmur  increases.  They  are  rarely  heard  to  the  left  of  the 
apex.  They  are  later,  softer,  shorter,  more  superficial;  they  vary  with 
inspiration,  expiration,  and  change  of  position;  and  the  heart  is,  as  a  rule, 
not  hypertrophied.  On  the  other  hand,  there  is  no  reason  to  believe  that 
the  distribution  of  the  murmur  due  to  functional  mitral  insufficiency  differs 
from  that  due  to  vegetations  upon  the  valves,  and  it  is  frequently  impos- 


432  DISEASES  OF  THE  HEART  AND  AORTA. 

sible  to  differentiate  between  the  two  conditions.1  The  common  statement 
that  murmurs  of  organic  origin  are  transmitted  to  the  axilla  while  those  of 
functional  origin  are  not  is  due  to  a  confusion  of  " functional"  with  " acci- 
dental" murmurs.  All  loud  and  rough  murmurs  are  transmitted  further 
than  soft  ones,  and  murmurs  due  to  vegetations  are  usually  louder  than 
functional  murmurs,  but  a  soft  murmur  of  organic  origin  is  probably  no 
louder  than  many  murmurs  of  functional  origin. 

The  murmur  due  to  tricuspid  insufficiency  is  heard  loudest  over  the 
lower  portion  of  the  sternum,  the  epigastrium,  and  often  also  to  the  right 
of  the  sternum.  That  of  aortic  sclerosis  or  aortic  stenosis  is  loudest  over 
the  second  and  first  right  interspace,  and  is  usually  transmitted  to  the 
carotid  and  axillary  arteries.  The  same  applies  to  the  murmur  due  to 
aneurism.  Moreover,  as  stated  by  Boy-Teissier,  it  is  always  meso-  or 
telesystolic,  and  therefore  follows  but  never  replaces  the  first  sound. 

The  Second  Sound. — The  second  sound  at  the  apex  and  over  the  aortic 
area  shows  no  special  change,  but  over  the  pulmonic  area  it  may  be  greatly 
accentuated.  This  is  not  always  the  case,  because,  as  seen  in  Fig.  183,  the 
pressure  in  the  pulmonary  artery  is  not  always  increased;  but  during  the 
course  of  a  mitral  insufficiency  the  intensity  of  the  second  pulmonic  may 
change.  In  interpreting  the  significance  of  this  change  it  must  be  remem- 
bered that  rise  of  pulmonary  pressure  may  occur  either  when  the  force  of 
both  ventricles  is  increasing  or  when  extreme  engorgement  of  the  pulmo- 
nary vessels  has  occurred.  In  the  former  case  it  will  be  accompanied  by  the 
general  signs  of  improvement  in  the  left  ventricle,  larger  pulse,  increased 
maximal  blood-pressure,  increased  pulse-pressure ;  in  the  latter  case  by  fail- 
ure of  the  left  ventricle.  Regarding  the  role  which  vasomotor  changes  in 
the  pulmonary  vessels  play  under  clinical  conditions  little  is  known;  but 
they  also  can  affect  the  intensity  of  the  second  pulmonic. 

Pulse.  —  The  pulse  in  mitral  insufficiency  shows  no  characteristic 
changes.  Dependent  upon  blood-pressure,  systolic  output,  and  pulse-pres- 
sure which  vary  considerably,  it  may  be  large  or  small,  hard  or  soft.  De- 
pendent upon  the  condition  of  the  heart  muscle  and  especially  of  the  left 
auricle,  it  may  be  regular  or  irregular.  The  condition  of  the  individual 
patient  at  any  single  stage  of  the  disease  must  be  viewed  in  the  light  of 
these  determining  factors. 

Blood=pressure. — As  has  been  seen  above,  the  sudden  production  of 
mitral  insufficiency  both  in  animals  and  on  the  model  is  followed  directly  by 
a  fall  of  blood-pressure  and  diminution  of  pulse-pressure,  unless  the  strength 
of  the  ventricle  and  its  systolic  output  be  increased.  Such  an  increase  does 
take  place,  however,  during  hypertrophy,  and  hypertrophy  of  the  left 
ventricle  is  the  rule  in  mitral  insufficiency.  Moreover,  when  the  output 
into  the  arteries  is  diminished  by  the  backflow  into  the  left  auricle,  these 
vessels  undergo  a  compensatory  constriction  and  narrow  the  blood  channel. 
However,  as  the  left  ventricle  hypertrophies,  its  systolic  output  increases 
at  the  expense  of  the  residual  blood.  These  two  compensatory  factors 
combine  to  maintain  the  blood-pressure  and  pulse-pressure  at  their  original 

1  The  confusion  of  the  terms  "hsemic"  (accidental)  and  "functional"  murmurs  so 
common  in  clinical  notes  seems  therefore  to  be  both  unnecessary  and  misleading,  and  should 
be  carefully  avoided. 


MITRAL  INSUFFICIENCY.  433 

level,  and  at  times  even  exceed  it.  For  example,  a  prominent  medical 
educator  who  has  a  mild  leak  at  the  mitral  valve  but  suffers  no  symptoms, 
has  a  maximal  pressure  of  140,  a  minimal  of  95,  and  a  large  full  pulse.  The 
compensation  in  this  case  has  more  than  balanced  the  disturbance  in  the 
circulation.  This  increase  of  pulse-  and  blood-pressure  is  not  always  indica- 
tive of  improvement,  but  may  occur  also  as  terminal  events  under  the 
stimulation  of  medullary  asphyxia  (see  page  38).  On  the  other  hand,  the 
presence  of  a  rather  small  pulse  and  rather  low  blood-pressure  and  pulse- 
pressure  may  merely  represent  the  natural  effect  of  the  lesion  unaltered  by 
compensatory  changes  on  the  one  hand,  or  on  the  other  may  represent  the 
failure  of  the  left  ventricle  to  maintain  the  circulation.  The  presence  of 
arteriosclerosis  may  in  itself  tend  to  modify  the  blood-pressure,  and  to 
increase  a  blood-pressure  and  pulse-pressure  that  would  otherwise  be  small. 
In  any  case  the  blood-pressure  shows  no  characteristic  features  in  mitral 
insufficiency,  and  the  figures  obtained  are  to  be  viewed  as  the  algebraic 
sum  of  various  circulatory  factors,  rather  than  as  absolute  measures  of 
cardiac  vigor.  It  must  be  remembered  further  that  the  cardiac  symptoms 
are  due  mainly  to  changes  in  the  pulmonary  circulation,  while  the  blood- 
pressure  changes  are  concerned  only  with  the  systemic. 

Arrhythmia. — The  action  of  the  heart  is  often  irregular  in  mitral  dis- 
ease, so  that  the  arrhythmia  in  these  conditions  is  frequently  described  as 
''the  mitralized  pulse,''  though  the  latter  is  more  frequently 
present  in  mitral  stenosis  than  in  mitral  insufficiency.  In  the  latter  case, 
owing  to  the  over  distention  of  the  left  auricle,  extrasystoles  arising  in  this 
chamber  are  sometimes  met  with.  Such  extrasystoles  may  persist  for  a  long 
time  and  give  rise  to  a  form  of  pulse  easily  confounded  with  the  typical  pulse 
of  auricular  fibrillation,  though  the  pulsation  in  the  neck  will  be  seen  to  be 
"  double  and  not  single  "  (see  page  134),  In  most  very  advanced  cases, 
however,  the  irregularity  is  due  to  auricular  fibrillation  with  absolutely 
irregular  pulse  and  a  positive  single  venous  pulse  with  distended  veins  (20). 
The  absolute  diagnosis  is,  however,  made  with  the  electro-cardiograph. 

The  origin  of  the  irregularity  is  probably  in  the  distended  left  auricle 
(cf.  also  page  118).  It  is  sometimes,  but  by  no  means  always,  accompanied 
by  paralysis  of  the  auricle,  as  shown  by  the  venous  tracings,  but  the  exact 
mechanism  by  which  this  form  of  irregularity  is  produced  requires  further 
investigation  in  order  that  its  diagnostic  and  prognostic  significance  may 
be  thoroughly  understood. 

The  condition  of  the  radial,  temporal,  and  other  arteries  may  vary 
considerably,  but,  especially  in  patients  above  40,  may  show  considerable 
grades  of  arteriosclerosis.  This  is  more  common  and  somewhat  more  exten- 
sive in  patients  suffering  from  any  cardiac  disease  than  in  persons  with 
normal  hearts  (Wild). 

Lungs. — Examination  of  the  thorax  and  lungs  in  mitral  insufficiency 
reveals  the  usual  signs  corresponding  to  the  pulmonary  changes  described 
above — small,  moist,  and  piping  rales  corresponding  to  the  bronchitis  often 
associated  with  hyper-resonance  on  percussion.  Over  areas  of  hydrothorax 
there  are  absolute  flatness  on  percussion,  absence  of  vocal  fremitus  and 
breath  sounds,  Koranyi's  flatness  over  the  lower  thoracic  spines,  and 
Grocco's  triangle,  paravertebral  dulness  to  the  left  of  the  midline. 

28 


434  DISEASES  OF  THE  HEART  AND  AORTA. 

Abdomen. — The  abdomen  rarely  shows  any  special  change  during  the 
milder  stages  of  the  disease.  Occasionally  one  finds,  as  in  a  young  girl 
recently  under  the  writer's  observation  in  the  Johns  Hopkins  Dispensary, 
the  remains  of  an  old  splenic  infarction,  characterized  by  enlargement, 
hardness,  and  tenderness  of  the  organ.  This  may  persist  for  some  months. 
Enlargement  and  pulsation  of  the  liver  and  ascites  (portal  stasis)  belong  to 
the  stage  of  broken  systemic  compensation  (see  page  206).  The  same  also 
applies  to  oedema  of  the  feet,  ankles,  and  legs,  which  occurs  in  the  mildest 
form  of  broken  compensation.  These  phenomena,  though  of  serious  import, 
are  by  no  means  harbingers  of  death,  for  with  proper  treatment  many  cases 
outlive  one  or  even  several  breaks  in  compensation  for  many  years. 

The  following  represent  the  course  of  typical  cases  of  mitral  insuf- 
ficiency. 

Case  of  Mitral  Insufficiency. 

C.  H.,  ship  carpenter,  aged  63,  first  admitted  to  the  Johns  Hopkins  Hospital  in  No- 
vember, 1899,  complaining  of  shortness  of  breath.  Family  history  negative.  The 
patient  has  always  been  a  robust  man.  He  gives  a  doubtful  history  of  rheumatism,, 
but  a  definite  history  of  pneumonia  five  years  before  admission.  No  venereal  his- 
tory.    He  has  always  been  a  hard  eater,  hard  drinker,  and  a  hard  worker. 

The  present  illness  began  with  attacks  of  paroxysmal  dyspnoea  upon 
exertion  eight  or  nine  months  before  admission.  Two  months  before  admission  an 
attack  came  on  spontaneously  while  in  a  warm  room.  During  the  past  month  he  has 
not  been  able  to  lie  down  in  bed  owing  to  dyspnoea  and  the  onset  of 
a  smothering  feeling.  He  has  had  no  cough,  no  haemoptysis.  Examination  on  this  admis- 
sion showed  a  stout,  well-nourished  man  with  mucous  membranes  a  trifle  purple  and  dilated 
venules  over  the  face.  His  chest  was  barrel  shaped  and  there  was  a  little  fluid  (flatness  and 
impaired  breath  sounds)  at  the  bases  behind. 

Heart. — Apex  was  situated  in  the  6th  interspace  16.5  cm.  from  the  midline.  The 
area  of  cardiac  dulness  reached  upward  to  the  second  costal  cartilage  and  5  cm.  to  the 
right  of  the  sternum.  There  is  a  well-marked  systolic  murmur  heard  over  the 
body  of  the  heart  and  over  the  anterior  part  of  the  axilla.  The  second  sound  is  every- 
where clear;  the  second  aortic  booming. 

The  liver  is  slightly  enlarged,  being  just  palpable;  the  spleen  is  not.  The  abdomen  is 
full,  the  flanks  bulge,  and  there  is  slight  movable  dulness  in  the  flanks.  Genitalia  normal. 
There  is  slight  oedema  of  the  ankles.  Blood  count  normal.  Urine  is  dark  sherry 
colored,  specific  gravity  1024,  acid,  contains  a  small  amount  of  albumin  and  some  hyaline 
and  granular  casts. 

The  patient  was  put  to  bed  on  soft  diet,  given  daily  purgation  with 
magnesium  sulphate  (30  Gm.,  oi),  also  8  doses  of  tincture  of  digitalis  (1  c.c,  n^xv) 
at  intervals  of  four  hours,  followed  up  by  strychnine  1.5  mg.  He  was  also  given 
potassium  iodide  1  Gm.  (gr.  xv)  after  meals. 

CEdema  disappeared  and  orthopncea  also,  so  that  within  ten  days  the  patient  could 
sleep  with  his  head  low  and  could  walk  without  dyspnoea.    He  then  left  the  hospital. 

He  was  next  seen  three  years  later,  having  been  perfectly  well  until 
he  took  cold  one  month  before,  since  when  he  had  shortness  of  breath  on  exertion  and 
on  lying  down.  He  had  some  cough  and  slight  swelling  of  the  feet.  The  physical 
condition  was  about  as  on  the  first  admission,  except  that  the  systolic  murmur 
entirely  replaced  the  first-  sound  and  was  well  heard  in  the  axilla. 
Maximal  blood-pressure  182  mm.  Hg.  He  again  improved  rapidly  and  left  the  hospital 
in  two  weeks. 

He  entered  the  hospital  again  one  year  later  with  the  same  signs,  the  liver  being  now 
2  cm.  below  the  costal  margin.  Once  more  he  improved  rapidly  under  treatment;  the  liver 
receded,  and  he  was  discharged,  only  to  be  readmitted  in  the  same  condition  five  weeks  later, 
when  symptoms  dated  from  exposure  to  the  wet.  He  then  had  some  tenacious  sputum 
streaked  with  blood  and  numerous  moist  rales  were  heard  everywhere  over  his  chest.  Re- 
covery was  once  more  uneventful. 


MITRAL  INSUFFICIENCY.  435 


COMPLICATIONS    AND    SEQUELAE. 

There  are  few  complications  and  sequelae  which  are  more  character- 
istic of  mitral  insufficiency  than  of  other  valvular  diseases.  Those  symp- 
toms due  to  pulmonary  engorgement;  bronchitis,  haemoptysis,  and 
pulmonary  oedema  have  already  been  discussed.  Embolism  from  loosening 
of  vegetations  upon  the  mitral  valve  or  of  clots  which  have  formed  in  the 
left  auricle  during  periods  of  stasis  is  an  occasional  occurrence,  especially 
in  severe  cases,  but  less  common  than  in  mitral  stenosis.  As  the  result 
of  this  there  may  be  the  production  of  infarcts  in  the  various  organs — 
spleen,  kidneys,  and  brain — and  of  ecchymoses  in  the  skin. 

In  contrast  to  mitral  stenosis,  pulmonary  tuberculosis  occurs  in  mitral 
insufficiency  with  the  same  frequency  as  in  otherwise  normal  individuals 
(Meisenburg) . 

As  may  be  seen  in  Fig.  166,  mitral  insufficiency  is  very  frequently  asso- 
ciated with  other  valvular  diseases,  29  per  cent,  of  all  the  cases  of  valvular 
disease  at  the  Johns  Hopkins  Hospital  being  accompanied  by  aortic  insuffi- 
ciency, 21  per  cent,  by  mitral  stenosis.  In  these  cases  the  mitral  insuffi- 
ciency is  sometimes  the  original  lesion,  the  other  lesion  resulting  from  a 
metastatic  infection  or  subsequent  organization.  On  the  other  hand,  the 
mitral  insufficiency  associated  with  aortic  insufficiency  may  also  be  a  func- 
tional one  due  to  overfilling  of  the  ventricles.  The  mitral  insufficiency 
which  appears  late  in  the  course  of  mitral  stenosis  is  due  to  the  inability  of 
the  thickened  valves  to  close.  Coronary  sclerosis,  as  shown  by  Wild,  is 
more  than  usually  common  in  chronic  valvular  disease,  and  hence  should 
be  borne  in  mind  in  establishing  the  prognosis. 

Pericarditis  is  one  of  the  common  complications,  especially  in  children, 
in  whom  adhesive  pericarditis  is  to  be  feared. 

Since  the  majority  of  cases  of  mitral  disease  are  of  rheumatic  origin, 
diseases  of  the  rheumatic  cycle,  tonsillitis,  articular  rheumatism,  chorea 
in  children,  and  affections  of  the  urticarial  group,  are  particularly  common. 
Of  these  arthritis  is  the  most  frequent  as  well  as  the  most  stubborn 
and  dangerous. 

TREATMENT. 

The  management  of  cases  of  mitral  disease  does  not  depart  in  any 
essential  particular  from  the  general  type  of  treatment  of  cardiac  disease. 
It  should  be  directed  to  three  ends: 

1.  Removing  the  overstrain; 

2.  Increasing  the  strength  of  the  heart; 

3.  Avoidance  of  infection,  and  removal  of  the  foci. 

In  the  mildest  cases,  the  insufficiency  shown  by  signs  but  not  by  symp- 
toms, due  especially  to  the  formation  of  a  new  vegetation,  it  is  most  impor- 
tant that  the  cardiac  tonicity  should  be  maintained,  that  the  amount  of 
leakage  should  thus  be  kept  down  to  its  minimum,  and  that  cardiac  hyper- 
trophy should  be  induced  before  symptoms  have  set  in.  It  is  therefore 
most  important  to  spare  the  heart  every  effort.  If  the  patient  is  seen  at 
the  onset  of  the  disease  he  should  be  kept  at  absolute  rest  in  bed  for  at 
least  a  couple  of  weeks  after  temperature  has  returned  to  normal  and  all 


436  DISEASES  OF  THE  HEART  AND  AORTA. 

signs  of  acute  disease  have  passed.  Too  much  care  cannot  be  exercised 
at  this  time,  since  this  is  the  crucial  epoch  in  determining  the  severity  of 
the  case.  It  is  important  not  only  to  maintain  the  tonicity  of  the  heart 
muscle  but  to  preserve  the  valves  from  all  further  injury  until  the  vegeta- 
tions have  become  thoroughly  organized  and  lined  with  endothelium,  and 
the  germs  have  disappeared  from  the  original  focus  of  infection.  When 
the  tonsil  is  the  source  of  infection,  it  should  be  completely  dissected 
out  as  soon  as  acute  infection  has  passed  off,  in  order  to  prevent  reinfec- 
tion of  the  valves  from  this  source.  The  results  obtained  in  the  Medical 
Clinic  of  the  Johns  Hopkins  Hospital,  where  this  practice  has  been  carried 
out  at  Prof.  Barker's  suggestion,  have  been  very  gratifying.  In  many 
cases  the  recovery  from  the  first  attack  has  been  more  rapid  than  had  been 
usual  before  this  treatment  had  been  resorted  to  (see  page  231),  and  it 
seems  probable  that  reinfection  of  the  valve  is  of  less  frequent  occurrence 
thereafter.  Similar  results  are  seen  in  gonorrhceal  endocarditis  after  treat- 
ment of  the  urethritis. 

In  these  mild  cases  drug  treatment  may  not  be  absolutely  necessary. 
In  how  far  Cloetta's  suggestion  as  to  the  early  use  of  digitalis  should  be 
carried  out  is  still  unsettled,  but  at  least  the  administration  of  strychnine 
in  doses  of  from  1  to  3  mg.  (-gV  to  ^V  gr.)  is  advisable  in  order  to  increase 
the  tonicity  of  the  heart  muscle.  However,  the  blood-pressure  and  hence 
the  strain  upon  the  valves  should  not  be  materially  increased  (not  more 
than  10  mm.  Hg),  and  the  dose  of  strychnine  should  be  reduced  if  it  rise 
above  this  level.    Digitalis  is  not  necessary  in  cases  of  this  type. 

The  bronchitis  which  frequently  accompanies  cases  of  this  type  does 
not  differ  greatly  from  the  ordinary  forms  of  chronic  bronchitis,  and  is 
associated  with  the  usual  pulmonary  bacteria  found  in  these  conditions — 
the  streptococcus,  pneumococcus,  influenza  bacillus,  Friedlander's  bacillus, 
etc.  Treatment  is  therefore  the  same  as  for  ordinary  bronchitis,  a  soothing 
steam  inhalation  being  very  useful.    The  following  is  to  be  recommended : 


Oleum  pini  sylvestris,  or 

Creosoti,  oiss;  5 

Tr.  benzoin,  co., 

Tr.  opii  camphorat.,  aa  oiiss         75 


A  teaspoonful  inhaled  with  steam  from  an  atomizer,  or  from  a  funnel 
above  a  glass  jar  into  which  a  teaspoonful  of  the  remedy  and  a  pint  of 
boiling  water  have  been  placed.  Codein  .015  to  .030  Gm.  (gr.  \  to  ^)  or 
heroin  2.5  mg.  (gr.  -^o  to  TV)  may  be  given  by  mouth  to  relieve  the  cough 
by  reducing  bronchial  secretion  and  irritability. 

Physical  Re=education. — When  the  stage  of  acute  symptoms  has  passed 
the  stage  of  re-education  begins.  The  heart  though  injured  must  be  trained 
to  perform  the  day's  work  without  strain.  To  do  this  the  heart  muscle 
must  be  stronger  than  normal;  it  must  have  hypertrophied.  The  process 
of  hypertrophy  after  valvular  lesion,  like  the  heart  hypertrophy  of  an  athlete 
in  training,  requires  time.  However,  the  amount  of  hypertrophy  setting 
in  after  a  valvular  lesion  is  greater  than  that  after  a  prolonged  period  of 
muscular  exercise,  and  hence  may  be  expected  to  take  a  longer  time.  At 
this  stage  Nauheim  baths  and  resisted  movements  may  be  dispensed  with 


MITRAL  INSUFFICIENCY.  437 

as  long  as  a  reasonable  supervision  is  kept  over  the  patient.  He  should 
never  be  allowed  to  become  either  very  tired  or  short  of  breath,  and  six 
months  or  a  year  should  elapse  before  he  is  allowed  to  run,  participate  in 
games,  severe  exercise,  or  manual  labor.  The  current  statement  that  the 
prognosis  is  doubtful  during  the  first  year  after  the  occurrence  of  a  valvular 
lesion  is  due  largely  to  the  intercurrence  of  acute  overstrain  of  the  heart 
muscle  before  hypertrophy  is  complete. 

The  condition  is  quite  different,  however,  when  the  mitral  insufficiency 
is  of  long  standing  before  it  is  encountered  by  the  physician,  as  is  frequently 
the  case  in  routine  examinations  for  life  insurance,  civil  service,  etc.  The 
disease  may  then  be  said  to  have  cured  itself  already,  and  beyond  gently 
admonishing  the  patient  against  over-exertion  no  further  precautions  are 
necessary.  It  is  often  unwise  to  inform  a  man  or  woman  of  nervous  tem- 
perament that  a  heart  lesion  is  present,  since  worry  may  in  itself  contribute 
to  the  cardiac  overstrain. 

Cases  of  functional  mitral  insufficiency  are  rarely  devoid  of  cardiac 
symptoms,  and  hence  will  be  considered  under  the  second  group. 

Treatment  of  the  Second  Stage. — The  second  stage  of  mitral  insuffi- 
ciency, in  which  dyspnoea  and  other  symptoms  of  cardiac  origin  are  present, 
represents  a  condition  of  chronic  cardiac  overstrain.  Indeed  it  is  the 
abnormal  severity  of  these  symptoms  following  some  slight  exertion  which 
usually  calls  attention  to  the  existence  of  the  lesion.  The  treatment  does 
not  depart  in  any  essential  particular  from  that  which  has  already  been 
discussed  in  the  case  of  chronic  overstrain  of  the  myocardium.  Just  as  in 
the  milder  cases  the  most  important  element  in  the  treatment  is  absolute 
rest  in  bed,  continued  until  long  after  symptoms  have  subsided.  The 
diet  should  at  first  be  very  light  (see  page  235),  and  should  be  very  gradually 
increased  after  symptoms  have  subsided.  As  in  the  milder  cases,  vigorous 
doses  of  strychnine  (2  to  3  mg.  [gr.  -^  to  2V]  every  four  hours)  should 
be  begun  at  once.  The  bowels  should  be  kept  moving  freely  by  means 
of  Seidlitz  powders,  Epsom  salts,  Hunyadi  water,  Mistura  ferri  aperiens, 
or  some  other  mild  laxative.  It  is  important  that  the  patient  should  sleep 
well  at  night,  and  trional  (1  Gm.  =  gr.  xv)  or  some  other  soporific  may  be 
given,  if  necessary  with  the  addition  of  codein  (15  mg.  =gr.  ss).  If  symp- 
toms have  not  diminished  after  a  couple  of  days  of  this  treatment,  digi- 
talis should  be  resorted  to  (see  page  245),  for  it  is  important  not  only  to 
reduce  the  strain  but  also  to  strengthen  the  heart  muscle  as  rapidly  as  pos- 
sible in  order  to  prevent  the  overstrain  from  becoming  permanent.  Indeed 
it  may  be  said  that  this  is  the  all-important  stage  in  the  course  of  mitral 
insufficiency  and  of  all  other  valvular  lesions,  the  stage  which  determines 
whether  the  patient  may  hope  to  return  to  a  life  of  activity  or  must 
look  forward  to  one  of  permanent  invalidism,  and  this  question  is  often 
decided  by  the  promptness  or  tardiness  with  which  the  symptoms  dis- 
appear when  the  patient  is  at  rest.  In  this  stage  the  primary  source 
of  infection  or  reinfection  should  be  treated  just  as  in  the  milder  ones,  but 
the  period  of  rest  should  be  longer  and  the  period  of  physical  re-edu- 
cation and  gymnastics  should  be  very  carefully  undertaken.  The 
more  systematic  methods,  such  as  those  of  Schott,  Herz  and  Oertel,  are 
especially  valuable,  as  are  also  the  Nauheim  baths.    The  important  factor, 


438  DISEASES  OF  THE  HEART  AND  AORTA. 

however,  is  that,  whatever  the  method  of  treatment,  the  patient  should 
never  be  allowed  to  become  fatigued  or  short  of  breath,  he  should  be 
gradually  trained  up  to  his  optimum  strength,  and  he  should  never  be 
allowed  to  attempt  to  exceed  his  limit. 

Treatment  of  the  Third  Stage. — In  the  third  stage  of  mitral  insuffi- 
ciency, that  of  broken  compensation,  the  burden  of  the  cardiac  fail- 
ure has  been  shifted  from  the  left  ventricle  to  the  right.  The  treatment 
therefore  follows  the  rules  laid  down  for  broken  compensation  due  to  any 
cause  whatever:  absolute  rest,  immediate  use  of  digitalis  (especially  along 
with  nitroglycerin,  sodium  nitrite,  or  erythrol  tetranitrate) ,  free  purgation, 
and  very  light  diet  being  the  essential  features.  Hypodermic  injections 
of  morphine  (8  to  15  mg.,  gr.  -J  to  I)  may  be  necessary,  but  they  should 
be  used  with  caution,  since  they  decrease  the  irritability  of  the  respiratory- 
centre  and  thus  lead  to  accumulation  of  C02  and  cardiac  asthma.  Since 
many  of  the  symptoms  are  due  to  a  high  pressure  in  the  vena  cava  and 
consequent  dilatation  of  the  right  auricle  and  ventricle,  venesection  is  often 
followed  by  great  improvement,  and  should  be  regarded  as  an  important 
therapeutic  measure  during  the  acute  stage  of  the  overstrain.  But  in 
the  presence  of  anaemia  it  should  not  be  resorted  to.  Intravenous 
strophanthin  (0.5  to  1  mg.)  is  of  the  greatest  value  when  the  symp- 
toms have  become  alarming,  and  should  be  followed  by  the  usual  course 
of  digitalis,  or  by  daily  intramuscular  injections  of  strophanthin. 

As  symptoms  subside,  the  condition  and  its  treatment  pass  into 
those  of  the  second  stage,  and  a  gradual  return  to  normal  may  occur. 
On  the  other  hand  the  symptoms  may  increase,  hydrothorax  and  ascites 
may  become  extensive  and  may  require  tapping,  and  the  oedema  may 
become  extreme.  To  diminish  these  it  may  be  advisable  to  use  diuretics, 
such  as  theobromin  acetate  (agurin),  theocin,  or  acettheocin  sodium,  or 
else  potassium  acetate  and  citrate. 

PROGNOSIS. 

Exactly  how  much  benefit  can  be  effected  by  treatment  varies  with 
each  individual  case,  and  depends  upon  factors  which  are  difficult  to  fore- 
tell. It  is  especially  true  of  mitral  insufficiency  that  while  there  is  fife 
there  is  hope,  for  the  patient  may  almost  completely  recover  from  one  or 
more  attacks  of  broken  compensation  and  yet  remain  comparatively  free 
from  symptoms  for  a  number  of  years. 

As  regards  the  prognosis  for  the  individual  attack  no  absolute  rule 
can  be  laid  down,  but  much  importance  may  be  attached  to  the  rapidity 
of  change  for  the  better  or  for  the  worse.  A  rapid  improvement  during 
the  first  two  days  may  be  construed  as  favorable  for  the  ultimate  outcome; 
a  slow  recovery  usually  indicates  a  severe  residuum  of  trouble;  an  increase 
of  symptoms  in  spite  of  treatment  is  of  grave  significance. 

Between  attacks  the  patient's  ability  to  hold  his  own  or  even  to  im- 
prove his  condition  depends  entirely  upon  his  ability  to  keep  himself  free 
from  overstrain  and  reinfection.  In  all  cases  the  physician  should  be  some- 
what guarded  in  his  statements  regarding  the  future. 


MITRAL  INSUFFICIENCY.  439 

BIBLIOGRAPHY. 

Mitral  Insufficiency. 

Krehl,  Geipel.     Quoted  on  page  324. 

Roy  and  Adami:  The  Failure  of  the  Heart  from  Overstrain,  Brit.  M.  J.,  Lond.,  1888,  i, 

1321  and  1395. 
Kiilbs.     Quoted  on  p.  290. 
Weber  and  Deguy:  Du  role  des  hsemorrhagies  intracardiaques  dans  les  retrecissement 

mitral,  Presse  med.,  Par.,   1898.     La  region  mitro-aortique ;    etude  anatomique  et 

pathologique,  Arch,  de  med.  exper.  et  d'anat.  path.,  Par.,  1897,  ix,  235. 
Meigs,  V.  A.:  A  New  Method  of  making  a  Hydrostatic  Test  of  the  Mitral  and  Tricuspid 

Valves,  Med.  News,  Phila.,  1884,  xlv,  533. 
Bleichroeder:  Die  Funktionspriifung  der  Mitralklappe,  Arch.  f.  path.  Anat.,  etc.,  Berl., 

1902,  clxix,  159. 
Gibson,  G.  A.:    Diseases  of  the  Heart  and  Aorta,  Edinb.  and  Lond.,  1898. 
Weiss,   O.,  and  Joachim,  G.:  Registrierung  und  Reproduktion  der  menschlichen  Herz- 

tone  und  Herzgerausche,  Arch.  f.  d.  ges.  Physiol.,  Bonn,  1908,  cxxiii,  341. 
Marey,  E.  J.:  La  circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Paris, 

1881. 
Gerhardt,  D.:  Ueber  die  Compensation  von  Mitralfehlern,  Arch.  f.  exper.  Pathol,  u.  Pharm., 

Leipz.,  1901,  xlv,  186. 
King,  T.  W.:  An  Essay  on  the  Safety-valve  Function  in  the  Right  Ventricle  of  the  Human 

Heart,  etc.,  Guy's  Hosp.  Rep.,  Lond.,  1837,  ii,  104. 
Osier,  W.,  and  Gibson,  A.  G.:  Modern  Medicine,  Phila.  and  N.  Y.,  1908,  iv,  205. 
Moritz,  F. :  Einige  Bemerkungen  zur  Frage  der  percutorischen  Darstellung  der  gesammten 

Vorderflache  des  Herzens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906,  lxxxviii,  276. 

Cf.  also  article  by  Dietlen  and  Simon  in  the  same  volume. 
Harris,  Th.:  Some  Clinical  and  Post-mortem  Observations  on  the  Cardiac  Dulness  in 

Cases  of  Mitral  Disease,  etc.,  Med.  Chron.,  Manchester,  1892,  xvii,  287. 
Groedel,  F.  M.:  The  Examination  of  the  Heart  by  the  Roentgen  Rays,  Arch.  Roentg. 

Ray  and  Allied  Phenom.,  Lond.,  1908. 
Hofmann,  Aug.     Quoted  on  p.  173. 
Gerhartz,  H. :  Zur  Frage  des  Stethoskops,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1907,  xc, 

501. 
Naunyn,  B.:  Ueber  den  Grund  weshalb  hin  und  wieder  das  systolische  Geriiusch  bei  der 

Mitralinsufficienz  am  lautesten  in  der  Gegend  der  Pulmonalklapp  zu  vernehmen  ist, 

Berl.  klin.  Wchnschr.,  1868,  v,  189. 
Boy-Teissier:  L'auscultation  retrosternale,  Rev.  de  Med.  Paris,  1892,  xii,  169. 
Wild,  R.:  A  Contribution  to  the  Pathology  of  the  Coronary  Arteries,  Med.  Chron.,  Man- 
chester, 1892,  xvi,  223. 
Meisenburg:  Ueber  das  gleichzeitige  Vorkommen  von  Herzklappenfehlern  und  Tuber- 

kulose,  Ztschr.  f.  Tuberk.,  etc.,  1902,  iii,  378. 


III. 

MITRAL  STENOSIS. 

HISTORICAL. 

After  mitral  insufficiency  the  most  common  affection  of  the  mitral 
valve  is  that  which  leads  to  mitral  stenosis.  This  condition  was  first  de- 
scribed by  John  Mayow  in  1669  in  the  case  of  a  young  man  who  died  after 
several  years  of  dyspnoea,  palpitation,  and  attacks  of  syncope.  "  At  autopsy 
he  found  dilatation  and  hypertrophy  of  the  right  ventricle  and  almost 
complete  closure  of  the  left  auriculoventricular  orifice  by  a  'cartilaginous 
product, '  so  that  the  blood  could  scarcely  traverse  the  left  ventricle  and 
was  compelled  to  flow  backward  to  the  pulmonary  vessels,  hence  the  disten- 
tion of  the  right  ventricle."  Vieussens  (1715)  described  similar  findings, 
noting  also  that  the  papillary  muscles  were  changed  to  small  short  tendons, 
and  that  the  right  ventricle  was  so  dilated  as  to  allow  reflux  of  blood  past 
the  tricuspid  valve.  He  further  noted  weakness  and  irregularity  of  the 
pulse,  and  ascribed  it  to  "too  small  quantity  of  blood  which  the  left  ven- 
tricle furnished  to  the  aorta  .  .  .  and  the  irregularity  of  its  contrac- 
tions." Senac  (1749)  and  others  described  cases,  so  that  the  lesion  became 
quite  familiar  to  pathologists  in  the  early  part  of  the  nineteenth  century. 


PATHOLOGICAL  ANATOMY  AND  PATHOGENESIS. 

Pathologically,  it  is  brought  about  by  a  chronic  inflammatory  process 
taking  place  in  the  tissue  of  the  valve  which  leads  to  thickening  and  fusion 
of  the  cusps.  By  this  fusion  the  valve  comes  to  form  a  sort  of  funnel,  some- 
times elongated,  sometimes  short 
and  shallow.  The  walls  are  much 
thicker  than  those  of  the  normal 
valve,  owing  to  a  chronic  infiltra- 
tion and  proliferation  of  the  con- 
nective tissue  within  them.  They 
are  usually  more  or  less  rigid,  some- 
times smooth,  sometimes  rough  from 
remains  of  old  vegetations  and  calci- 
fications, and  the  auricular  surface 
is  often  puckered  or  thrown  into 
folds.  The  lower  margin  of  the 
valve  is  attached  to  the  chordse 
tendinese,  which  become  shortened 

and   thickened   very   early  in   the   process.     The   orifice  thus  formed  is 
sometimes  circular,  sometimes  oval  or  button-holed,  sometimes  irregular 
(Fig.  189).     According  to  Sansom,  the  funnel  shape  is  more  common  in 
440 


Fig.  189.  —  Human  heart,  showing  mitral  (M) 
and  tricuspid  (T)  stenosis.  Viewed  from  above. 
The  auricles  have  been  cut  through. 


MITRAL  STENOSIS.  441 

children,  while  the  buttonhole  is  more  common  in  adults  and  represents 
a  lesion  of  longer  duration.  The  orifice  may  often  become  very  small 
before  death  ensues,  sometimes  barely  large  enough  to  admit  a  goose-quill 
(Sansom).  In  some  long-standing  lesions  the  margin  of  the  valve  may 
become  so  thick  and  stiff  (sometimes  calcified,  cartilaginous,  or  ossified) 
that  it  does  not  close  during  ventricular  systole;  in  others  the  edges 
become  retracted  so  that  they  no  longer  cover  the  orifice.  In  either  case 
secondary  mitral  insufficiency  may  result. 

Occurrence. — According  to  the  studies  of  Lockhart  Gillespie,  mitral 
stenosis  is  most  common  in  women,  increasing  in  frequency  up  to  the 
age  of  29.  In  men  it  is  scarcely  more  than  half  as  common,  but  reaches 
its  maximum  frequency  a  decade  later.  The  males  affected  die  earlier  than 
the  females,  however;  the  average  period  of  death  being  from  30  to  39  with 
the  former,  while  with  the  latter  it  is  40  to  49.  The  presence  of  the  double 
mitral  lesion  does  not  shorten  the  average  period  of  life. 

Etiology. — As  regards  etiology,  Cheadle,  Samways,  Duroziez,  and 
Dyce  Duckworth  agree  that  rheumatism  is  the  etiological  factor  in  at 
least  60  per  cent,  to  78  per  cent,  of  the  cases,  other  acute  infections,  chlo- 
rosis (Goodhart),  chronic  nephritis,  gout,  arteriosclerosis,  and  puerperal 
infections  representing  the  other  etiological  factors.  Potain  also  believes 
that  pulmonary  tuberculosis  is  an  important  factor,  but  this  is  disputed 
by  many  writers;  most  of  whom  agree  with  Traube  that  tuberculosis  is 
far  less  frequent  (5  per  cent.)  in  the  presence  of  mitral  stenosis  than  in 
normal  individuals  (12  per  cent.)  or  in  those  with  other  heart  lesions 
(Meisenburg,  Tileston). 

Pathogenesis. — As  regards  pathogenesis,  Huchard  (I.e.)  divides  the 
cases  of  mitral  stenosis  into  three  groups: 

1.  The  congenital  form,  resulting  from  fetal  endocarditis,  which, 
as  Sansom  has  shown,  is  very  rare. 

2.  The  endocarditic  form  of  infectious  origin  (due  especially  to 
rheumatism,  scarlet  fever,  measles,  typhoid  fever,  smallpox,  etc.),  resulting 
from  the  organization  and  fusion  of  old  vegetations.  This  is  the  most  com- 
mon form,  since  rheumatism  alone  can  be  demonstrated  as  an  etiological 
factor  in  about  70  per  cent,  of  the  cases. 

3.  The  sclerotic  form,  which  is  associated  with  general  arterio- 
sclerosis, gout,  and  plumbism.  In  this  group  no  traces  of  endocarditic  vege- 
tations occur  upon  the  valve,  and  the  process  is  more  closely  allied  to  that 
within  the  vessel  walls  in  arteriosclerosis.  Under  this  group  should  also  fall 
the  large  group  of  cases  associated  with  chlorosis  and  other  anaemias  in 
which  no  other  causal  factor  is  present  to  explain  the  presence  of  the  lesion. 
Goodhart,  who  lays  especial  stress  upon  this  group,  believes  that  the 
chronic  overstrain  of  the  anaemic  heart  muscle  is  followed  by  oedema 
and  petechiae  in  the  substance  of  the  mitral  valve,  as  has  been  demonstrated 
experimentally  by  Roy  and  Adami.  He  thinks  that  this  oedema  is  followed 
by  cellular  infiltration  and  finally  by  proliferation  of  fibrous  tissue  resulting 
in  the  mitral  stenosis.  While  this  view  is  suggestive,  no  careful  histological 
or  experimental  studies  have  been  made  to  bear  it  out.  On  the  other  hand, 
it  must  be  remembered  that  most  anaemic  and  gouty  persons  are  subject  to 
repeated  slight  infections  which  might  suffice  to  produce  chronic  changes  in 


442 


DISEASES  OF  THE  HEART  AND  AORTA. 


the  heart  during  the  lapse  of  years.  Weber  and  Deguy  have  shown  that 
hemorrhage  occurs  often  in  the  valves  after  labor,  etc.  This  is  followed 
by  infiltration  and  organization  and  finally  by  sclerosis  of  the  valve. 


PATHOLOGICAL    PHYSIOLOGY. 

The  nature  of  the  disturbance  to  the  circulation  in  mitral  stenosis  was 
already  discerned  by  Vieussens  in  1715,  who  noted  that  owing  to  the  inabil- 
ity of  the  blood  to  pass  through  the  mitral  orifice  with  sufficient  rapidity, 
it  had  become  dammed  back  in  the  pulmonary  veins  and  pulmonary  arte- 
ries, increasing  the  work  of  the  right  ventricle  and  leading  to  insufficiency  of 
the  tricuspid  valve.  At  the  same  time  the  force  of  the  pulse  (blood-pressure) 
and  amplitude  of  the  pulse  were  diminished,  owing  to  the  diminution  of  the 
blood  which  entered  or  was  forced  out  of  the  left  ventricle.  Vieussens 
noted  further  that  the  force  and  rhythm  of  contraction  were  irregular. 


NORMAL 


ii 

BROKEN 

PULMONARY 

COMPENSATION 


III 

BEGINNING 

FAILURE  OF  LEFT 

VENTRICLE 


Fig.  190. — Diagram  showing  the  changes  in  the  circulation  due  to  mitral  stenosis.  The  stage  of 
perfect  compensation  is  not  shown,  since  there  are  practically  no  pressure  changes.  II  represents  the 
stage  at  which  pulmonary  compensation  is  broken  but  systemic  circulation  has  not  yet  become  affected. 
Ill  represents  the  stage  in  which  there  is  broken  pulmonary  compensation,  and  the  left  ventricle  has  failed 
to  maintain  the  arterial  pressure.  The  last  pressure  changes  in  the  last  stage,  with  broken  systemic  com- 
pensation as  well,  correspond  exactly  to  those  in  the  last  stage  of  mitral  insufficiency.    (Compare  with  Fig.  26.) 

The  changes  of  pressure  corresponding  to  these  phenomena  have  been  studied  experi- 
mentally by  Bettelheim  and  Kauders,  D.  Gerhardt,  and  MacCallum  and  McClure,  who  have 
found  that  the  production  of  a  mild  grade  of  experimental  stenosis  causes  distinct  rise 
in  the  mean  pressure  within  the  left  auricle,  the  pulmonary  veins 
and   the  pulmonary  artery. 

Filling  of  the  Ventricles. — The  effect  of  the  stenosis  upon  the  filling 
of  the  ventricles  as  shown  in  the  volume  curve  has  recently  been  investi- 
gated by  the  writer,  aided  by  Mr.  J.  M.  Wolfsohn.  As  shown  in  Fig.  191, 
the  first  effect  of  the  mitral  stenosis  is  to  slow  the  inflow  into  the  left  ven- 
tricle. As  a  result  of  this  the  left  auricle  is  more  than  usually  full  at  the 
time  of  its  systole,  and  forces  an  unusually  large  quantity  of  blood  into  the 
ventricle  (Fig.  192,  as).  This  increase  in  auricular  output  at  first  suffices 
to  complete  the  filling  of  the  ventricle,  but  as  the  lesion  progresses  a  little 
further  even  this  fails  to  do  so  and  the  amount  of  blood  entering  the  ven- 
tricle falls  below  normal.     As  a  consequence  of  this,  the  ventricle  forces 


MITRAL  STENOSIS. 


443 


less  blood  into  the  aorta,  the  arterial  blood-pressure  falls  and  the  pulse- 
pressure  diminishes.  This  is  the  condition  as  observed  in  the  experiment. 
In  man,  however,  where  the  pathological  change  is  a  gradual  one,  the 
arteries  gradually  accommodate  themselves  by  constriction  of  their  chan- 
nels until  the  blood-pressure  has  returned  to  about  its  normal  level. 
The  pressure  in  the  systemic  veins  is  diminished,  as  has  been  shown  by 
Kornfeld. 

LIGATURE  TIGHTENED 


VOL. 


CAR. 


Fig.  191. — Volume  of  the  ventricles  in  experimental  mitral  stenosis.  (Kindness  of  the  Johns 
Hopkins  Hospital  Bulletin.)  Tracings  obtained  from  a  dog's  heart  in  experimental  mitral  stenosis. 
VOL.,  volume  curve;  CAR.,  carotid  pressure.  The  arrow  indicates  the  moment  at  which  the  stenosis 
was  produced.  The  filling  of  the  ventricles  (downstroke)  was  slowed,  diastasis  (horizontal  part  of  curve) 
sets  in  prematurely,  and  the  part  of  the  curve  due  to  auricular  systole  (second  downstroke)  becomes 
more  pronounced.     The  heart  rate  is  practically  unchanged. 


S  D 

NORMAL 


S        D 
II 


S    D 
III 


S    D 
IV 


Fig.  192. — Diagram  illustrating  the  variations  in  the  volume  curve  of  the  ventricles  in  increasing 
degrees  (I,  II,  III,  IV)  of  mitral  stenosis.  S,  systole;  D,  diastole,  AS,  inflow  into  the  ventricles  due  to 
systole  of  the  auricles.    (Compare  with  Fig.  13.) 

As  the  narrowing  of  the  mitral  orifice  progresses,  a  further  change 
occurs  in  the  filling  of  the  heart.  It  now  requires  a  greater  difference  in 
pressure  to  drive  the  blood  from  auricle  to  ventricle  and  as  a  consequence 
it  is  seen  that  during  a  great  part  of  diastole  little  or  no  blood  is  flowing  in. 
Diastole  is  thus  divided,  according  to  Henderson's  terminology  (cf.  page 
11), into  three  periods: 

I.  A  period  of  early  diastole,  during  which  the  ventricle  fills  with  moderate  rapidity, 

though  more  slowly  than  normally. 
II.  A  period  of  diastasis  (Henderson),  during  which  little  or  no  filling  occurs.  Experi- 
ments upon  the  excised  heart  (cf .  page  12)  indicate  that  the  mitral  valves  close 
suddenly  just  at  the  beginning  of  this  period  and  remain  completely  or  almost 
completely  closed  until  the  next. 
III.  This  is  followed  by  the  third  event  of  diastole,  when  more  blood  is  driven  into  the 
ventricle  by  the  forcible  contraction  of  the  left  auricle.  The  latter  must  now  con- 
tract more  forcibly  than  ever  and  as  a  consequence  hypertrophies.  Indeed  Ger- 
hardt  has  shown,  from  the  autopsies  of  two  cases  with  very  mild  grades  of  stenosis, 
that  hypertrophy  of  the  left  auricle  is  the  first  change  resulting  from  the  lesion, 
and  that  hypertrophy  of  the  right  ventricle  is  a  later  phenomenon.  Pulmonary 
congestion  always  occurs,  however,  and  in  all  but  the  very  mildest  cases  hypertrophy 
of  the  right  ventricle  results. 


444  DISEASES  OF  THE  HEART  AND  AORTA. 

With  further  narrowing  the  filling  of  the  left  ventricle  diminishes,  its 
total  volume  and  systolic  output  diminish,  and  the  blood-pressure  would  fall 
were  this  not  compensated  by  vasoconstriction.  The  stretching  of  the 
walls  of  the  left  auricle  resulting  from  stasis  may  act  as  a  stimulus  and 
give  rise  to  extrasystoles  or  may  predispose  to  paroxysmal  tachycardia; 
and  when  the  overdistention  is  great,  it  may  lead  to  auricular  fibrillation 
and  absolute  irregularity  (Lewis,  see  page  118).  At  first  the  spells  of  irregu- 
larity occur  in  transitional  attacks  coming  on  during  the  periods  of  overstrain 
and  subsiding  under  treatment,  but  as  the  disease  advances  the  irregularity 
becomes  permanent.  Persistent  irregularity  due  to  extrasystoles  (Fig.  199) 
is  occasionally  met  with.  When  the  auricle  becomes  paralyzed  and  its  walls 
become  fibrous,  the  heart-rate  remains  regular.  The  chamber  may  then  be 
dilated  to  hold  2500  c.c.  (Miiller)  or  even  3000  c.c.  (Minkowski).  The  irreg- 
ularity may  disappear  when  the  work  of  the  heart  is  relieved,  or  its  strength 
is  increased  by  digitalis  (see  Fig.  199),  when  the  presystolic  rumble 
reappears.  As  the  lesion  progresses  further,  the  stasis  in  the  pulmo- 
nary circulation  increases,  and  broken  compensation  follows,  just  as  it 
does  in  mitral  insufficiency. 

As  can  be  seen  from  the  above  description,  the  problem  of  maintain- 
ing compensation  in  mitral  stenosis  is  quite  different  from  that  in  mitral 
insufficiency.  In  the  latter  condition  the  important  factor  was  seen  to  be 
the  emptying  of  the  left  ventricle,  whereas  in  mitral  stenosis  the 
difficulty  lies  in  the  filling  of  this  chamber,  and  the  hypertrophy 
necessary  to  bring  this  about  affects  not  the  left  but  the  right  ven- 
tricle and  the  left  auricle.  Since  this  can  be  accomplished  only  by  increas- 
ing the  pulmonary  engorgement,  it  is  evident  that  after  the  lesion  has 
reached  a  certain  stage  perfect  compensation  becomes  impossible,  and  the 
re-establishment  of  compensation  is  always  more  difficult  than  in  a  corre- 
sponding grade  of  mitral  insufficiency. 

SYMPTOMS    AND    SIGNS. 

The  symptoms,  color,  and  general  appearance  of  patients  with  mitral 
stenosis  are  very  much  the  same  as  in  those  with  mitral  insufficiency, 
except  that  they  are  somewhat  more  pronounced  and  more  persistent. 
Haemoptysis  and  precordial  pain  are  more  frequent  than  in  mitral  insuffi- 
ciency, as  are  also  attacks  of  pulmonary  oedema. 

Hofbauer,  Alexander,  Miecslaw,  Frischauer,  and  Osier  have  called 
attention  to  the  hoarseness  and  stenotic  (brassy)  cough  as 
a  symptom  in  mitral  stenosis.  Osier  has  shown  at  autopsy  that  under 
these  conditions  the  left  recurrent  laryngeal  nerve  is  compressed  against 
the  arch  of  the  aorta  and  the  ligamentum  Botalli  by  the  dilated  left  auricle, 
and  then  undergoes  degenerative  changes. 

Andre  Petit  recognizes  three  clinical  groups  of  persons  with  mitral  stenosis: 
I.  The  chlorotic  type  affecting  mainly  young  girls.  The  skin  and  mucous  mem- 
branes are  pale,  the  complexion  sallow.  The  patients  readily  become  short  of 
breath,  are  subject  to  nose-bleeds,  menstrual  disturbances,  dyspepsia,  constipation, 
and  nervousness.  Only  auscultation  reveals  the  nature  of  the  disease. 
II.  The  pseudotuberculous  type  in  young  women,  characterized  by  repeated 
attacks  of  bronchitis,  dry,  hacking  cough,  and  haemoptysis,  especially  at  menstrual 


MITRAL  STENOSIS.  445 

periods.  The  patients  are  pale  and  emaciated  and  closely  resemble  consumptives 
in  appearance. 
III.  The  dyspnoeic  type  into  which  any  of  the  other  types  may  merge.  There  is 
dyspnoea  on  exertion,  frequently  also  attacks  of  cardiac  asthma  at  night.  These 
patients  usually  have  flushed  faces,  with  slight  dull  tinge  of  cyanosis  (the  typical 
mitral  facies),  due  to  imperfect  aeration  of  the  blood  in  the  lungs. 

PHYSICAL    EXAMINATION. 

Except  for  the  findings  in  the  immediate  vicinity  of  the  heart,  the 
results  of  physical  examination  in  cases  of  mitral  stenosis  are  practically 
the  same  as  in  mitral  insufficiency.  The  pulse,  however,  is  rarely  of  as 
long  volume  as  in  the  latter,  and  the  pulse-pressure  is  usually  smaller. 
Irregularity  is  about  as  common  and  is  of  the  same  type  (absolute  irregular- 
ity, with  or  without  auricular  paralysis)  in  both  conditions. 

The  Cardiac  Impulse. — The  findings  about  the  heart  are,  however, 
characteristic.  The  apex  impulse,  sometimes  in  the  normal  position  and 
sometimes  out  in  the  axilla,  is  usually  well  marked,  sudden,  short,  and 
tapping  or  flapping.  This  peculiar  appearance  is  due  to  the  seesaw  move- 
ments of  the  chest  wall  over  the  right  and  left  ventricles.  There  is  a  wavy 
movement  in  the  third,  fourth,  and  fifth  interspaces,  which  when  accurately 

timed  or  recorded  is  found  to  consist  of  a  systolic 
retraction  of  these  interspaces  over  the  hyper- 
trophied  right  ventricle  (see  page  297).  The 
systolic  impulse  of  the  pulmonary  artery  may 
sometimes  be  seen  in  the  second  left  interspace 
at  the  sternal  margin. 

Palpation.  —  The  findings  of  palpation  are 
perfectly  characteristic.  At  the  apex,  and 
usually  over  this  area  only,  the  shock  of  the 
first  sound  can  be  felt,  short,  sharp,  and  tap- 
ping. In  the  typical  cases,  up  to  the  last  stage 
(auricular  paralysis)  this  is  preceded  by  a  short 
presystolic  thrill,  having  a  "purring"  character 
(fremissement  cataire,  Corvisart,  Laennec), 
Fig.  193.— Diagram  showing  the     leading  up  to  the  shock  which  accompanied  the 

JR^vi£  SSSSS     first  .souncL     Tt    can    be    increased    by    slight 
notic  mitral  orifice.  exercise.     It   is,    as    a    rule,    sharply   localized 

about  the  apex  in  an  area  of  about  3  cm.  in 
diameter  (or  about  the  size  of  a  stethoscope  bell),  probably  because  it  is 
produced  by  the  impact  of  the  narrow  stream '  driven  by  the  forcible 
auricular  contraction  directly  against  the  apical  portion  of  the  walls  of 
the  left  ventricle. 

Indeed  Oestreich,  Lenhartz,  and  Burk  have  shown  that  this  stream  may  finally  cause 
a  bulging  of  the  ventricular  wall  at  the  point  where  it  has  been  striking.  The  vibra- 
tions transmitted  from  the  chordae  tendineee  and  papillary  muscles  are  also  factors  in  its 
production. 

Occasionally  a  tap  or  thrill  is  also  to  be  felt  in  early  or  mid-dia- 
stole accompanying  the  third  heart  sound  or  the  diastolic  rumbles 
about  to  be  described.  The  sensation  thus  imparted  by  the  presystolic 
thrill  and  the  tapping  first  shock  are  so  characteristic  that  the  diagnosis 


446 


DISEASES  OF  THE  HEART  AND  AORTA. 


of  mitral  stenosis  may  often  be  established  from  palpation  alone.  The 
shock  accompanying  the  second  sound  is  usually  very  distinct,  and  becomes 
markedly  accentuated  as  the  pulmonary  area  is  approached. 

Percussion. — The  typical  area  of  dulness  on  percussion  and  the  cardiac 
outline  as  seen  by  the  X-ray  (Groedel)  often  show  the  outline  of  the  left 
ventricle  (lower  border  and  lower  half  of  left  border)  to  be  normal,  though 
in  almost  equal  frequency  it  is  extended  to  the  left.  Thus,  in  32  cases 
Sansom  found  the  left  ventricle 

Normal  in 12 

Hypertrophied  in 9 

Dilated  in 5 

Dilated  and  hypertrophied  in. .  3 

Small  in 3 

Thin  walled  in 1 

Above,  the  area  of  dulness 
extends  higher  and  further  to  H  \f      \n  ) 

the  left  than  normal,  often 
reaching  as  high  as  the  second 
rib  (though  usually  not  above 
the  third)  and  embracing  an  area 
of  2  to  5  cm.  in  the  second  left 
interspace. 

As  shown  by  the  autopsies  of  Th.  FiG>  194._Cardiac  outline  and  distribution  of  the 

Harris,  this  area  of  dulness  COrre-  presystolic  rumble  in  mitral  stenosis.  The  area  of  cardiac 
sponds     to      the      dilated      conus       dulness  is  indicated  by  a  light  line,  the  cardiac  flatness  by 

a  r  t  e  r  i  o  s  u  s  and  dilated  pulmonary  * heavJ line-  .  The  afa  °™r  whif  the  presystolic  rum- 
+t,  j'l  ^  i  nj.  ble  and  snapping  hrst  sound  are  heard  is  indicated  by  a 
artery  and  not  to  the  dilated  ^  lett  circie.  The  relation  of  these  sounds  to  the  cardiac  cycle 
auricle.  Except  when  general  failure  is  shown  in  the  small  diagram  at  the  left.  The  systolic 
has  set  in  the  right  border  of  the  retraction  over  the  right  ventricle  is  indicated  by  the 
heart  is  normal,  but  the  cardiac  flat-  mver  e  car  10gram. 
ness  may  be   increased  and  reach  to 

the  right  sternal  margin  (hypertrophy  of  the  right  ventricle) .  The  typical  area  of  cardiac 
dulness  in  mitral  stenosis  is  therefore  a  short,  wide  oval  with  a  bulging  upon  its  upper 
left  margin  (Fig.  194). 

Auscultation. — Presystolic  Rumble. — The  auscultatory  findings  in  mitral 
stenosis  are  quite  unique,  and  usually  furnish  the  basis  for  diagnosis.  The 
characteristic  sign  is  a  rumbling  or  echoing  sound  in  late  diastole  (auriculo- 
systolic  in  time),  increasing  in  crescendo  up  to  the  beginning  of  the  first 
heart  sound.  Like  the  presystolic  thrill  and  the  diastolic  sounds,  this 
presystolic  rumble  is  usually  heard  over  an  area  of  2-3  cm.  only,  at  or  a 
little  to  the  right  of  the  apex. 

The  rumble  and  the  first  sound  thus  come  to  have  the  phonetic  equivalent  of  Trup, 
tr-rr-rup,  Turrup  (Steel),  Rou  fut  (Duroziez).  It  was  first  described  by  Gendrin  in 
1842  and  by  Fauvel  in  1843  in  cases  of  mitral  insufficiency,  but  its  diagnostic  significance 
was  definitely  established  by  W.  T.  Gairdner,  of  Edinburgh,  in  1861.  Gairdner  and  the 
older  writers  considered  it  to  be  produced  by  systole  of  the  left  auricle  (auricular-systolic) 
driving  the  blood  forcibly  through  the  narrow  mitral  orifice.  This  view  has  been  practi- 
cally proved  by  the  observations  of  James  Mackenzie  that  the  presystolic  murmur  is  present 
only  when  the  venous  tracing  shows  contractions  of  the  auricles,  and  disappears  when  the 
auricle  no  longer  pumps.  The  protodiastolic  and  mid-diastolic  rumbles  remain,  however, 
but  they  may  be  very  hard  to  distinguish  from  the  presystolic  (auriculosystolic)  murmurs, 
especially  when  the  heart-rate  is  rapid.    T.  S.  Hart  (Med.  Rec,  1911,  lxxx,  2)  claims  to 


MITRAL  STENOSIS. 


447 


have  heard  crescendo  presystolic  murmurs  in  four  cases  of  auricuar  fibrillation,  but 
his  observations  require  confirmation.  The  graphic  records  of  Weiss  and  Joachim 
show  the  rumble  to  be  auriculosystolic.  T.  Lewis  (Heart,  1912-1913,  iv,  241)  has  recorded 
the  sounds  of  Einthoven's  method  and  finds  that  the  presystolic  rumble  precedes  ven- 
tricular systole  by  .05  to  .22  second,  the  period  of  auriculoventricular  conduction,  and 
that  when  auricular  fibrillation  is  present,  the  sounds  run  through  the  entire  diastole  and 
are  never  confined  to  the  presystolic  period. 


Fig.  195. — Radiograph  from  a  case  of  mitral 
stenosis,  taken  with  the  plate  behind  the  patient, 
showing  increase  of  the  shadow  due  to  the  dilated 
left  auricle.  (Kindness  of  Prof.  C.  M.  Cooper.)  The 
left  ventricle  is  not  dilated. 


Fig.  196. — Diagram  representing  the  shadows 
shown  in  Fig.  195.  The  broken  line  indicates  the 
outline  of  a  normal  heart.  The  arrow  indicates  the 
enlargement  upward  in  the  transvere  oblique  diam- 
eter. LA,  left  auricle;  PA,  pulmonary  artery; 
AO.  aorta;  LV,  left  ventricle. 


CAROTID 


SOUND 


Snapping  First  Sound. — The  nature  of  the  first  heart  sound  is  also  char- 
acteristic. It  is  short  and  sharp,  and  may  resemble  the  second  sound  so 
closely  as  to  be  mistaken  for  the  latter.  This  is  especially  common  in  cases 
in  which  the  second  sound  is  not  well  heard  at  the  apex. 

Fenwick  and  Overend  believed  that  it  was  of  higher  pitch  than  the  normal  first  sound, 
but  this  is  not  borne  out  by  the  curves  of  Weiss  and  Joachim,  who  found  waves  of  about 
normal  pitch  but  of  much  greater  amplitude  (Fig.  197).  It  is  possible 
that    Fenwick    and    Overend    may 

have  heard  higher  overtones  than  p    l  p    * 

accompany  the  normal  heart  sound. 
According  to  Haycraft,  it  is  the 
valvular  element  which  imparts  the 
high-pitched  notes  to  the  first  sound, 
and  this  is  naturally  accentuated  in 
mitral  stenosis,  for  the  stiff  mitral 
valve  plays  a  greater  role  in  sound 
production  than  in  the  normal. 

Broadbent  and  Acland  be- 
lieved that  the  ventricular  walls 
"close  down  rapidly  because  their 
cavity  is  not  distended  with  blood" 
and  thus  give  rise  to  a  more  sudden 
sound.  However,  the  snapping 
sound  is  quite  as  pronounced  in  the  numerous  cases  in  which  the  ventricle  is  dilated;  and 
moreover,  on  the  other  hand,  the  cardiometer  shows  that  diminution  in  ventricular  volume 
occurs  at  exactly  the  same  rate  as  in  the  normal  heart.1 

1  On  account  of  the  smaller  amount  of  blood  discharged  at  the  usual  rate,  the  duration 
of  systole  is  shorter;  but  Einthoven's  tracings  show  that  the  duration  of  the  first  sound  is 
normal. 


Fig.  197. —  Graphic  record  of  carotid  pulse  and  heart 
sounds  in  mitral  stenosis.  (After  Weiss  and  Joachim.)  Upper 
line,  carotid  pulse ;  middle  line,  phonogram ;  lower  line, 
time  in  Toii  seconds  ;    P,  presystolic  rumble;  1,  2,  heart  sounds. 


448 


DISEASES  OF  THE  HEART  AND  AORTA. 


This  applies  only  to  the  first  sound  produced  in  the  left  ventricle, 
and  hence  heard  only  over  a  small  area  about  the  apex  from  which  it  is 
transmitted  for  a  short  distance  upward  and  to  the  right.  Over  the  right 
ventricle  the  first  sound  is  normal  until  the  latter  stages  of  the  disease, 
when  it  is  often  replaced  by  the  murmur  of  tricuspid  insufficiency.  The 
second  sound  at  the  apex  is  usually  faint,  and  may  even  become  quite 
inaudible  in  the  latter  stages  of  the  disease,  probably  owing  to  the  low 
arterial  blood-pressure,  but  over  the  pulmonic  area  it  is  markedly  accen- 
tuated. 


INTRAVENTRICULAR 
PRESSURE 


VENTRICULAR  3 
VOLUME  2 

CURVES 

I 

N 


SOUNDS 

CORRESPONDING  TO 

VOLUME 

CURVES 


3 


Fig.  198. — Diagram  showing  the  relations  of  the  various  sounds  heard  in  uncomplicated  mitral 
stenosis  to  events  in  the  filling  and  emptying  of  the  ventricle.  N,  normal.  Light,  heavy,  broken,  and  dot- 
ted lines  correspond  with  sounds  whose  base  lines  are  made  with  these  lines. 


Digital  Imitation  of  the  Presystolic  Rumble  and  Snapping  First  Sound. — While  the 
ordinary  vowel  and  consonant  sounds  fail  to  give  any  close  imitation  of  the  sounds  heard 
in  mitral  stenosis,  these  may  be  quite  closely  reproduced  by  the  method  of  H.  L.  Smith 
(page  170),  tapping  on  the  knuckles  with  four  fingers  in  rapid  succession. 

Systolic  Murmur  in  Mitral  Stenosis  with  Mitral  Insufficiency. — Since  the  mitral  cusps 
are  much  deformed  and  thickened  in  mitral  stenosis,  and  the  chordse  tendineae  shortened, 
it  is  not  surprising  that  leakage  at  this  valve  should  be  present  in  the  greater  number  of 
cases  (Fig.  179).  The  group  of  signs  due  to  the  insufficiency  of  the  valve  associated  with 
stenosis  do  not  present  striking  differences  from  the  signs  of  the  former  lesion  when  existing 
alone.  Hypertrophy  of  the  left  ventricle  occurs  in  almost  all  these  cases,  and  the  heart  is 
enlarged  horizontally  to  the  left.  A  blowing  systolic  murmur  accompanies  and  follows  the 
snapping  first  sound;  and  occasionally,  when  the  second  sound  at  the  apex  is  absent  or 
very  soft,  this  murmur  may  seem  to  be  diastolic.  Careful  timing  by  comparison  with  the 
shocks  and  the  time  of  the  pulmonic  second  sound,  however,  will  prevent  this  error. 


MITRAL  STENOSIS. 


449 


Sounds  in  Early  and  Mid=diasto!e. — The  sounds  heard  in  early  and  mid- 
diastole,  however,  are  quite  as  well  marked  as  is  the  presystolic  murmur. 
These  sounds  are  of  three  types: 

1.  An  early   diastolic  sound,  the  third   sound  of  a  proto- 

1  2  3 

diastolic  gallop  rhythm  (rup  -  tat  -  ta) ,  which  Bouillaud  observed  in  1841 
in  association  with  mitral  stenosis.  This  sound  is  heard  in  about  65  per 
cent,  of  all  cases  of  mitral  stenosis  (Steell).  Though  somewhat  louder  it 
does  not  seem  to  differ  from  the  third  sound  of  the  normal  heart  in  mode 
of  production,  and  is  probably  due  to  the  sharp  closure  of  the  mitral  cusps 
when  the  period  of  rapid  ventricular  filling  has  come  to  an  end.  It  is  there- 
fore to  be  regarded  as  a  "closing  snap"  of  the  mitral  (Hirschfelder,  1.  c), 
and  not  as  an  "opening  snap"  as  thought  by  Duroziez,  Sansom,  and  Potain. 
As  the  filling  of  the  ventricle  is  somewhat  less  complete  than  normal,  this 
sound  occurs  a  trifle  early  (Thayer).  That  it  should  be  louder  and  more 
readily  produced  is  due  to  the  rigidity  of  the  altered  mitral  valve. 


Fig.  199. — Venous  pulse  of  a  patient  with  mitral  stenosis  during  an  attack  of  acute  heart  failure. 
A.  Tracing  taken  on  Dec.  4,  1907.  The  presystolic  rumble  has  disappeared.  The  a  (auricular)  wave  is 
absent  from  the  venous  pulse.  There  is  absolute  arrhythmia.  B.  Tracing  taken  five  days  later,  after 
return  of  compensation.  The  presystolic  rumble  has  returned;  the  a  wave  is  present  on  the  venous  pulse. 
The  rhythm  is  regular.     The  arrows  mark  the  time  when  auricular  contraction  should  occur. 


2.  One  of  the  commonest  sounds  in  mitral  stenosis  is  a  rumble 
in  early  or  in  mid-diastole  of  the  same  character  as  the  pre- 
systolic rumble.  According  to  Huchard,  it  may  resemble  the  sound  of  a 
flag  fluttering  in  the  breeze,  causing  the  cardiac  cycle  to  resemble  the  words 

1  2 

"rup  -  tat -rarou."  This  rumble  may  follow  almost  immediately  after 
the  second  sound.  It  may  last  throughout  diastole  and  be  continuous 
with  the  presystolic  rumble,  or  it  may  be  separated  from  the  second  sound 
and  also  from  the  presystolic  by  short  intervals.  On  the  other  hand,  when 
the  presystolic  rumble  has  disappeared  during  auricular  paralysis  it  may  be 
the  only  sound  heard  during  diastole. 

These  rumbles  occur,  therefore,  at  the  time  when  the  blood  is  flowing  rapidly  into  the 
left  ventricle.  At  this  phase  of  diastole,  owing  to  the  stasis  in  the  pulmonary  veins,  the 
auricular  pressure  is  relatively  high.  It  is,  therefore,  not  surprising  that  the  stream  pass- 
ing through  the  narrowed  auricular  channel  under  about  the  same  pressure  should  give 
rise  to  a  rumble  similar  to  that  produced  later  in  diastole  when  the  same  stream  is  pro- 
pelled through  the  same  orifice  at  about  the  same  rate  by  the  force  of  the  auricular  con- 
traction. Nor  is  it,  therefore,  surprising  that,  as  shown  by  Mackenzie,  the  early  diastolic 
29 


450  DISEASES  OF  THE  HEART  AND  AORTA. 

rumbles  produced  by  a  pressure  which  is  continually  diminishing  should  be  always 
decrescendo  in  character,  while  the  presystolic  rumbles  produced  by  the  rapidly 
increasing  auricular  contraction  should,  on  the  contrary,  be   crescendo. 

3.  A  blowing  diastolic  murmur  not  unlike  the  ordinary  mur- 
mur of  aortic  insufficiency  is  occasionally  heard  in  mitral  stenosis  (Graham 
Steell,  Huchard,  Cabot  and  Locke,  Bard).  This  murmur,  however,  never 
replaces  the  second  sound  as  does  the  aortic  murmur,  but  follows  it  after 
a  short  pause.  It  becomes  louder  and  lasts  longer  as  the  pulse-rate  dimin- 
ishes. The  murmur  is  intense  at  the  apex,  but  is  also  heard  above  and 
to  the  left  of  the  latter.  It  is  not  heard  over  the  aortic  area  nor  over  the 
sternum,  though  sometimes  heard  at  the  upper  left  sternal  margin.  Whether 
this  murmur  is  caused  by  a  secondary  functional  insufficiency  of  the  pul- 
monary valves,  due  to  dilatation  of  the  right  ventricle  (cf.  page  493),  or  is 
a  cardiopulmonary  murmur  (cf.  page  178)  induced  by  the  increased  activity 
of  the  right  ventricle,  is  still  unsettled.  It  is  probable  that  each  is  met  with 
in  some  cases. 

STAGES    OF    MITRAL    STENOSIS. 

It  is  difficult  to  divide  the  course  of  mitral  stenosis  into  well-defined 
stages.  From  a  physiological  and  diagnostic  stand-point  it  might  be  con- 
venient to  distinguish  four  stages, — which  differ  slightly  from  those  de- 
scribed by  Broadbent  (I.e.).  These  are  characterized  by  the  following 
phenomena: 

First  Stage.  —  Presystolic  rumble,  snapping  first  sound  and  second 
sound  are  well  heard  at  the  apex, — compensation  is  good,— the  left  auricle 
contracting  forcibly  as  shown  by  the  presystolic  rumble,  also  the  left  ven- 
tricle as  shown  by  well-marked  second  sound.  The  second  pulmonic  sound 
is  increased.  The  sounds  of  early  and  mid-diastole  may  or  may  not  be 
present.  Broadbent  says  of  this  stage,  "  I  have  never  known  serious  symp- 
toms to  arise  from  the  condition  of  the  heart,  and  I  have  seen  serious  ill- 
nesses of  different  kinds  passed  through  without  the  intervention  of  embar- 
rassment of  the  circulation." 

Second  Stage. — The  presystolic  rumble  and  first  sound  persist  and  the 
early  and  mid-diastolic  rumbles  may  be  present,  but  the  second  sound  at 
the  apex  has  completely  or  almost  completely  disappeared.  This  indicates 
that  the  force  of  the  left  ventricle  is  beginning  to  diminish  (Fig.  190,  III), 
but  the  left  auricle  is  still  contracting  forcibly.  At  this  stage  the  presystolic 
rumble  is  sometimes  mistaken  for  the  first  heart  sound  and  the  snapping 
first  sound  for  the  second,  so  that  if  there  is  a  systolic  murmur  present  a 
diagnosis  of  mitral  insufficiency  may  be  made,  and  a  less  severe  prognosis 
is  sometimes  given.  This  error  may  be  avoided  by  carefully  timing  the 
heart  sounds  by  palpation  or  by  noting  the  change  in  sounds  on  gradually 
passing  the  stethoscope  from  base  to  apex. 

Third  Stage. — The  presystolic  rumble  and  thrill  have  disappeared.  The 
snapping  first  sound  and  sounds  of  early  diastole  persist;  the  second  sound 
at  the  apex  may  or  may  not  be  heard.    Fibrillation  of  the  auricles  has  set  in. 

Overlapping  of  Second  and  Third  Stages. — In  some  cases  this  occurs 
earlier  than  the  disappearance  of  the  first  sound  at  the  apex,  and  these  two 
stages  overlap  or  may  even  replace  one  another  chronologically. 


MITRAL  STENOSIS. 


451 


This  depends  upon  the  relative  strength  of  left  ventricle  and  left  auricle,  as  well  as 
upon  the  degree  to  which  the  mitral  orifice  is  narrowed;  for  a  comparatively  weak  left 
auricle  sometimes  fails  without  materially  affecting  the  cardiac  filling,  while,  on  the  other 
hand,  a  vigorously  beating  auricle  may  produce  a  loud  sound  while  forcing  a  small  amount 
of  blood  through  the  narrowed  orifice,  and  yet  the  amount  of  blood  thus  entering  the  left 
ventricle  may  be  too  small  to  maintain  the  arterial  blood-pressure  and  to  cause  a  distinct 
second  sound. 

Dyspnoea,  haemoptysis,  and  the  usual  features  of  stasis  in  the  pulmo- 
nary circulation  occur  in  the  second  and  third  stages  of  the  disease. 

Fourth  Stage. — Broken  systemic  compensation,  venous  stasis,  oedema 
of  the  extremities,  enlargement  of  the  liver,  gastric  and  digestive  disturb- 
ances, ascites,  hydrothorax,  and  all  the  other  features  of  broken  compen- 
sation of  the  right  ventricle  set  in.  In  the  later  stages  there  are  well-marked 
signs  of  tricuspid  insufficiency,  positive  venous  pulse,  and  positive  pulsa- 
tion of  the  liver. 

PULSE. 

Exactly  as  in  mitral  insufficiency,  permanent  irregularity  of  the  pulse 
due  to  the  numerous  extrasystoles  may  occur  quite  early  in  cases  where 
both  the  presence  of  the  presystolic  rumble  and  the  venous  pulse  tracing 


CAR. 


JUG. 


3.0  5.0  Z.&  4.0  2.8         4.0        3.8 


Fig.  200. — Permanent  arrhythmia  in  a  case  of  mitral  stenosis,  showing  persistence  of  the  auricular 
contractions  (o  wave)  upon  the  venous  pulse.  The  right  auricle  (at  least)  is  still  contracting.  The  tracing 
shows  the  presence  of  persistent  auricular  extrasystoles. 

show  that  the  auricles  are  still  contracting  forcibly  (Fig.  200).  Owing  to 
the  greater  circulatory  disturbance  entailed  in  the  filling  of  the  left  ventricle, 
arrhythmia  causes  a  somewhat  greater  circulatory  disturbance  in  mitral 
stenosis  than  in  insufficiency,  although  in  neither  is  it  a  harbinger  of  immedi- 
ate clanger  and  it  may  last  for  years.  The  pulse  is  usually  small  in  mitral 
stenosis,  owing  to  the  contracted  condition  of  the  radial  and  other  medium- 
sized  arteries. 

The  blood-pressure  is,  as  a  rule,  very  little  changed,  owing  to  the  com- 
pensatory changes  in  the  arterial  bed.  The  most  common  change  is  a 
diminution  in  pulse-pressure  due  to  a  rise  in  the  minimal  pressure  brought 
about  by  the  vasoconstriction.  A  large  pulse-pressure,  such  as  is  frequently 
seen  in  well-compensated  mitral  insufficiency,  is  not  common  in  mitral 
stenosis. 

DIAGNOSIS. 

In  the  absence  of  aortic  insufficiency  and  adherent  pericardium  the 
diagnosis  of  mitral  stenosis  is  comparatively  simple,  and  is  based  upon  the 
presence  of  the  presystolic  or  diastolic  rumble  or  thrill  at  the  apex,  together 
with  a  short  snapping  first  sound  in  this  region,  a  markedly  accentuated 
second  pulmonic  sound,  and  a  large  P  wave  upon  the  electrocardiogram. 


452  DISEASES  OF  THE  HEART  AND  AORTA. 

However,  it  sometimes  happens  that  these  signs  appear  only  occasion- 
ally while  the  patient  is  under  observation. 

Some  years  ago  the  writer  had  under  his  care  for  several  months  a  patient  with  per- 
nicious anaemia  in  whom  a  presystolic  murmur  was  heard  on  only  one  occasion,  though  the 
heart's  action  was  fairly  vigorous  and  regular.  A  gallop  rhythm  had  been  present  during 
her  entire  illness.    The  diagnosis  of  a  mild  grade  of  mitral  stenosis  was  verified  at  autopsy. 

Occasionally,  on  the  other  hand,  the  patient  is  seen  after  auricular 
paralysis  has  set  in  and  when  there  is  no  diastolic  rumble  present  whatever 
and  only  the  sounds  of  the  second  and  third  stages.  Such  cases  show  the 
need  of  frequent  auscultation  of  the  patient. 

Differentiation  between  Aortic  Insufficiency  and  Mitral  Stenosis. — In 
the  presence  of  aortic  insufficiency  it  must  be  remembered  that  the  presys- 
tolic and  diastolic  murmurs  described  by  Austin  Flint  may  closely  simulate 
those  arising  in  mitral  stenosis  (see  page  473)  ^  In  aortic  insufficiency  the 
thrill  is  rarely  as  well  marked  as  in  mitral  stenosis,  and  the  first  sound  is 
rarely  sufficiently  short  and  snapping  to  be  mistaken  for  mitral  stenosis. 
The  two  conditions  were  found  together  in  4.2  per  cent,  of  the  1781  cases 
of  valvular  disease  at  the  Johns  Hopkins  Hospital, — i.e.,  in  about  one- 
seventh  of  all  the  cases  of  mitral  stenosis  and  one-tenth  of  all  the  cases  of 
aortic  insufficiency,  so  that  it  is  not  a  condition  of  extreme  rarity.  When, 
as  not  infrequently  happens,  the  mitral  stenosis  is  the  first  condition  present, 
there  is  no  difficulty,  as  the  late  diastolic  blow  of  mitral  stenosis  is  rare  and 
scarcely  ever  mistaken  for  aortic  insufficiency.  But  when  the  aortic  insuffi- 
ciency is  the  first  lesion  to  occur,  the  diagnosis  of  the  second  lesion  becomes 
much  more  difficult.  Occasionally  in  doubtful  cases  a  slight  exercise 
or  a  few  forced  expirations  with  glottis  closed  (Valsalva's  experiment)  will 
increase  the  work  of  the  left  auricle  and  cause  the  presystolic  thrill  and 
rumble  to  become  so  intense  that  the  presence  of  mitral  stenosis  is  unmis- 
takable. A  diagnosis  should  never  be  made  unless  the  heart  has  been 
examined  in  various  stages  of  its  activity.  In  spite  of  such  precautions 
errors  are  not  infrequent,  and  are  made  by  the  most  skilful  observers.  It 
must  be  frankly  confessed  that  there  are  many  cases  in  which  the  diagnosis 
cannot  be  made  with  any  degree  of  certainty. 

According  to  Phear,  adhesive  pericarditis  can  also  be  mistaken  for 
mitral  stenosis,  since  occasionally  a  presystolic  rumble  may  occur,  due  no 
doubt  to  the  stretching  of  the  fibrous  strands  under  the  influence  of  the 
auricular  contraction  of  the  ventricular  filling,  and  here  also  the  diagnosis 
of  two  coexistent  lesions  should  be  made  with  caution. 

Presystolic  Gallop  Rhythm. — Another  condition  which  on  rare  occa- 
sions may  be  confounded  with  mitral  stenosis  is  one  of  slight  cardiac  weak- 
ness in  which  there  is  a  presystolic  gallop  rhythm.  Under  these  circum- 
stances, as  Sewall  states,  the  ventricles  are  overfilled  with  blood  and  the 
auricle  encounters  some  difficulty  in  forcing  blood  into  them.  There  may 
even  in  some  cases  be  a  slight  functional  stenosis  like  that  discussed  on 
page  172.  Sewall  believes  that  under  these  conditions  the  contraction  of 
the  auricle  becomes  audible  and  may  even  be  mistaken  for  mitral  stenosis. 

Quite  recently  the  writer  has  had  under  his  care  in  the  Johns  Hopkins  Dispensary 
a  girl  of  13  years  who  presented  this  picture.  She  had  had  a  slight  attack  of  rheumatism 
and  tonsillitis  and  shortly  afterwards  began  to  have  palpitation,  weakness,  nervousness, 


MITRAL  STENOSIS.  453 

and  a  little  pain  in  the  precordium  and  around  the  lower  part  of  the  left  axilla.  On  exami- 
nation the  heart  was  not  enlarged,  but  the  shock  accompanying  the  first  sound  was  quite 
sharp  and  there  was  a  well-defined  impulse  which  began  with  vibrations  that  suggested  a 
presystolic  thrill.  These  were  somewhat  increased  on  exercise.  The  second  pulmonic 
was  not  abnormally  accentuated.  The  pulse-rate  was  120  and  regular.  There  was  no 
anaemia.  The  signs  were  not  quite  definite  enough  to  warrant  a  diagnosis  of  mitral  stenosis. 
The  patient  was  given  digitalis  for  a  few  days  and  this  was  followed  by  a  prolonged  treat- 
ment with  iron,  quinine,  and  strychnine.  She  improved  steadily,  and  for  several  weeks 
past  no  presystolic  sounds  or  impulse  can  be  elicited  even  by  quite  severe  exercise.  As  it 
seems  quite  unlikely  that  an  auricular  paralysis  would  set  in  coincident  with  these  condi- 
tions of  improvement,  and  in  the  absence  of  any  arrhythmia,  it  seems  most  likely  that  this 
case  represented  one  of  very  loud  presystolic  gallop  rhythm,  and  that  no  organic  lesion 
is  present. 

Case  of  Mitral  Stenosis  with  Insufficiency,  Angina  Pectoris,  and 
Pulmonary  Sclerosis. 

O.  A.  K.,  farmer,  aged  34,  was  admitted  to  the  Johns  Hopkins  Hospital,  June  2, 
1903,  complaining  of  heart  trouble  and  shortness  of  breath.  Family  history 
negative.  Patient  has  always  been  healthy  except  for  c  h  o  r  e  a  at  14  and  acute 
articular  rheumatism  at  18.  He  is  rather  subject  to  headaches.  Has  smoked  and 
drunk  in  excess,  but  for  the  past  few  years  does  so  in  great  moderation.  He  is  much  ex- 
posed to  the  weather. 

For  the  past  six  or  seven  years  he  has  been  short  of  breath  and  has  had 
pain  over  the  heart.  Six  months  before  admission  he  developed  ascending 
oedema,  which  disappeared  under  treatment,  but  his  breath  remained  short  and  the 
oedema  reappeared  within  a  couple  of  months.  During  the  past  month  he  has  had  spells 
of  dizziness   and  fainting  during  exertion  and  had  one  chill  followed  by  fever. 

On  examination  the  patient  is  seen  to  be  a  well-nourished  man  with  anxious  appear- 
ance and  flushed  face,  deeply  cyanotic.  He  is  quite  dyspnoeic.  The  teeth  are 
bad;  the  pharynx  is  injected.  The  veins  of  the  neck  are  prominent,  but  do  not  pulsate. 
The  chest  is  full,  and  coarse  rales  are  everywhere  heard. 

Heart.  — The  apex  impulse  is  seen  in  the  6th  left  interspace  12  cm.  from 
the  midline.  Dulness  extends  upward  to  the  second  left  interspace  and  4  cm.  to  the  right 
of  the  sternum.  There  is  a  loud  systolic  murmur  heard  over  the  entire  heart 
and  left  axilla.  The  heart's  action  is  irregular  in  force  and  rhythm.  Pulse-rate  76.  The 
radial  is  somewhat  sclerotic.    Maximal  blood-pressure  130  mm.  Hg. 

His  liver  and  spleen  were  not  enlarged.    There  was  no  oedema  of  the  feet. 

He  was  kept  in  bed,  purged  freely,  given  tincture  of  digitalis 
(8  doses  of  1  c.c.  [n\xv]  each).  During  the  following  two  months  his  condition  im- 
proved markedly,  in  spite  of  the  occurrence  of  a  fibrinous  pleurisy.  His  dyspnoea 
diminished  and  he  felt  much  improved.  Coincident  with  this  improve- 
ment a  presystolic  rumble  and  thrill  gradually  appeared  and  a  snap- 
ping first  sound  preceded  the  systolic  murmur.  Three  months  after  admis- 
sion his  cyanosis  had  almost  entirely  disappeared.  The  heart  was  still  enlarged  (the  apex 
11  cm.  from  the  midline);  a  well-marked  presystolic  thrill  was  felt  and  a  presystolic  mur- 
mur was  heard  at  the  apex.  The  first  sound  was  snapping  and  was  accompanied  and 
followed  by  a  loud  blowing  systolic  murmur. 

The  blood-pressure  during  his  stay  in  the  hospital  ranged  between  12  0  and 
135  mm.   Hg. 

After  leaving  the  hospital  at  this  time  the  patient  felt  well  for  about  six  weeks, 
during  which  period  he  could  even  run  for  a  car  without  distress.  Then  he  caught  a 
cold  which  persisted  for  four  months,  being  aggravated  by  exertion.  He  had  two  more 
fainting  spells  on  exertion.  Oedema  returned,  the  lower  extremities  and 
of  late  even  the  face  and  eyes  being  swollen.    Urine  less  frequent  than  normal. 

On  readmission  he  was  very  cyanotic  and  very  dyspnoeic. 
Moist  rales  were  heard  over  the  entire  chest.  The  apex  is  now  in  the  6th  left 
interspace  15.5  cm.  from  the  midline.  The  presystolic  rumble  and  sys- 
tolic murmur  are  well  heard,  as  at  the  last  discharge.  Red  blood-corpuscles  5,000,000; 
haemoglobin  105  per  cent.;  leucocytes  5500. 


454  DISEASES  OF  THE  HEART  AND  AORTA. 

On  the  night  of  admission  the  patient  felt  bad  and  had  attacks  during 
which  he  felt  faint  and  "  saw  stars."  Venesection  caused  much  r  e  1  e  i  f 
in  the  symptoms  and  the  blood-pressure  rose  from  120  mm.  Hg  to  140  mm. 
The  patient's  condition  then  gradually  improved,  but  on  January  24  he  had  a  definite 
attack  of  precordial   pain   and  constriction   lasting  1-3  minutes. 

Feb.  23.  Has  had  pain  in  head  and  the  left  side  of  the  face  due  to  a  beginning  otitis 
media. 

During  the  next  few  weeks  he  had  several  attacks  of  angina  pec- 
toris, the  pain  being  usually  most  marked  behind  the  lower  part  of  the  sternum.  In 
one  attack  it  radiated  to  the  left  shoulder  and  down  the  left  arm  to  the  hand  (left  ventric- 
ular pain). 

On  April  20  he  complained  of  pain  in  the  left  axilla  and  back,  com- 
ing in   paroxys  ms   lasting  for   15-20  minutes    (left  auricular  pain) . 

May  6.  Sputum  bloody.  From  this  time  on  he  gradually  improved, 
cyanosis  and  dyspnoea  almost  disappeared,  and  he  was  discharged  in  August 
in  fair  condition.  From  that  time  until  his  readmission  in  November  he  suffered  from 
numerous  attacks  of  angina  pectoris,  beginning  in  the  left  hand  and 
passing  up  the  arm  to  the  shoulder  and  heart.  He  also  had  an  attack  of  rheu- 
matism and  severe  tonsillitis.  His  physical  condition  was  like  that  on  pre- 
vious admission,  but  the  anginal  attacks  were  more  frequent.  He  was  given  hypodermic 
injections,  sometimes  of  morphine,  sometimes  of  distilled  water,  to  relieve  them. 
His  condition  gradually  improved,  most  markedly  after  venesec- 
tion. Toward  the  end  of  his  stay,  while  up  and  about,  he  became  subject  to  sudden 
paroxysms  of  acute  dyspnoea  (respirations  130  per  minute),  with  small  moist  rales  filling 
the  lungs  (acute  pulmonary  oedema) .  These  persisted  in  spite  of  repeated  rest  and  digitalis 
treatments.  He  was  discharged  on  July  11,  1905,  seven  months  after  admission.  (Edema 
and  dyspnoea  returned  within  ten  days,  and  he  was  soon  back  in  the  hospital  again.  Dur- 
ing this  admission  he  never  thoroughly  rallied.  His  blood-pressure  remained 
low,  105  mm.  maximal  pressure  (as  compared  with  120-130  mm.  on  previous  ad- 
missions). The  pulse  was  irregular.  Rales  were  constantly  present  in  his  chest.  The 
liver  was  palpable.  A  slight  pleurisy  developed  on  October  13  and  he  died  on  Octo- 
ber 20. 

At  autopsy  the  mitral  orifice  was  found  to  have  the  form  of  a  small 
button -hole  barely  admitting  the  tip  of  the  little  finger  (about  5  mm.  in  diameter). 
The  left  auricle  was  dilated  and  hypertrophied.  The  left  ventricle 
was  not  dilated,  but  was  much  hypertrophied,  its  walls  being  15  mm.  thick.  The  right 
auricle  and  ventricle  were  much  dilated,  the  tricuspid  orifice  admitting  four  fingers 
(13-14  cm.  in  circumference).  The  coronary  arteries  were  patent  but  showed 
scattered  areas  of  sclerosis.  There  were  old  fibrous  patches  upon  the  pericardium. 
The  pulmonary  arteries  were  markedly  sclerotic;  the  sclerosis  extended 
into  their  smaller  branches.  The  aorta  and  peripheral  arteries  showed  less  sclerosis.  There 
were  also  chronic  passive  congestion  of  the  other  viscera,  anaemic  infarctions  of  the  spleen, 
hemorrhagic  infarction  of  the  lungs,  acute  bronchitis,  bronchopneumonia, 
acute  ulcerative  follicular  colitis,  old  tuberculous  foci  in  the  lymph-glands  and  lungs, 
chronic  adhesive  pleuritis,  and  adhesive  peritonitis. 


COMPLICATIONS. 

As  seen  by  the  table  in  Fig.  179  mitral  stenosis  is  frequently  associated 
with  other  valvular  lesions.  Mitral  insufficiency,  present  in  one-half  of  the 
Johns  Hopkins  cases  and  in  75  per  cent,  of  Steell's  cases,  may  be  regarded 
as  an  essential  part  of  the  disease  rather  than  a  special  complication,  and 
its  presence  does  not  shorten  the  average  length  of  life. 

The  association  of  aortic  disease,  and  indeed  of  any  additional  burden 
upon  the  circulation,  increases  the  gravity  of  the  condition. 

Tricuspid  stenosis  is  an  occasional  concomitant,  though  rarely  as  often 
found  as  by  Samways,  who  encountered  it  in  severe  grade  in  24  out  of  196 


MITRAL  STENOSIS.  455 

autopsies  upon  cases  of  mitral  stenosis,  and  in  mild  grade  in  8  additional 
cases.  In  the  Johns  Hopkins  Hospital  it  was  found  clinically  7  times  among 
298  cases  of  mitral  stenosis. 

A  certain  degree  of  myocarditis  is  the  rule,  especially  in  cases  in  the 
third  and  fourth  decades. 

Acute  pericarditis  is  quite  common  in  the  youthful  rheumatic  cases, 
frequently  leaving  a  residual  adherent  pericardium,  a  lesion  which  aggra- 
vates the  condition  considerably  and  greatly  shortens  the  life  of  the  patient. 

One  of  the  most  important  and  dangerous  complications  arising  with 
mitral  stenosis  is  pregnancy   (see  Chapter  I X) . 

Thrombosis  in  the  Left  Auricle. — Another  not  uncommon  complication 
of  mitral  stenosis,  more  than  any  other  valvular  lesion,  is  thrombosis  within 
the  left  auricle.  This  may  occur  even  while  the  auricle  is  still  contracting 
vigorously,  as  shown  by  the  presystolic  thrill  and  rumble.  The  thrombus 
may  remain  quiescent  in  the  tip  of  the  auricle  or  it  may  obstruct  the  pul- 
monary veins.  Sometimes  it  is  so  large  as  to  stop  up  the  narrow  mitral 
orifice  and  kill  the  patient.  More  frequently  it  is  small  enough  to  pass 
through,  and  if  carried  on  by  the  blood  current  gives  rise  to  a  small  area  of 
embolism. 

Embolism. — Embolism  of  the  middle  cerebral  artery  may  give 'rise  to 
paralysis  or  aphasia.  Embolism  in  other  organs  gives  rise  to  corresponding 
signs  and  symptoms. 

Pulmonary  embolism  and  infarction  are  caused  by  thrombi  from  the 
right  auricle  and  ventricle;  and  hence  are  due  to  secondary  stasis  in  the 
latter  and  not  primarily  to  the  mitral  stenosis.  However,  as  failure  of  the 
right  ventricle  is  particularly  common  in  mitral  stenosis,  pulmonary  embolism 
is  especially  frequent  in  this  disease. 

A  few  months  ago  a  patient  was  admitted  to  the  medical  service  of  the 
Johns  Hopkins  Hospital  with  gangrene  and  anaesthesia  of  both  lower  ex- 
tremities, due  to  plugging  of  the  abdominal  aorta  by  such  an  embolus.  He 
has  a  well-marked  mitral  stenosis,  with  purring  presystolic  thrill  and  loud 
presystolic  rumble,  showing  that  his  left  auricle  was  contracting  vigorously. 
Needless  to  say,  nothing  could  be  done  to  relieve  him,  and  he  died  within 
a  few  days. 

TREATMENT   OP   MITRAL   STENOSIS. 

As  regards  indications  for  treatment,  cases  of  mitral  stenosis  fall  into 
several  groups. 

I.  1.  Compensated  cases  with  regular  pulse-rate. 

2.  Occasional  extrasystoles  with  some  cardiac  weakness  or  occasional 
attacks  of  paroxysmal  tachycardia. 

II.  Paroxysmal   or   permanent   arrhythmia   with   or   without   broken 
compensation. 

III.  Broken  compensation. 

In  the  mildest  and  most  chronic  forms  the  treatment  is  mainly  prophy- 
lactic and  the  patients  may  often  be  kept  free  from  symptoms  for  years  by 


456  DISEASES  OF  THE  HEART  AND  AORTA. 

maintaining  a  carefully  regulated  life,  by  taking  special  precautions  against 
overstrain,  anaemia,  and  infectious  diseases. 

All  foci  of  infection  should  be  carefully  looked  for  and  eradicated. 
Diseased  tonsils  and  abscessed  teeth  should  be  removed,  furuncles  and  foci 
of   pyorrhoea  alveolaris   vigorously   treated,   suppurations   of    the   various 
sinuses  and  of  the  sexual  organs  treated  or  drained. 
-"-"'    When  bronchitis  is  present  it  may  bring  on  a  vicious  circle: 

Bronchial 
congestion  and 
infection 


/  \ 


Pulmonary    ^ Reinfection  of  and  increase 

stasis  of  cardiac  lesion, 

and  therefore  it  should  be  treated  carefully. 

The  patient  should  be  protected  as  far  as  possible  from  draughts  and 
severe  weather,  and  the  bronchial  condition  relieved  with  inhalations.  The 
writer  has  found  the  following  mixture  especially  soothing: 

R  Menthol 2  G.  ^ss 

Eucalyptol 5  3  iss 

Camphor 5  3  iss 

Tr.  benzoin  co 30  %  i 

Alcohol 45  ^  iss 

Sig.     One  teaspoonful  in  boiling  water  for  inhalation. 


Pulmonary  tuberculosis,  though  not  extremely  uncommon,  must  not 
be  overlooked ;  and  must  be  vigorously  treated  by  the  usual  methods .  Anaemia 
is  such  a  potent  factor  in  keeping  up  the  cedema  infiltrations  of  the  valves 
that  when  present  it  deserves  special  attention.  Anaemic  patients  should  be 
given  complete  rest  and  diet  rich  in  eggs  and  milk,  some  form  of  iron, 
especially  Vallet's  mass  (0.3  G.,  gr.  v),  Blaud's  pills,  or  the  saccharated 
oxide  of  iron  (Ferrum  oxidatum  saccharatum, — one  teaspoonful  in  water). 
When  the  haemoglobin  is  low,  arsenic  (Fowler's  or  Donovan's  solution)  may 
be  given. 

The  patients  whose  compensation  in  itself  remains  good  but  who  suffer 
occasionally  from  the  palpitation  and  discomforts  attending  extrasystoles 
and  paroxysmal  tachycardia  which  owe  their  origin  to  the  distended  left 
auricle  present  a  condition  which,  though  as  a  rule  not  dangerous,  is  difficult 
to  relieve,  for  it  bears  a  closer  relation  to  the  heightened  irritability  than  to 
lessened  contractibility  of  the  heart  muscle  (see  page  108). 

Drugs  of  the  digitalis  series  affect  this  condition  only  occasionally,  and 
no  remedy  has  thus  far  proved  of  great  use. 

The  cheerful  side,  however,  is  found  in  the  fact  that  in  many,  though  by 
no  means  the  majority  of  instances,  the  patient's  actual  strength  and  his 
outlook  may  not  be  seriously  impaired  by  the  occurrence  of  these  disturbances. 
Extrasystoles,  when  not  associated  with  signs  of  cardiac  failure  or  weakness, 


MITRAL  STENOSIS.  457 

may  be  disregarded,  even  though  when  accompanied  by  cardiac  weakness 
they  may  have  a  serious  import.  The  same  is  true  of  paroxysmal  tachycardia, 
although  in  the  latter  the  cardiac  failure  due  to  the  paroxysm  itself  may  be 
entirely  out  of  proportion  to  the  slight  disturbance  of  the  circulation  from 
the  mitral  stenosis.  The  management  of  this  condition  is  discussed  on 
page  700. 

Mitral  Stenosis  with  Absolute  Arrhythmia  and  Auricular  Fibrillation. — 
It  is  in  the  cases  of  mitral  stenosis  with  transitory  or  permanent 
arrhythmia  resulting  from  fibrillation  of  the  auricle  that,  as  Mackenzie 
and  Lewis  have  shown,  the  most  brilliant  improvements  are  to  be  obtained 
(page  256). 

In  these  cases  the  symptoms  are  to  a  great  extent  due  in  part  to  stasis 
in  the  left  auricle,  pressure  upon  the  bronchi  and  the  recurrent  laryngeal 
nerve,  congestion  of  the  pulmonary  circulation,  and  at  times  cedema  of  the 
lungs,  and  in  part  to  diminished  filling  of  the  arterial  blood-vessels. 

This,  as  the  experiments  of  Hirschfelder  and  Wolfsohn  have  shown,  is 
due  largely  to  the  fact  that  in  mitral  stenosis  the  ventricles  fill  more  slowly 
than  normally  during  diastole,  and  moreover  that  in  this  condition  the  pump- 
ing action  of  the  auricles  assumes  a  role  of  importance  about  equal  to  that  of 
the  passive  filling;  so  that,  when  the  latter  factor  is  eliminated  by  fibrillation 
and  the  diastoles  are  shortened  by  a  rapid  heart-rate,  the  filling  of  the  ven- 
tricle is  greatly  impeded,  the  pulmonary  circulation  becomes  overfilled,  and 
the  outflow  into  the  arteries  becomes  diminished.  — 

In  mitral  stenosis  more  than  in  any  other  condition  the  value  of  digitalis 
shows  itself,  but  by  no  means  always  to  the  same  degree.  Indeed,  no  other 
valvular  lesion  furnishes  such  striking  contrasts  in  the  usefulness  of  digitalis. 
If  the  heart  is  regular  and  rapid  digitalis  may  be  entirely  without  avail,  since 
its  effects  in  slowing  the  regular  heart  are  slight  at  best.  In  pure  mitral  steno- 
sis the  effect  on  tonus  does  not  show  itself  at  all,  since  the  left  ventricle  is 
not  dilated;  but  where  any  considerable  grade  of  mitral  insufficiency  and 
dilatation  exist,  the  favorable  effect  of  the  drug  in  these  conditions  may  mani- 
fest itself.  In  the  paroxysmal  tachycardia  and  auricular  flutter  which  occur 
in  mitral  stenosis  more  than  in  any  other  condition,  digitalis  is  of  little  use 
unless  it  acts  first  to  convert  the  allorrhythmia  into  an  auricular  fibrillation. 

But  it  is  in  the  condition  of  auricular  fibrillation  which  occurs  more 
commonly  in  old  cases  of  mitral  stenosis  than  in  any  other  condition  that 
digitalis  exerts  the  most  striking  effects  ever  seen  in  the  practice  of  medi- 
cine— the  rapid  heart  becomes  slow,  the  respiratory  distress  disappears, 
swelling  of  liver  and  legs  vanishes,  the  patient's  strength  rapidly  returns,  and 
all  the  desired  therapeutic  effects  may  be  brought  about  in  many  cases  by 
the  proper  administration  of  the  drug. 

In  order  to  secure  the  full  benefit  in  these  cases,  as  stated  on  page  256, 
the  drug  must  be  administered  in  sufficient  doses  over  a  sufficient  period  of 
time  and  must  be  kept  up  as  long  as  the  arrhythmia  lasts.  In  general,  three 
or  four  doses  of  50  minims  of  the  (physiologically  standardized)  tincture  of 
digitalis  at  four  hourly  intervals,  followed  by  fifteen-minim  (1  c.c.)  doses 
until  the  pulse-rate  falls  below  70,  will  suffice  to  bring  about  improvement 
without  danger  of  cumulative  action.     If  the  larger  doses  are  continued  too 


h^r 


458  DISEASES  OF  THE  HEART  AND  AORTA. 

long,  the  period  of  full  benefit  may  be  only  transitory,  and  may  be  replaced 
by  several  weeks  during  which  the  patient  may  be  troubled  by  palpitation 
("  uncomfortable  thumping  "  of  the  heart),  weakness,  and  peculiar  sensa- 
tions in  the  extremities,  which  one  patient  of  the  writer's  described  as  "  feeling 
as  though  her  limbs  were  empty." 

The  two  extremes,  therefore,  of  too  much  and  too  little  digitalis  must  be 
carefully  avoided  in  each  case,  if  the  best  results  are  to  be  attained,  but  the 
amount  of  digitalis  and  the  time  necessary  to  bring  this  about  vary  with  each 
individual,  and  indeed  with  each  attack.  To  slow  the  pulse  and 
keep  it  slow  must  be  the  aim  in  those  patients. 

In  unfortunate  contrast  to  these  cases  of  mitral  stenosis  with  absolute 
arrhythmia  are  the  patients  whose  pulse,  in  spite  of  failing  compensation, 
remains  regular,  either  because  the  muscle  of  the  auricle  becomes  atrophied 
or  because  it  remains  strong  enough  to  carry  out  its  share  of  coordinate  con- 
tractions throughout. 

In  these  patients  the  effect  of  digitalis  is  confined  to  its  action  on  force 
and  on  tonicity. 

In  the  milder  cases  of  cardiac  failure,  and  especially  those  in  which  the 
latter  has  been  of  short  duration,  this  treatment  alone  may  suffice;  but  in 
patients  whose  heart  has  been  weak  and  rapid  for  some  time  it  no  longer  has 
much  effect  in  slowing  the  heart.  This  may  be  on  account  of  exhaustion  of 
the  vagi,  or  else  be  due  to  the  simultaneous  stimulation  of  the  accelerators. 
Accordingly,  in  cases  of  this  type,  digitalis,  and  other  drugs  as  well,  cannot 
be  relied  upon,  and  treatment  must  be  directed  along  the  lines  of  rest,  grad- 
uated exercise,  and  careful  regulation  of  life. 

In  the  acute  heart  failure  of  mitral  stenosis  with  pulmonary  oedema, 
various  methods  for  tiding  over  the  crisis  must  be  resorted  to.  Atropine 
(0.5  to  1  mg.,  gr.  jyo  to  -$-$)  may  be  given  to  diminish  the  secretion  into 
the  bronchi  and  alveoli,  inhalations  of  amyl  nitrite  and  hypodermic  injections 
of  nitroglycerin  (0.5  to  1.5  mg.,  gr.  jyo  to  -jV)  to  lessen  the  peripheral  resist- 
ance; and  as  quickly  as  possible  an  attempt  should  be  made  to  increase  the 
force  of  the  heart  with  an  intravenous  injection  of  strophanthin  (0.5  to 
1  mg.,  gr.  jfo  to  eV)- 

If  the  patient  is  not  anaemic,  a  prompt  venesection  with  removal  of 
300  to  500  c.c.  of  blood  will  do  more  than  anything  else  to  relieve  the 
circulation,  and  should  be  resorted  to  promptly,  but  never  before  the 
haemoglobin  has  been  taken.  If  the  latter  is  in  the  vicinity  of  70  per 
cent.,  venesection  should  be  used  only  under  exceptional  circumstances, 
for  there  is  danger  of  impoverishing  the  blood  too  greatly  and  bringing 
on  cardiac  weakness  from  anaemia.  In  such  cases  a  gradual  cutting  off 
of  the  venous  return  by  bandages  upon  both  arms  and  both  legs,  as  recom- 
mended by  v.  Tabora  and  Tornai  (page  233),  has  been  found  to  have 
a  similar  action  without  removing  the  blood-corpuscles  from  the  body  and 
thus  without  bringing  on  the  symptoms  of  anaemia.  Care  must  be  taken 
that  the  bandages,  which  for  this  purpose  may  well  be  composed  of  ordi- 
nary elastic  tape,  must  compress  the  arm  at  a  pressure  well  below  the 
diastolic  pressure,  so  as  to  impede  the  backflow  through  the  veins  but  not 
the  flow  through  the  arteries. 


PLATE  XVIII. 


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Typical  electrocardiogram  from  a  case  of  mitral  stenosis  showing  large  P  wave. 


EXSYS 


. 

\  Sm0****h$  *ftV*» 

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.  'm^sH  **p**» 

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Electrocardiogram  from  a  case  of  mitral  stenosis  with  permanent  arrhythmia  due  to  auricular  fibrillation, 
fclectrocaraiogram     ghowing  qqq  extrasy3toIo  (EX.SYS.)  arising  in  the  right  ventricle. 


MITRAL  STENOSIS.  459 

W.  Arbuthnot  Lane  and  later  (1902)  Sir  Lauder  Brunton  suggested 
that  in  the  light  of  modern  surgical  technic  it  might  be  possi- 
ble to  slit  the  narrowed  valve  with  a  fine  knife 
and  thus  remove  the  stenosis.  The  experiment  of  slitting  the  mitral  valve 
has  been  performed  by  Cushing  and  Branch  in  hearts  of  normal  dogs.  It 
does  not  present  extreme  difficulties,  but  the  recoveries  were  few,  in  spite 
of  the  fact  that  the  heart  muscle  of  these  dogs  was  in  good  condition. 
Bernheim  in  the  same  laboratory  arrived  at  similar  results.  Lauder 
Brunton  had  advocated  the  operation  only  for  cases  which  were  otherwise 
doomed;  and  it  is  evident  that  here  the  danger  from  a  weakened  myocar- 
dium would  be  far  greater.  Moreover,  even  if  successful,  the  mechanical 
effect  of  suddenly  converting  a  severe  mitral  stenosis  into  a  severe  mitral 
insufficiency  would  impose  an  intense  strain  upon  the  heart,  and  might, 
even  in  that  way,  do  more  harm  that  good. 

PROGNOSIS. 

In  spite  of  the  numerous  complications  and  the  progressive  character 
of  the  lesion,  the  average  duration  of  life  in  mitral  stenosis  is  not  extremely 
short,  being  33  years  for  males,  38  for  females.  This  is  due  to  the  fact  that 
the  pathological  process  is  usually  a  slow  and  very  chronic  one,  and  with 
careful  avoidance  of  infectious  diseases  and  overstrains,  it  may  remain  dor- 
mant for  years.  Lenhartz  has  seen  a  woman  with  mitral  stenosis  pass  through 
seven  pregnancies  without  trouble. 

When  heart  failure  and  persistently  rapid  heart  rate  set  in,  the  prog- 
nosis depends  upon  the  presence  or  absence  of  auricular  fibrillation.  If  the 
heart  rate  is  regular,  digitalis  can  do  little  and  the  prognosis  may  be  highly 
unfavorable.  If  there  is  fibrillation,  digitalis  can  usually  be  counted  on  to 
slow  the  heart  rate,  and  amelioration  may  set  in,  in  even  the  most  desperate 
cases. 

In  severe  cases  with  prolonged  stasis,  embolism  is  always  to  be  feared. 

BIBLIOGRAPHY. 

Mitral  Stenosis. 

Mayow,  John,  and  Vieussens.    Quoted  from  Huchard,  Maladies  du  cceur,  vol.  iii,  3d  ed., 

Paris,  1905. 
Sansom,  A.  E.:  The  Pathological  Anatomy  and  the  Mode  of  Development  of  Mitral 

Stenosis  in  Children,  Am.  J.  M.  Sci.,  Phila.,  1908,  xcix,  229. 
Gillespie,  A.  Lockhart:  An  Analysis  of  2368  Cases  Admitted  with  Cardiac  Lesions  into  the 

Royal  Infirmary,  Edinburgh,  Edinb.  Hosp.  Rep.,  1898,  v,  31. 
Cheadle.    Quoted  from  Sansom. 

Samways,  D.  W.:  Mitral  Stenosis,  a  Statistical  Inquiry,  Brit.  M.  J.,  1898,  i,  364. 
Duroziez.    Quoted  from  Petit. 
Duckworth,  Dyce:  On  the  Etiology  of  Mitral  Stenosis,  St.  Barth.  Hosp.  Rep.,  Lond.,  1877, 

xiii,  263. 
Goodhart,  J.  H.:  On  Anaemia  as  a  Cause  of  Heart  Disease,  Lancet,  Lond.,  1880,  i,  479. 
Meisenburg:  Ueber  das  gleichzeitige  Vorkommen  von  Herzklappenfehlern  und  Lungen- 

schwindsucht,  Ztschr.  f.  Tuberkl.  u.  Heilstattenwesen,  1902,  iii,  378. 
Tileston,  W. :  Passive  Hyperemia  of  the  Lungs  and  Tuberculosis,  J.  Am.  M.  Asso.,  Chicago, 

1908,  1,  1179. 


460  DISEASES  OF  THE  HEART  AND  AORTA. 

Bettelheim,  K.,  and  Kauders,  F.:  Experimentelle  Untersuchungen  ueber  die  kiinstlich 

erzeugte  Mitralinsufficienz  und  ihren  Einfluss  auf  Kreislauf  und  Lunge,  Klin,  exper. 

Unters.  a.  d.  Lab.  S.  v.  Basch,  Berl.,  1891,  i,  144. 
Kornfeld,  S.:  Experimentelle  Beitrag  zur  Lehre  vom  Venendruck  bei  Fehlern  des  linken 

Herzen,  ibid.,  1892,  ii,  126. 
Gerhardt,  D.:  Ueber  die  Compensation  von  Mitralfehlern,  Arch.  f.  exper.  Pathol,  u.  Phar- 

makol.,  Leipz,  1901,  xlv,  186. 
MacCallum,  W.  G.,  and  McClure,  R.:    On  the  Mechanical  Effects  of  Mitral  Stenosis  and 

Insufficiency,  Tr.  Ass.  Am.  Phys.,  Phila.,  1906,  xxi,  5;  also  Bull.  Johns  Hopkins  Hosp., 

Baltimore,  1906,  xvii,  260. 
Hirschf elder,  A.  D. :  The  Volume  Curve  of  the  Ventricles  in  Experimental  Mitral  Stenosis 

and  its  Relation  to  Physical  Signs,  Bull.  Johns  Hopkins  Hospital,  Baltimore,  1908,  xix. 
M  tiller,   G.:   Ungewohnliche  Dilatation  des  Herzens  und  Ausfall    der  Vorhofsfunction, 

Ztschsr.  f.  klin.  Med.,  Berl.,  1905,  Ivi,  520. 
Harris,  Th.     Quoted  on  p.  426. 
Petit,  A.:  Retrecissement  mitrale,  Traite  de  Med.  (Charcot,  Bouchard,  Brissand),  Paris, 

1893,  v,  247. 
Corvisart,  J.  N.:  An  Essay  on  the  Organic  Diseases  of  the  Heart,  etc.,  translated  by  Jacob 

Gates,  Phila.,  1812. 
Gendrin  and  Fauvel:  Arch,  de  Med.,  Paris,  1843,  Ser.  iv,  i,  1.    Quoted  from  Gairdner. 
Gairdner,  W.  T.:  A  Short  Account  of  Cardiac  Murmurs,  Edinb.  M.  J.,  1861,  vii,  428;  also 

Clinical  Medicine,  1862. 
Mackenzie,  James:  The  Study  of  the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903. 

The  Extrasystole,  etc.,  I,  Quart.  J.  M.,  Lond.,  1907,  i,  131,  481. 
Minkowski,  O.:  Demonstration  eines  Herzens  mit  ungewohnlich  starker  Dilatation  der 

Vorhofe,  Munchen.  med.  Wchnschr.,  1904,  li,  182. 
Hofbauer:   Rekurrenslahmung   bei    Mitralstenose,    Wien.   klin.   Wchnschr.,    1902.      Also 

Alexander:  Berl.  klin.  Wchnschr.,  1904;  and  Frischauer:  Wien.  klin.  Wchnschr..  1905. 

Quoted   from    Thorel,    C:      Pathologie    der    Kreislauforgane,    Lubarsch-Ostertag's 

Ergebnisse  der  Path.,  Wiesb.,  1907,  ii,  iite  Abth.,  386. 
Osier,  W. :  De  la  paralysie  du  nerf  recurrent  gauche  dans  les  affections  mitrales,  Arch,  des 

malad.  d.  cceur,  Par.,  1909,  ii,  73.    Reviewed  in  an  editorial,  J.  Am.  M.  Ass.,  Chicago, 

1909,  liii,  35. 
Einthoven,  W.,  with  the  assistance  of  Flohil  and  Battaerd:    Die  Registrirung  der  mensch- 

lichen  Herztone  mittelst  des  Saitengalvanometers,  Arch.  f.  d.  ges.  Physiol.,  Bonn, 

1907,  cxvii,  461. 
Brockbank,  E.  M.:  The  Murmurs  of  Mitral  Disease,  Edinb.  and  Lond.,  1899. 
Fenwick,  W.  S.,  and  Overend,  W.:  The  Production  of  the  First  Cardiac  Sound  in  Mitral 

Stenosis,  Am.  J.  M.  Sci.,  Phila.,  1893,  ex,  123. 
Haycraft,  J.  B.:  The  Cause  of  the  First  Sound  of  the  Heart,  J.  Physiol.,  Camb.,  1890,  xi, 

486. 
Broadbent,  W.  H.,  and  J.  F.  H.:  Heart  Disease  and  Aneurism,  N.  Y.,  1906. 
Acland.    Quoted  from  Fenwick  and  Overend. 
Steell,  G. :  The  Auscultatory  Signs  of  Mitral  Obstruction  and  Regurgitation,  Med  Chron., 

Manchester,  1888,  viii,  89.    The  Diagnosis  of  Mitral  Regurgitation  through  a  Con- 
stricted Orifice,  ibid.,  1891-2,  xv,  361.     The  Conduction  of  the  Murmur  of  Mitral 

Regurgitation,  ibid.,  1892,  xvi,  116.     The  Distinction  between  Mitral  Stenosis  and 

Muscle-failure  in  Certain  Heart  Cases,  ibid.,  1892-3,  xvii,  24.    The  Auscultatory  Signs 

of  Mitral  Stenosis;  a  Statistical  Inquiry,  ibid.,  1895,  N.  S.  iii,  409.    Case  of  Mitral 

Stenosis  Presenting  a  Widely  Distributed  Tc-and-fro  Murmur  Resembling  that  of 

Aortic  Incompetence,  ibid.,  1896-7,  N.  S.  vi,  174.      Mitral  Stenosis,  Internat.  Clin., 

Phila.,  1898,  s.  viii,  iii,  1411. 
Huchard:  1.  c,  p.  673. 
Cabot,  R.  C,  and  Locke,  E.  A.:  On  the  Occurrence  of  Diastolic  Murmurs  without  Lesions 

of  the  Aortic  or  Pulmonary  Valves,  Bull.  Johns  Hopkins  Hosp.,  Baltimore,  1903,  xiv, 

115. 
Bard,  L.:  Die  Phvsikalische  Zeichen  der  Mitralstenose,  Samml.  klin.  Vort.,  Leipz.,  No.  45. 

Inn.  Med.  No.  137,  1907. 


MITRAL  STENOSIS.  461 

Flint,  A.:  The  Mitral  Cardiac  Murmurs,  Am.  J.  M.  Sc,  1886,  xci,  27. 

Phear,  A.  G.:  On  Presystolic  Apex  Murmur  without  Mitral  Stenosis,  Lancet,  Lond.,  1895, 

ii,  718. 
Weber  and  Deguy:     Du  role  des  hsemorrhagies  intracardiaques  dans  le  retrecissement 

mitral,  Arch,  de  Med.  Exper.,  Par.,  1897,  and  Presse  med.,  Par.,  1898. 
Sewall,  H. :  A  Common  Modification  of  the  First  Heart  Sound,  etc.,  Trans.  Ass.  Am.  Phys., 

Phila.,  1909,  and  Am.  J.  M.  Sc,  1909. 
Brunton,  T.  Lauder:  Preliminary  Note  on  the  Possibility  of  Treating  Mitral  Stenosis  by 

Surgical  Methods,  Lancet,  Lond.,  1902,  i,  352.     Discussed  by  Shaw,  L.  E.,  ibid., 

1902,  i,  619. 
Cushing,  H.  W.,  and  Branch,  J.  R.  B.:    Experimental  and  Clinical  Notes  on  Chronic  Val- 
vular Lesions  in  the  Dog  and  their  Possible  Relation  to  a  Future  Surgery  of  the  Cardiac 

Valves,  J.  Med.  Research,  1908,  xii. 
Bernheim,  B.  M.:  Experimental  Surgery  of  the  Mitral  Valve,  Johns  Hopkins  Hospital 

Bull.,  Baltimore,  1909,  xx,  107. 


IV. 

AORTIC  INSUFFICIENCY. 


HISTORICAL. 

Our  knowledge  concerning  lesions  of  the  aortic  valves  producing  leak- 
age at  that  orifice  (aortic  insufficiency,  aortic  regurgitation,  aortic  incom- 
petency) dates  from  1705,  when  the 
English  anatomist  Cowper  first  de- 
scribed the  occurrence  of  stiffening 
and  thickening  of  the  valves  so  that 
they  "did  not  apply  adequately  to 
each  other,  whence  it  happened  some- 
times that  the  blood  in  the  great 
artery  would  recoil  and  interrupt  the 
heart  in  its  systole."  Shortly  after 
this,  and  quite  independently  of  Cow- 
per, Vieussens  (1715)  described  two 
similar  cases,  noting  also  the  presence 
of  a  very  full  quick  pulse,  like  the 
rebound  of  a  tightly-stretched  cord, 
associated  with  palpitation  of  the 
heart  so  severe  that  it  prevented  lying 
down.  Morgagni  also  described  sev- 
eral cases,  in  one  of  which  he  recog- 
nized both  aortic  insufficiency  and 
aortic  stenosis.  Hodgkin  in  1829  de- 
scribed a  number  of  cases,  and  also 
noted  for  the  first  time  the  diastolic 
murmur,  but  did  not  recognize  any 
diagnostic  features;  so  that  the  clear 
clinical  picture  of  aortic  insufficiency  may  be  said  to  date  from  the 
publication   of   Dominic   Corrigan  in   1832. 


'/:      •;'■■     \\\ 


K%^ 


wk;«ms* 


Fig.  201.  —  Specimen  showing  vegetations 
upon  the  aortic  valves.  The  arrow  points  to  the 
vegetation. 


PATHOLOGICAL    ANATOMY. 

Modern  classifications  of  aortic  insufficiency  differ  little  from  that  of 
Corrigan,  and  we  distinguish,,  as  he  did — 

1.  Organic  forms  of  aortic  insufficiency  due  to  pathological  changes  in  the  valves. 

2.  Functional  or  relative  aortic  insufficiency  due  to  dilatation  of  the  mouth  of  the 

aorta  (Fig.  202,  D). 

The  organic  forms  of  aortic  insufficiency  may  be  of  three  types: 

1.  Endocarditic,  due  to  the  occurrence  of  inflammatory  changes  upon  the  valves, 
usually  vegetations,  occasionally  to  calcified  atheromatous  plaques  (Fig.  202,  A). 

462 


AORTIC   INSUFFICIENCY. 


463 


2.  Rupture  of  the  valves,  sometimes  from  mechanical  strain,  sometimes  from  ulcera- 

tion (Fig.  202,  B). 

3.  Sclerotic  shrivelling  of  the  cusps,  usually  associated  with  arteriosclerosis   (Fig. 

202,  C),  especially  the  syphilitic  form. 

1.  The  pathology  of  the  endocarditic  lesions  has  been  sufficiently  dis- 
cussed in  a  preceding  chapter  (page  398),  since  they  represent  quite  typi- 
cal vegetations.  This  form  of  lesion  results  from  the  usual  causes  of 
endocarditis,  especially  rheumatism,  scarlet  fever,  pneumonia,  as  well  as 
gonorrhceal,  puerperal,  septicemic,  and  other  acute  infections  (see  page 
401).  It  is  the  most  common  form  in  persons  below  thirty-five,  whereas 
the  sclerotic  is  more  common  in  later  life. 

2.  Rupture  of  the  valves  is  one  of  the. less  frequent  but  by  no  means 
rare  occurrences,  and  usually  takes  place  suddenly  during  a  period  of  great 
muscular  strain,  such  as  wrestling,  lifting  a  heavy  weight,  drawing  a  heavy 
burden,  or  even  during  a  bicycle  race  (Huchard) ,  or  else  after  severe  blows 
upon  the  chest  (Osier).  Under  these  circumstances,  as  has  been  seen, 
the  blood-pressure  may  suddenly  rise  to  a  tremendous  height  (see  page  200), 


Fig.  202. — Schematic,  showing  the  various  forms  of  lesion  producing  aortic  insufficiency.     A.  Vegetation. 
B.  Perforation.     C.  Arteriosclerotic  shrinking.     D.  Dilatation  of  the  aorta. 


and  the  blood  stream  tears  its  way  through  the  valve  at  the  weakest  point — 
usually  near  the  base  of  the  sinus  of  Valsalva.  The  ruptured  valve  may 
have  an  apparently  normal  structure,  but  probably  contains  minute  areas 
of  degeneration,  since  it  is  impossible  to  rupture  a  normal  valve  experi- 
mentally by  subjecting  it  to  the  highest  pressures  that  are  ever  reached  in 
the  animal  body.  In  many  cases  the  ruptured  valves  show  arteriosclerotic 
changes  which  have  tended  to  weaken  the  tissue.  Where  endocarditic 
changes  are  already  present,  rupture  or  perforation  of  the  valve  takes  place 
spontaneously  and  at  ordinary  or  even  lowered  blood-pressures. 

3.  The  sclerotic  form  is  the  most  common  type  of  the  lesion,  and  is  brought 
about  by  a  progressive  fibrosis  of  the  valve  tissue  in  which  contraction,  thicken- 
ing, calcification,  aneurismal  dilatation  or  perforation  of  the  valve  may  be  pres- 
ent. The  process  is  in  all  the  essentials  similar  to  that  in  mesarteritis  and  is 
usually  associated  with  the  latter.  Here  also  extensive  vascularization  accom- 
panies the  fibrosis  (Fig.  172) .  In  any  individual  case  the  symptoms  depend  upon 
the  size  of  the  leak  as  well  as  upon  the  state  of  the  peripheral  vessels  and  heart. 

Although  the  usual  etiological  factors,  old  age,  hard  work,  tobacco,  lead 
poisoning,  nephritis,  etc.,  are  responsible  for  aortic  insufficiency,  one  of  the 
most  frequent  and  most  striking  single  factors  is  syphilis  (Osier).  Citron, 
Collins  and  Sachs,  Longcope,  and  others  have  found  positive  Wassermann 
reactions  in  about  half  their  cases,  and  Pearce  (Arch.  Int.  Med.,  1910,  vi, 
478),  who  has  tabulated  the  cases  reported  by  a  number  of  authors,  has  found 


464  DISEASES  OF  THE  HEART  AND  AORTA. 

it  positive  in  85  out  of  207  cases  (41  per  cent.),  while  in  other  valvular  diseases 
it  was  a  little  more  than  half  as  frequent  (23  per  cent.). 

When  the  cases  of  aortic  insufficiency  arising  in  childhood  and  those 
directly  traceable  to  rheumatic  infection  are  excluded,  the  proportion  due 
to  syphilis  looms  a  great  deal  larger.  A  certain  number  of  cases,  however, 
are  due  to  the  other  causes  of  arteriosclerosis,  infectious  diseases,  hard  work, 
worry,  heredity,  tobacco,  alcohol,  lead  poisoning. 

Sex. — In  women  aortic  insufficiency  is  far  less  frequent  than  in  men, 
constituting  8.4  per  cent,  of  all  heart  lesions  in  the  former  as  compared  with 
28.5  per  cent,  in  the  latter  (Gillespie). 

Moreover,  as  shown  by  Romberg  and  Hasenfeld,  the  presence  of  aortic 
insufficiency  from  causes  other  than  sclerosis  in  itself  leads  to  the  produc- 
tion of  general  arteriosclerosis,  and  hence  the  presence  of  any  other  form 
of  the  lesion  predisposes  to  the  superposition  of  sclerosis. 

Functional  Aortic  Insufficiency. — The  existence  of  leaks  at  a  dilated  aortic  orifice 
was  already  suspected  by  Corrigan,  especially  when  there  was  an  aneurism  near  the  base  of 
the  ascending  arch.  This  has  been  verified  by  subsequent  observers  and  a  diffusely  dilated 
aorta  with  insufficiency  of  the  valves  is  not  a  rare  finding.  As  regards  the  presence  of  tran- 
sitory leaks  from  dilatation  Gibson  has  also  shown  experimentally  that  such  a  dilata- 
tion may  occur  as  a  result  of  too  high  pressure  in  the  excised  heart,  and  Stewart  claims  to 
have  produced  it  by  cutting  the  aortic  ring  muscle.  But  since  transitory  aortic  insufficiency 
does  not  often  accompany  the  high  blood-pressures  of  uraemia,  meningitis,  and'brain  tumor, 
it  is  probable  that  this  factor  plays  little  role  clinically.  The  cases  of  supposed  functional 
aortic  insufficiency  are  rare,  but  Anders  has  reported  a  considerable  number.  In  some  at 
least  it  is  possible  that  the  phenomena  (diastolic  murmur,  collapsing  pulse,  etc.)  are  due 
to  other  causes,  especially  functional  pulmonary  insufficiency.  Cardiopulmonary 
murmurs,  like  those  described  by  Potain,  must  also  be  excluded.  However,  the  possi- 
bility of  functional  aortic  insufficiency  must  be  borne  in  mind  by  the  clinician;  but  it  can 
rarely  be  verified,  and  the  clinical  diagnosis  is,  at  best,  hazardous. 


Fig.  203. — Effect  of  aortic  insufficiency  in  the  mechanical  model.  (After  Marey.)  The  horizontal 
line  shows  the  point  of  production  of  aortic  insufficiency.  P.V.,  intraventricular  pressure;  PR,  arterial 
pressure;  O,  auricular  systole.  The  diastolic  pressure  in  the  ventricle  after  aortic  insufficiency  is  consid- 
erably higher  than  in  the  normal  condition  and  approximates  the  diastolic  pressure  in  the  aorta.  The 
wavelet  o',  due  to  contraction  of  the  auricle,  is  less  marked. 

PATHOLOGICAL    PHYSIOLOGY. 

The  mechanical  effects  of  aortic  insufficiency  upon  the  circulation  were 
first  studied  experimentally  in  horses  and  dogs,  as  well  as  on  the  mechanical 
model,  by  Marey  and  Chauveau. 


AORTIC   INSUFFICIENCY. 


465 


They  produced  the  lesion  by  pushing  a  probe  down  one  carotid  artery  and  through  a 
cusp  of  the  aortic  valve,  while  they  registered  the  pulsation  in  the  other  carotid  by  means 
of  a  cannula.  They  were  thus  able  to  reproduce  the  phenomena  observed  clinically, 
especially  the  occurrence  of  the  murmurs,  the  violent  beating  of  the  heart  and  arteries, 
and  the  large  collapsing  pulse  which  had  been  described  by  Corrigan.  They  were  also 
able  to  reproduce  these  phenomena  in  a  mechanical'  model  of  the  circulatory  system. 

The  experiments  of  Marey  and  Chauveau  on  animals  have  been  repeated  and  con- 
firmed by  Cohnheim,  Rosenbach,  de  Jaager,  Kornfeld,  Romberg  and  Hasenfeld,  and  those 
upon  the  model  by  Moritz.  The  subject  was  again  investigated  under  the  writer's  direction 
by  Dr.  H.  A.  Stewart  in  the  Johns  Hopkins  Medical  Clinic.  The  method  employed  by 
Stewart  differed  from  that  of  previous  observers  in  the  fact  that  he  recorded  simultaneously 
the  volume  of  the  ventricles,  the  maximal  and  minimal  blood-pressures,  and  the  pulse- 
curve  from  the  carotid  artery.  He  found  in  animals,  as  had  been  shown  by  Marey  upon 
the  mechanical  model,  that  the  production  of   aortic    insufficiency    is    at 


NORMAL 


II 

COMPENSATED 

LOW  PERIPHERAL 

RESISTANCE. 


Ill 

COMPENSATED 

HIGH  PERIPHERAL 

RESISTANCE 


IV 

BROKEN 
PULMONARY 

COMPENSATION 


Fig.  204. — Diagram  of  the  circulation  in  aortic  insufficiency.  The  vertical  black  bars  represent  the 
volume  of  the  left  ventricle,  the  shaded  portions  representing  the  residual  blood,  the  portions  indicated  by 
the  white  arrows  showing  the  amount  of  blood  regurgitating,  the  solid  black  indicating  the  systolic  output. 
The  black  arrows  indicate  the  change  in  condition  or  pressure  that  has  taken  place.  MAX,  MIN,  maxi- 
mal and  minimal  blood-pressures.  The  white  curve  indicates  the  absolute  sphygmogram  corresponding. 
AO,  PA,  RA,  LA  as  in  previous  diagrams.     (Compare  with  Fig.  26.) 

once  followed  by  a  great  fall  in  pressure:  during  diastole,  which  is,  at 
least  in  part,  due  to  the  regurgitation  into  the  ventricle.  This  great  fall  in  diastolic  pressure 
is  the  most  characteristic  feature  of  aortic  insufficiency. 

The  actual  amount  of  blood  regurgitating,  both  in  animals  (Stewart) 
and  in  model  experiments  (Moritz),  is  usually  not  more  than  one-tenth  of  the  total 
forced  out  at  each  systole,  though  MacCallum  has  sometimes  found  larger  quan- 
tities. Simple  calculations  of  the  pulse-pressure  in  Fig.  214  show  that  this  amount  of 
leakage  during  diastole  would  account  for  the  low  diastolic  pressure. 

The  factors  influencing  leakage  are :  (1)  the  size  of  the  hole  in  or  between 
the  valves;  (2)  the  head  of  pressure  in  the  aorta;  (3)  the  length  of  time 
during  which  leakage  occurs. 

Cardiac  Tonicity. — The  experiments  performed  by  Stewart  and  the 
writer  indicate  that  the  chief  factor  antagonizing  the  reflux  is  the  elasticity 
of  the  heart  muscle,  or  the  cardiac  tonicity. 

It  is  evident  that,  with  a  given  lesion  and  a  constant  heart  rate,  the 

factor  affecting  the  regurgitation  is,  therefore,  the  antagonism  between  the 

height  of  blood-pressure  during  diastole,  on  the  one  hand,  and  the  cardiac 

tonicity,  on  the  other.     However,  the  pressure  within  the  ventricle  is  not 

30 


466 


DISEASES   OF   THE   HEART   AND    AORTA. 


constant  throughout  diastole,  but  is  continually  increasing;  while  the  pres- 
sure in  the  aorta  is  continually  decreasing,  and  the  reflux  will  cease  alto- 
gether at  the  instant  when  pressure  within  the  ventricle  +  cardiac  tonicity 
=  pressure  within  the  aorta.  Consequently,  the  lower  the  pressure  in  the 
aorta  (diastolic  pressure)  or  the  higher  the  cardiac  tonicity,  the  earlier  this 
will  occur  and  the  less  will  be  the  amount  of  blood  regurgitating. 


AORTIC  PRESSURE 
INTRAVENTRICULAR  PRESSURE 

AMOUNT  OF  BLOOD 
REGURGITATING 


Fig.  205. — Diagram  showing  how  the  high  cardiac  tonicity  (T  +)  hastens  the  equilibrium  between  aortic 
pressure,  intraventricular  pressure,  and  tonicity,  and  thus  diminishes  the  amount  of  blood  regurgitating. 

It  was  found,  however,  that  whenever  this  occurred  the  hearts 
dilated  and  the  animals  died.  Those  animals  which  survived  the  shock  of 
the  operation  were  able  to  increase  their  systolic  output  by  the  amount 
regurgitated,  and  thus  in  spite  of  the  lesion  to  keep  the  maximal  pressure 
at  the  same  height  as  before.  In  these  animals  positive  intraventricular 
pressure  during  diastole  acts  as  a  load  to  the  heart  muscle,  which  responds 


WIMMAMMAA 


T  + 


NORMAL 


DILATATION 


DIMINUTION    IN    VOLUME 


Fig.  206. — Effect  of  rupturing  an  aortic  valve  in  a  dog,  showing  a  transitory  dilatation  followed  by  a 
permanent  diminution  in  size.  (After  Stewart.)  CAR.,  carotid;  VOL.,  volume  of  the  ventricles.  Down- 
strokes  represent  systole,  upstrokes  diastole.  The  maximal  blood -pressure  remains  unchanged  (122  mm. 
Hg),  the  minimal  pressure  falls  from  90  to  45  mm.  Systolic  output  is  somewhat  increased,  a-b  repre- 
sents the  tonicity  of  the  ventricles  before  producing  the  lesion;  c-d  represents  tonicity  after  the  lesion.  A 
represents  the  point  at  which  the  aortic  valve  was  ruptured. 

by  increased  tonicity,  and  fills  somewhat  less  completely  than  it  otherwise 
would;  so  that  the  total  volume  of  the  ventricles  after  aortic  insufficiency, 
just  as  after  any  other  strain,  may  be  smaller  than  before  it.  In  these  hearts 
total  volume  is  decreased,  systolic  output  increased,  and  residual  blood 
greatly  decreased. 

Romberg  and  Hasenfeld  (1.  c.)  have  denied  that  this  increased  tonicity  is  always 
beneficial,  claiming  that  by  inhibiting  the  inflow  from  the  auricle  it  impedes  the  circulation. 
However,  Kornfeld  found  that  the  pressure  in  the  left  auricle  is  not  affected  by  experi- 


AORTIC   INSUFFICIENCY.  467 

mental  aortic  insufficiency  as  long  as  the  strength  of  the  left  ventricle  remains  unimpaired. 
According  to  MacCallum  (Johns  Hopkins  Hosp.  Bull.,  1911,  xxii,  197),  the  nourishment 
of  the  myocardium  (and  hence  the  force  of  the  heart)  is  largely  influenced  by  the  general 
blood-pressure.    There  is  an  optimum  pressure  for  each  heart. 

As  regards  the  role  played  by  tonicity  in  aortic  insufficiency  two  views 
are  held: 

1.  Romberg  and  Hasenfelcl  claim  that  an  increased  tonicity  hindering 
the  influx  of  blood  from  the  auricle  is  distinctly  harmful. 

2.  Stewart  and  the  writer  have  shown  that  the  most  dangerous  event 
in  experimental  aortic  insufficiency  is  overdilation,  and  this  is  antagonized 
by  increase  in  tonicity.  Moreover,  Cloetta  has  found  that  the  hearts  of 
rabbits  with  experimental  aortic  insufficiency  which  had  been  treated  with 
digitalis  were  less  dilated  and  were  much  stronger  than  those  of  normal 
rabbits.  Almost  all  the  influences  which  bring  about  increased  systolic 
output  are  the  same  as  produce  increase  in  tonicity.  Fear  of  evil  results 
from  this  cause  seems,  therefore,  quite  unwarranted. 

Blood=pressure. — As  regards  blood-pressure,  it  was  found  that  when 
the  peripheral  resistance  was  increased,  as  by  clamping  the  thoracic  aorta, 
the  force  of  the  heart-beat  increased  correspondingly,  and  both  maximal 
and  minimal  (systolic  and  diastolic)  pressures  increased  about  equally 
and  pulse-pressure  remained  high.  With  the  increase  in  diastolic  pressure 
upon  clamping,  the  regurgitation  through  the  orifice  increased  (Fig.  214), 
and,  as  systolic  output  changed  no  further,  the  heart  dilated  considerably, 
showing  that  high  peripheral  pressure  represents  the  condition  which 
produces  the  greatest  embarrassment  of  the  circulation.  With  the  increase 
in  peripheral  pressure,  however,  the  form  of  the  pulse  curve  changed 
from  collapsing  to  flat-topped  and  anacrotic,  a  fact  which  will  be  referred 
to  later. 

Rate. — Corrigan  thought  that  if  the  heart  were  slowed  and  diastole 
were  prolonged  the  heart  would  undergo  great  dilatation,  but  in  the  experi- 
ments performed  by  Stewart  and  the  writer  it  can  be  seen  that  this  dilata- 
tion soon  reaches  its  limit,  and  the  volume  of  the  ventricles  need  not  exceed 
the  normal  volume  for  the  same  rate  (Fig.  206).  This  is  due  to  the  fact 
that,  as  the  aortic  pressure  falls  during  a  prolonged  diastole,  it  approaches 
the  intraventricular  pressure,  and  the  above-mentioned  equilibrium  is 
soon  reached. 

As  a  result  of  experiments  upon  animals,  it  would  appear,  therefore, 
that  the  conditions  most  favorable  to  the  heart  are  low  peripheral  resist- 
ance and  moderately  high  tonicity;  and,  as  will  appear  later,  therapy  should 
be  directed  toward  this  end. 

Pulmonary  Circulation. — As  stated  above,  Kornfeld's  experiments 
show  that  the  aortic  lesion  has  no  effect  upon  the  pulmonary  circulation  as 
long  as  the  left  ventricle  is  acting  powerfully.  When  the  left  ventricle 
begins  to  fail,  pulmonary  stasis  and  rise  in  auricular  pressure  occur  (Korn- 
feld) ,  which,  as  Stewart  and  the  writer  have  found,  are  frequently  associated 
with  the  occurrence  of  a  functional  mitral  insufficiency.  Pulmonary  stasis 
in  aortic  insufficiency  is,  therefore,  a  secondary  phenomenon  dependent 
upon  failure  of  the  left  ventricle.  The  clinical  importance  of  this  fact  will 
be  referred  to  subsequently. 


468  DISEASES   OF   THE   HEART   AND    AORTA. 

Hypertrophy. — As  a  result  of  the  increased  strain  upon  the  left  ventricle, 
the  walls  of  this  chamber  undergo  great  hypertrophy.  The  cavity  of  the  left 
ventricle,  owing  to  the  regurgitation  during  diastole,  is  often  much  dilated, 
especially  in  the  infrapapillary  or  aortic  portion  of  the  chamber. 

The  left  auricle,. on  the  other  hand,  is  rarely  hypertrophied.  The  right 
ventricle,  however,  usually  shows  some  hypertrophy,  resulting  either  from 
slight  increase  in  pulmonary  pressure  or  from  continuity  of  the  fibres  with 
those  of  the  left  ventricle. 

SYMPTOMS. 

The  symptomatology  of  aortic  insufficiency  differs  considerably  from 
that  of  the  mitral  lesions.  When  the  lesion  is  well  compensated  and  no 
pulmonary  stasis  occurs,  dyspnoea  may  not  appear  for  years,  and  in  the 
meantime  the  patient  may  enjoy  excellent  health.  On  the  other  hand, 
he  may  also  be  considerably  annoyed  by  the  throbbing  of  his  arteries, 
headache,  roaring  in  the  ears,  by  loss  of  memory,  by  periods  of  depression 
often  alternating  with  periods  of  great  exhilaration,  by  the  appearance  of 
motes  or  muscse  volitantes  before  the  eyes. 

Hallucinations  of  sight,  especially  that  of  the  veiled  gray  figure,  of  hearing 
(rhythmic  knocking  or  bell-tolling),  and  of  smell  are  relatively  common  in  aortic  disease, 
and  are  usually  associated  with  pain  in  the  precordium  or  down  the  arms  and  tenderness 
over  the  upper  left  chest  (Head) .  Head  states  that  these  always  disappear 
when  mitral   insufficiency  sets  in. 

There  are  often  pains  over  the  heart,  especially  over  the  base,  and 
down  the  left  arm,  and  typical  attacks  of  definite  angina  pectoris.  These 
symptoms  are  especially  common  in  the  sclerotic  forms,  in  the  later  stages 
of  the  disease,  but  may  occur  even  when  the  coronary  arteries  are  unaffected. 
After  the  break  in  compensation,  dyspnoea  is  usually  intense,  and  the  patient 
is  compelled  to  sit  up  in  bed,  not  only  on  account  of  shortness  of  breath 
but  also  on  account  of  extreme  palpitation. 

Cheyne-Stokes  respiration  (of  the  cardiac  type)  is  some- 
what more  common  in  aortic  insufficiency  than  in  other  forms  of  cardiac 
disease.  This  is  probably  due  to  lack  of  oxygen  in  the  medulla,  leading  to 
rapid  breathing  and  overventilation  of  the  lungs. 

Sudden  agonizing  attacks  of  cardiac  asthma  are  very 
frequent,  accompanied  by  intense  orthopncea,  in  which  the  patient  gasps  for 
breath  for  several  minutes  or  even  half  an  hour.  Whether  this  is  brought  on 
by  overfilling  of  the  left  ventricle  and  pulmonary  stasis  or  by  anaemia  of  the 
medulla,  or  by  both  factors,  is  still  uncertain.  Sudden  death  may  occur 
during  such  attacks,  and  is  indeed  more  common  in  aortic  insufficiency  than 
in  other  forms  of  valvular  disease.  Both  the  maximal  and  the  minimal 
pressures  may  be  high  up  to  the  instant  of  death,  as  in  one  case  observed 
by  the  writer  in  which  the  blood-pressures  were  150  mm.  Hg  and  110  mm. 
respectively  until  the  instant  when  the  pulse  suddenly  ceased. 

PHYSICAL    EXAMINATION. 

The  appearance  of  persons  suffering  from  aortic  insufficiency  is  usually 
quite  characteristic.  The  eyes  are  bright,  with  conjunctivae  moist,  the 
pupils  often  dilated  and  palpebral  slits  wide,  giving  a  peculiar  staring  ap- 


AORTIC   INSUFFICIENCY.  469 

pearance  which  sometimes  for  an  instant  suggests  exophthalmic  goitre. 
The  sclera?  are  usually  pale  and  bluish.  The  cheeks  are  somewhat  sunken, 
the  complexion   usually  pale    and   sallow   (aortic  facies). 

One  of  the  features  which  at  once  attracts  the  attention  of  the  observer, 
as  already  the  case  with  Vieussens  in  1715,  is  the  intense  and  sudden  visi- 
ble pulsation  in  the  arteries,  especially  the  carotids,  temporals,  and 
brachials.  Often  this  pulsation  is  so  great  as  to  shake  the  entire  head, 
even  when  the  patient  is  asleep  (Frankel).  There  is  sometimes  a  visible 
pulsation  of  the  entire  uvula  (F.  Miiller)  and  of  the  arteries  in  the  retina 
(Becker). 

Not  only  the  larger  but  also  the  smaller  arteries  pulsate  visibly,  as 
can  be  seen  in  the  so-called  capillary  pulse  (Quincke),  the  to-and- 
fro  movement  of  the  red  border  of  an  area  of  hypersemicskin  synchronous 
with  each  pulse-wave.  This  can  be  observed  at  any  place  where  an  area 
of  erythema  borders  upon  an  area  of  pallor,  especially  along  the  margin 
of  an  area  of  skin  which  has  been  caused  to  redden  by  slight  friction,  beneath 
the  finger-nails,  or  in  the  lips  or  gums  when  gently  compressed  with  a  glass 
slide.  This  appearance  coupled  with  the  presence  of  the  bounding  and 
collapsing  pulse  is  usually  very  typical.  Indeed,  it  is  said  that  Oppolzer 
won  his  professorship  at  Vienna  by  casually  making  a  diagnosis  of  aortic 
insufficiency  while  walking  down  the  wards  of  the  hospital  and  merely 
resting  his  hand  upon  the  dorsum  of  the  patient's  foot. 

However,  Oppolzer  might  readily  have  come  to  grief  had  he  encountered  one  of  those 
not  very  rare  cases  in  which  all  these  phenomena  result  from  arteriosclerosis  alone.  Lenn- 
hoff,  v.  Weissmayer,  and  Huber  have  termed  these  cases  pseudo-aortic  insuffi- 
ciency. In  these  cases  the  arteries  are  large  and  rigid  and  there  is  a  high  pulse-pressure 
but  no  other  manifestations  of  aortic  insufficiency.  The  whole  phenomenon  is  due  to  a 
high  pulse-pressure  in  rigid  arteries  (page  359). 

The  chest  and  lungs  show  no  abnormalities  until  the  later  stages  of 
the  disease  are  reached  and  pulmonary  congestion  has  set  in  with  bronchitis, 
pulmonary  oedema,  or  hydrothorax. 

Cardiac  Impulse. — Over  the  heart  there  is  usually  some  bulging  of  the 
chest  wall,  and  usually  a  well-defined  apex  beat  in  the  fifth  or  sixth  inter- 
space to  the  left  of  the  mammillary  line.  The  impulse  is  systolic  in  time 
and  heaving  in  character  (dome-like,  "choc  en  dome"),  owing  to  the  fact 
that  the  entire  apex  is  usually  made  up  of  the  hypertrophied  left  ventricle 
(Bamberger).  In  the  second  right  interspace  there  is  often  another 
systolic  impulse,  caused  by  the  throbbing  aorta,  which  may  lead  to  the 
suspicion  of  aneurism. 

On  palpation  nothing  abnormal  is  noted  except  that  the  second  aortic 
shock  is  often  lacking.  In  about  40-50  per  cent,  of  the  cases  a  pre- 
systolic thrill  (Thayer)  and  in  15  per  cent,  a  tapping  systolic  shock 
may  be  felt  at  the  apex.  This  is  very  similar  to  that  observed  in  mitral 
stenosis  but  less  intense,  while  in  most  cases  the  impulse  is  strong  and 
heaving.  In  about  16  per  cent,  of  Thayer's  cases  an  actual  mitral  stenosis 
was  present  as  well,  and  this  association  must  always  be  borne  in  mind. 
Systolic  thrills  are  often  felt,  especially  over  the  aortic  area,  caused  by  the 
roughenings  of  the  aortic  valves,  and  also  over  the  apex  in  cases  where 
mitral  insufficiency  is  present. 


470 


DISEASES   OF  THE   HEART   AND   AORTA. 


Percussion  and  X=ray  Shadow. — As  stated  above,  the  cardiac  outline 
in  aortic  insufficiency  shows  a  marked  elongation  of  the  long  axis  (L),  due 
to  the  hypertrophy  and  dilatation  of  the  left  ventricle.  There  is  little 
increase  in  the  transverse  diameter  (Q),  so  that  the  area  of  cardiac  dulness 


BLOWING 
DIASTOLIC  MURMUR 

BLOWING 

DIASTOLIC  MURMUR 
(AXILLARY) 
PRESYSTOLIC 
RUMBLE  (FLINT) 


Fig.  207. — Area  of  cardiac  dulness  and  distribution  of  the  cardiac  sounds  and  murmurs  in  aortic 
insufficiency.  Heavy  curved  line,  outline  of  the  heart;  heavy  straight  line,  longitudinal  diameter. 
Parallel  lines  indicate  the  distribution  of  the  aortic  diastolic  murmur.  Black  dot  indicates  maximum 
intensity.  Small  circle  indicates  the  distribution  of  the  presystolic  rumble  (Flint).  Small  diagram  at  the 
left  indicates  the  murmur  heard  in  each  area. 

and  the  X-ray  show  (Figs.  207,  208,  and  209)  the  form  of  a  narrow  elongated 
oval  whose  long  axis  is  inclined  more  obliquely  downward  than  is  that  of 
the  normal  heart.    In  this  way  it  presents  a  marked  antithesis  to  the  out- 


Fig.  208. — Radiograph  of  a  case  of  aortic  insuf- 
ficiency, showing  elongation  of  the  long  axis  of  the 
heart.  (Kindness  of  Prof.  C.  M.  Cooper.)  The  plate 
is  at  the  back  of  the  patient,  the  tube  in  front. 


Fig.  209. — Diagram  of  Fig.  208,  showing  the 
hypertrophy  of  the  left  ventricle.  The  broken  line 
indicates  the  normal  cardiac  outline;  the  arrow  indi- 
cates the  direction  of  enlargement;  AO  indicates 
the  shadow  of  the  dilated  aortic  arch. 


line  of  mitral  stenosis,  in  which  the  oval  is  a  broad  and  rather  short  one, 
and  to  the  broad,  elongated  oval  of  mitral  insufficiency.  The  X-ray  shadow 
often  shows  a  marked  dilatation  of  the  aortic  arch,  which  may  correspond 
to  an  area  of  dulness  in  the  second  right  interspace  and  over  the  adjacent 
portions  of  the  sternum,  but  this  can  be  differentiated  from  aneurism  by 


AORTIC   INSUFFICIENCY.  471 

fluoroscopic  examination  with  oblique  illumination.  Indeed,  examination 
with  the  X-ray  shows  this  condition  to  be  much  more  frequent  than  had 
previously  been  suspected,  and  discloses  many  cases  of  dilated  aorta  which 
had  previously  been  regarded  as  true  aneurisms.1  On  the  other  hand,  the 
tremendous  strain  upon  the  vessel  walls  in  aortic  insufficiency  tends  to 
bring  about  the  formation  of  aneurisms,  and  the  latter  is  a  relatively  fre- 
quent complication  of  aortic  insufficiency. 

The  Aortic  Diastolic  Murmur.— The  characteristic  and  almost  pathog- 
nomonic sign  of  aortic  insufficiency  is  the  blowing,  hissing,  or  occasionally 
musical  murmur  heard  over  the  heart  in  early  diastole.  This  murmur  was 
first  described  by  Hodgkin  in  1829  as  " a  constant  bruit  de  scie, 
which  presented  this  peculiarity,  that  it  was  double,  attending  the  systole 
as  well  as  the  diastole."  1  However,  it  remained  for  Corrigan  (1832)  to 
recognize  its  diagnostic  significance.  The  murmur  is  caused  by  the  regurgi- 
tant stream  passing  through  the  orifice  between  the  closed  valves,  and  its 
quality,  like  the  noise  made  by  a  jet  of  steam,  depends  upon  the  size  and 
character  of  the  opening  and  the  pressure  in  the  vessel  during  diastole 
rather  than  upon  the  size  of  the  orifice.  Indeed,  a  small  leak  passing 
through  a  narrow  orifice,  especially  with  irregular  and  calcified  walls,  at 
a  high  diastolic  pressure,  may  cause  a  much  more  intense  murmur  than 
a  large  leak  through  a  wide  orifice  (cf.  page  176).  Balfour  even  goes  so  far 
as  to  state  that  when  the  diastolic  murmur  is  loud  over 
the  base  but  not  over  the  carotid  artery  the  regur- 
gitation is  small,  whereas  when  it  is  loud  over  the  arteries  but  not 
heard  over  the  base  the  leak  is  a  large  one.  In  occasional  cases  of  ulcera- 
tive endocarditis  separation  of  an  entire  cusp  may  occur  without  the  pres- 
ence of  the  characteristic  murmur.  Moreover,  it  is  frequently  observed 
that  the  diastolic  murmur  is  totally  absent  when  the  heart  is  rapid  and 
weak,  but  reappears  as  the  rate  falls  and  the  force  of  the  beat  increases. 
The  consistency  of  the  valves  also  plays  a  considerable  role.  A  rigid  and 
calcified  orifice  forms  a  better  sounding-board  and  gives  rise  to  a  louder 
and  more  roaring  murmur. 

As  to  the  region  in  which  it  is  best  heard,  the  statements  of  different 
authors  vary.  The  following  list  shows  the  region  of  maximum  intensity 
given  by  various  authors: 

V.  Jurgenson Second  right  interspace  and  adjacent  portions  of 

sternum. 

Gerhardt Left  of  sternum. 

Romberg Second  and  third  left  interspaces. 

Huchard Third  right  costal  cartilage. 

Sibson Lower  part  of  left  margin  of  sternum. 

Broadbent Sternum  near  origin  of  third  left  costal  cartilage. 

Osier Midsternum,   third   costal   cartilage,   or  along  left 

border  of  sternum  as  low  as  ensiform. 

Cole  and  Cecil  have  called  attention  to  the  fact  that  in  many  cases  of 
aortic  insufficiency  the  diastolic  murmur  not  only  can  be  heard  but  under- 
goes an  accentuation  as  the  stethoscope  passes  outward  from  the  apex 
into  the  left  axilla.    The  writer  can  confirm  this  observation. 

1Aortic  insufficiency  with  dilatation  of  the  aortic  arch  is  sometimes  termed  Hodgson's  disease. 


472 


DISEASES   OF   THE   HEART    AND    AORTA. 


The  discrepancies  in  the  statements  of  the  different  observers  may  be  due  to  the 
direction  taken  by  the  regurgitant  stream.  Foster,  Balfour,  and  Grocco  suggested  that 
this  might  depend  upon  the  aortic  segment  which  happened  to  be  affected.  It  is  easy  for 
any  one  to  demonstrate  to  his  own  satisfaction  that  this  view  is  at  least  partially  correct. 
A  calf's  heart  may  be  obtained  from  a  butcher's  shop  and  a  cannula  connected  with  a  pres- 
sure bottle  inserted  into  the  aorta.  A  window  is  cut  into  the  left  ventricle,  and  a  hole  is 
then  made  in  one  of  the  aortic  leaflets.  A  regurgitant  stream  issues  from  the  hole,  taking  a 
direction  nearly  perpendicular  to  the  plane  of  the  valve.  The  stream  emerging  from  a 
hole  in  the  left  cusp  strikes  the  septum,  that  from  the  posterior  cusp  strikes  the  left  wall 
of  the  ventricle  in  the  vicinity  of  the  apex  or  anterior  papillary  muscle,  while  that  from 
the  right  cusp  strikes  against  the  anterior  cusp  of  the  mitral  valve.  The  higher  the  pressure 
under  which  these  streams  pass  the  more  their  direction  is  deflected  toward  the  apex.  A  mod- 
erate change  in  pressure  will  make  a  great  difference  in  the  direction  taken  by  the  stream. 


Fig.  210. — Direction  of  the  primary  regurgitant  streams  in  aortic  insufficiency.  (Schematic.)  I.  Re- 
gurgitant streams  passing  through  orifices  in  the  aortic  cusps.  II.  1,  Direction  taken  by  a  stream  regurgi- 
tating at  low  pressure;  2,  direction  of  stream  regurgitating  througn  the  same  orifice  at  high  pressure.  III. 
A,  direction  naturally  taken  by  a  stream  regurgitating  through  an  orifice  in  the  aortic  cusp;  B,  direction 
to  which  the  stream  through  the  same  orifice  is  deflected  by  irregularities  upon  the  surface  of  the  vegetation. 


If  the  orifice  from  which  the  stream  emerges  is  an  irregular  one  like  that  at  the  margin 
of  a  vegetation,  the  direction  of  the  stream  may  be  totally  deflected  from  its  original  course 
(Fig.  210)  and  this  is  probably  the  case  in  most  clinical  conditions.  The  regurgitant  stream 
continues  as  a  well-defined  jet,  whose  sound  would  naturally  be  loudest  near  the  point 
where  it  strikes  and  which  would  be  transmitted  more  or  less  nearly  in  the  direction  of  its 
course.  The  walls  of  the  heart  and  the  chorda?  tendinese  aid  in  transmitting  these  murmurs  for 
some  distance  beyond  their  point  of  impact.  The  correctness  of  these  hypotheses  has  been 
verified  by  S.  Engh  in  a  series  of  very  careful  experiments  done  in  the  pharmacological 
laboratory  of  the  University  of  Minnesota. 

It  is  evident,  therefore,  that  the  mere  variations  in  the  direction  of 
the  regurgitant  streams  due  to  the  form  of  the  leak,  the  blood-pressure, 
and  the  position  of  the  heart  may  give  rise  to  the  greatest  variations  in 
the  point  at  which  the  murmur  is  maximal,  and  may  account  for  the  dis- 
crepancies in  the  clinical  findings  of  excellent  observers. 

Murmurs  over  the  Arteries. — Owing  to  the  roughening  of  the  aortic 
valves  and  sometimes  to  the  presence  of  aortic  stenosis,  a  systolic  murmur 
is  also  heard  over  the  aortic  area  and  transmitted  along  the  blood  stream 
to  the  arteries. 

In  the  carotid  and  brachial  arteries  a  diastolic  or  to-and-fro  murmur 
may  also  be  heard.  This  was  described  by  Corrigan  in  1832  and  by  Da 
Costa  Alvarenga  in  1856,  but  it  is  most  frequently  and  easily  heard  over 
the  femoral  arteries,  where  it  was  first  noticed  by  Bouillaud  and  described 
by  his  pupil,  Duroziez,  in  1861.  It  is  usually  known  as  Duroziez's 
double  murmur.  The  diastolic  portion  is  probably  due  to  a  slight 
regurgitant  stream  from  the  periphery  toward  the  larger  arteries. 


AORTIC   INSUFFICIENCY. 


473 


VOL 


Flint's  Presystolic  Rumble. — Another  and  very  important  murmur  is 
the  presystolic  rumble  heard  only  at  the  apex  (Flint  murmur),  first  de- 
scribed by  Austin  Flint  in  1862  in  cases  of  aortic  insufficiency  without  any 
mitral    involvement.      This   rumble   is  in 
every   respect    similar  to    that    of   mitral 
stenosis,   and   it  is  extremely  difficult  to 
determine   whether    the    latter  is   absent. 

Indeed,  Flint,  in  his  original  paper,  supposed 
that  the  murmur  was  due  to  the  existence  of  a 
functional  narrowing  of  the  orifice  between  the 
mitral  cusps,  which,  as  Baumgarten  (1843)  and 
Hammernjk  had  shown,  was  closed  at  the  beginning 
of  auricular  systole.  Guiteras  and  Thayer  believe 
that  the  murmur  is  due  to  the  vibration  of  the  ante- 
rior cusp  of  the  mitral  valve  set  in  motion  by  the 
regurgitant  stream.  Thayer  and  also  Gibson  deny 
the  existence  of  such  a  functional  stenosis.  How- 
ever, the  writer  has  been  able  to  show  on  the  excised 
heart,  by  the  method  of  Baumgarten  and  Gad,  that 
although  the  mitral  valve  usually  opens  along  its 
entire  extent,  yet  when  the  pressure  within  the  ven- 
tricle is  increased,  the  separation  of  the  cusps  occurs 
at  only  a  small  portion  of  the  line  of  closure  (Fig.  212) . 

An  actual  functional  stenosis  is,  there- 
fore, present  exactly  as  assumed  by  Flint. 
Snapping  First  Sound. — The  first  sound 
at  the  apex  in  30  per  cent,  of  these  cases 
has  the  snapping  character  present  in  mitral 
stenosis,  but  more  commonly  is  loud  and 

booming.     The  systolic  murmur  transmitted  to  the  left  axilla  is  present 
in  many  cases  in  which  mitral  insufficiency  is  associated. 

Aortic  Second  Sound. — When  there  is  great  destruction  or  great  retrac- 
tion of  the  aortic  cusps  and  they  do  not  ap- 
proximate, the  second  sound  may  completely 
disappear;  but  if  the  edges  are  sclerotic  or 
calcified,  or  covered  with  hard  vegetations, 
the  closure  may  even  cause  an  intensification 
of  the  second  sound,  in  spite  of  the  presence 
of  a  larger  regurgitation. 

Third  Heart  Sound. — Besides  these  sounds 
Prof.  Thayer  has  called  attention  to  the  ex- 
treme frequency  of  a  loud  third  heart  sound 
(protodiastolic  gallop  rhythm)  in  aortic  insuf- 
ficiency, associated  with  the  protodiastolic 
wave  upon  the  cardiogram.  If,  as  has  been  sug- 
gested by  Hirschfelder,  Gibson,  and  Thayer, 
this  sound  is  due  to  the  closing  snap  in  diastole, 
it  is  quite  natural  that  it  should  be  unusually  loud  in  aortic  insufficiency 
when  the  mitral  valves  are  forcibly  clapped  together  by  the  high  diastolic 
pressure  in  the  ventricle.  It  can  be  readily  shown  on  excised  hearts  that 
the  snap  is  then  more  abrupt  than  under  normal  conditions. 


Fig.  211. — Relation  of  murmurs  in 
aortic  insufficiency  to  the  cardiac  cycle. 
PR.,  intraventricular  pressure;  VOL.,  vol- 
ume curve  of  the  ventricles.  1,  simple 
aortic  diastolic  murmur;  2,  Flint  presys- 
tolic rumble  and  aortic  diastolic  murmur; 
3,  presystolic  rumble,  diastolic  murmur, 
and  third  sound;  4,  mitral  and  aortic  in- 
sufficiency murmurs  replacing  both  sounds 
(machinery  murmur). 


mitral 


aortic 


Fig.  212. — Functional  mitral  ste- 
nosis in  aortic  insufficiency  as  demon- 
strated on  the  excised  heart  by  Baum- 
garten's  method.    (Semi-schematic.) 


474 


DISEASES   OF   THE   HEART   AND    AORTA. 


BLOOD-PRESSURE. 

The  blood-pressure  in  patients  with  aortic  insufficiency  presents  the 
same  characteristics  as  in  experimental  animals, — namely,  a  constantly 
high  pulse-pressure.  This  may  be  due  either  to  a  considerable 
fall  in  the  minimal  pressure  (as,  for  example,  maximal  pressure  120,  mini- 
mal 50),  as  is  most  common  in  the  endocarditic  group,  or  to  a  considerable 
rise  in  the  maximal  pressure  with  relatively  little  change  in  the  minimal 
(170  and  90  respectively),  such  as  is  usual  in  the  arteriosclerotic  form. 
Occasionally  one  encounters  cases  in  which  an  aortic  diastolic  murmur 
and  normal  pulse-rate  are  present  with  normal  maximal  and  minimal  pres- 
sures (120  and  90),  but  all  the.  experimental  evidence  indicates  that  in 
these  cases  the  leak  must  be  a  small  one,  just  as  is  the  case  in  animal  experi- 
ments when  a  thrombotic  deposit  plugs  the  hole  in  a  punctured  valve 
(see  page  398).  In  such  cases,  therefore,  there  is  a  definite  lesion  of  the 
aortic  valves,  producing  but  little  leakage  yet  a  well-marked  murmur. 
Any  disturbances  to  the  circulation  in  such  a  case  are  due  to  sclerotic  and 
myocardial  factors  rather  than  to  the  aortic  lesion.  Although  this  class 
of  cases  has  not  been  studied  extensively,  it  seems  probable  that  a  careful 
functional  diagnosis  based  upon  the  blood-pressure  findings  might  prove 
very  useful  for  prognosis. 


Fig.  213. — Variations  in  the  form  of  the  pulse-wave  encountered  clinically  in  aortic  insufficiency. 
Marey.)     1,  normal  form;  2,  collapsing  (Corrigan);  3,  4,  5,  6,  anacrotic  pulse. 


(After 


PULSE. 


The  typical  pulse  of  aortic  insufficiency  is  very  characteristic,  and 
since  the  time  of  Corrigan  has  been  known  as  the  Corrigan  pulse  (water- 
hammer  pulse,  see  page  68).  The  wave  is  large,  with  a  quick  upstroke 
(pulsus    celer   et   altus)  and  sudden  fall,  leaving  the  artery  quite 


AORTIC   INSUFFICIENCY. 


475 


small  and  soft  during  diastole  (collapsing  pulse).1  In  the  typical  sphygmo- 
gram  these  characteristics  are  very  marked.  The  criterion  for  designat- 
ing a  pulse-tracing  as  collapsing  is  not  the  steepness  of  the  up-and-down 
strokes,  for  these  depend  chiefly  upon  the  speed  at  which  the  smoked  sur- 
face is  travelling,  but  lies  in  the  fact  that  the  dicrotic  notch  in  the 
collapsing  pulse  falls  below  the  middle  of  the  pulse- 
wave,  while  in  the  normal  and  anacrotic  pulse  it  lies  above  the  middle 
(Mackenzie  and  Broadbent).  Since  Marey  and  Huerthle  have  shown  that 
the  systolic  period  occupies  the  time  before  the  dicrotic  notch  and  the 


£SEC. 


CAROTID 


VOLUME  OF 
VENTRICLES 


VOLUME  OF 
VENTRICLES 


Fig.  214. — Tracings  from  a  dog  with  experimental  aortic  insufficiency,  showing  the  conversion  of  a 
collapsing  (A)  into  an  anacrotic  pulse  (B)  by  clamping  the  descending  aorta.  (After  Stewart.)  A,  before; 
B,  after  clamping.  The  figures  on  the  first  pulse  curves  indicate  the  time  from  the  base  to  the  summit  of 
the  pulse- wave.  The  figures  on  the  second  wave  indicate  maximal  and  minimal  pressures  in  the  carotid. 
Downstrokes  upon  the  volume  curve  represent  systole.  Clamping  the  aorta  causes  the  ventricle  to  dilate 
somewhat,  and  to  fill  more  quickly  in  diastole. 

diastolic  after  it,  it  is  but  a  paraphrase  to  state  that  in  the  collapsing  pulse 
over  half  the  fall  of  pressure  occurs  during  systole,  while 
in  the  normal  pulse  the  fall  occurs  chiefly  during  diastole.  Moreover 
the  volume  curves  by  Stewart  and  the  writer  have  shown  that  the  collapse 
occurs  while  the  blood  is  still  flowing  out  of  the  ventricle  into  the  aorta, 
and  not  at  the  time  when  the  regurgitation  is  occurring.  On  the  other 
hand,  increasing  the  peripheral  resistance,  either  by" clamping 
the  descending  aorta  or  by  the  administration  of  adrenalin,  etc.,  which 


1  Corrigan  called  attention  to  the  fact  that  elevating  the  arm  caused  the  pulse  to 
have  a  more  collapsing  quality,  but  Stewart  has  shown  that  this  is  due  to  hastening  the 
venous  return  and  not  to  increased  regurgitation.  It  can  be  prevented  by  slightly  con- 
stricting the  arm. 


476  DISEASES   OF  THE   HEART   AND   AORTA. 

caused  an  actual  increase  in  the  amount  of  blood  regur- 
gitated, caused  the  collapsing  form  of  the  pulse-wave  to 
be  replaced  by  one  of  typically  anacrotic  form  (Fig.  214). 
The  pulse-pressure,  however,  remained  high.  Moreover,  the  pulse-tracings 
of  Marey  (Fig.  213)  showed  almost  all  possible  variations  of  form  to  occur 
in  cases  of  aortic  insufficiency,  and  Stewart  found  that  the  collapsing  pulse 
was  absent  in  42  per  cent,  of  the  tracings  at  the  Johns  Hopkins  Hospital. 
There  is  also  a  certain  number  of  cases  in  which  the  clinical  note  describes 
the  pulse  as  collapsing,  while  no  such  character  appears  on  the  tracing.  In 
these  cases  there  is  usually  a  large  pulse-pressure,  and  the  discrepancy  is  due 
to  the  fact  that  the  finger  appreciates  the  amount  of  the  changes  in  pressure 
while  the  sphygmograph  records  mainly  the  suddenness  of  the  change. 
The  cause  of  the  collapsing  character  of  the  pulse  seems  to  be  the  dila- 
tation of  the  peripheral  arteries,  but  the  backflow  into  the  ventricle  during 
diastole  depletes  the  aorta  just  before  the  onset  of  systole  and  this  state 
gives  rise  to  the  very  high  pulse-pressure  and  large  pulse  volume.1 

Hasenfeld  and  Romberg  have  shown  that  these  vessels  become  greatly 
dilated  after  the  lesion  has  been  produced,  and  Stewart  has  shown  that 
this  is  due  to  a  stimulation  of  the  depressor  nerve  at  the  aortic  ring  which 
the  increase  in  intraventricular  pressure  may  render  continuous.  An  entirely 
new  light  upon  the  collapsing  pulse  has  been  shown  by  the  studies  of  Hewlett 
and  van  Zwaluwenberg  (cf .  page  68)  who  found  that  the  predicrotic  fall  in 
the  normal  and  in  the  dicrotic  pulse  is  due  to. actual  reflux  of  blood  from  the 
peripheral  arteries  to  the  aorta,  and  that  the  collapsing  pulse  of  aortic  insuf- 
ficiency is  due  to  a  similar  reflux  but  occurring  in  a  much  greater  degree. 

It  is  sometimes  thought  that  the  absence  of_a  collapsing 
pulse  in  a  case  of  aortic  insufficiency  indicates  the  presence  of  aortic 
stenosis.     However,   as  not  only  the  above-mentioned  experiments  but 

many  autopsy  findings 
demonstrate,  this  is  not 
the  case.  It  merely  indi- 
cates that  there  is  high 
peripheral  resistance, 
which  is  common  in  arte- 

Fig.  215. — Radial  pulse  tracings  from  patient  (R.  C.)  showing 
extrasystoles  (E)  which  are  probably  of  ventricular  origin.     The       riOSClerOSiS. 

heavily  shaded  portion  represents  the  systolic  period  in  one  cardiac  Pll1«P  =  rflfp     TVlP 

cycle.     The  pulse  is  collapsing.  * 

pulse-rate  depends  largely 
upon  the  degree  of  compensation,  being  little  faster  than  normal  in  cases 
without  symptoms,  but  usually  ranging  from  80  to  120  in  hospital  cases. 
The  pulse-rate  is  usually  regular;  but  when  the  heart's  action  is  very 
labored,  ventricular  extrasystoles  may  result  from  the  over-distention, 
and  thus  produce  an  irregular  or  a  bigeminal  pulse. 

Case  of  Aortic  Insufficiency. 

R.  M.  C,  colored  laborer,  aged  46,  entered  the  hospital  on  May  20,  1904,  complain- 
ing of  soreness  and  swelling  of  the  abdomen  and  shortness  of  breath.  He  has 
always  been  healthy  except  for  measles,  mumps,  and  whooping-cough  as  a  child,  diph- 

1  MacCallum,  in  his  otherwise  excellent  article,  confuses  collapsing  pulse  with  high 
pulse-pressure,  and  thus  vitiates  his  conclusions. 


AORTIC   INSUFFICIENCY.  477 

theria  at  21,  and  chills  and  fever.  He  has  had  gonorrhoea  but  denies  syphilis. 
He  passes  water  once  a  night.  He  has  worked  hard,  exposed  to  wet  and  cold  and  doing 
heavy  lifting.    Does  not  use  alcohol  or  tobacco. 

About  two  years  before  admission  he  had  cough,  palpitation,  short- 
ness of  breath  on  exertion,  and  some  orthopnoea,  of  which  he  was  cured 
at  the  dispensary.  The  present  trouble  began  about  two  months  ago,  with  violent 
beating  of  the  heart  and  shortness  of  breath  which  were  worse  at  night.  These  symp- 
toms came  on  in  paroxysms,  which  may  be  produced  by  stooping  down.  He  has 
severe  paroxysmal  coughing  spells.  During  the  past  few  days  his  abdomen  has 
been   swollen,   but  his  feet  have  not  been  at  all  so. 

The  patient  is  a  poorly  nourished  man,  propped  up  in  bed  without  respiratory  dis- 
tress. There  is  marked  pulsation  visible  in  all  the  large  arteries, 
and  a  to-and-fro  murmur  can  be  elicited  over  them  by  heavy  pressure  with  the 
stethoscope.  The  lungs  are  clear  on  percussion  and  auscultation,  except  for  a  few  coarse 
mucous  rales  at  both  bases. 

Heart.  —  There  is  considerable  pulsation  over  the  precordium,  the  apex  being 
located  in  the  seventh  left  interspace  18  cm.  from  the  midline.  Dulness 
extends  upward  to  the  second  left  interspace  and  5  cm.  to  the  right  of  the  midline  in  the 
fourth  interspace.  There  is  a  well-defined  presystolic  thrill  over  the  apex. 
A  blowing  systolic  murmur  replaces  the  first  sound  and  is  heard  over  the  whole  axilla,  also 
a  short  blowing  diastolic  murmur  and  a  short  presystolic  rumble 
(Flint  murmur).  Passing  inward  and  upward  the  sounds  are  replaced  by  a  loud  to- 
and-fro  murmur,  loudest  over  the  insertion  of  the  fourth  rib  and  scarcely 
heard  to  the  right  of  the  sternum.  In  the  second  right  interspace  the  systolic  mur- 
mur is  very  harsh  and  the  first  sound  is  loud;  the  diastolic  murmur  is  well  heard, 
The  pulse  is  of  good  volume,  regular,  markedly  water-hammer  in  charac- 
ter.    Maximal   blood-pressure    170  mm.   Hg. 

Abdomen  is  full ;  the  hepatic  dulness  extends  9  cm.  below  the  costal  margin  ; 
the  liver  is  soft  and  tender.    There  is  well-marked  oedema  of  the  legs. 

Red  blood-corpuscles  5,000,000;    haemoglobin  75  per  cent.;    leucocytes  75  per  cent. 

He  was  put  at  rest,  soft  diet,  and  given  1  c.c.  of  tincture  of  digi- 
talis and  strychnine,  1.5  mg.  (gr.  £s)  every  four  hours,  and  purged  freely. 
He  immediately  improved.  The  cedema  disappeared,  and  within  three  weeks  he 
was  up  and  about,  feeling  well,  with  a  pulse-rate  of  80-90  per  minute.  He  was 
discharged  on  June  16.  His  shortness  of  breath  and  cedema  returned,  however, 
within  a  week,  and  he  re-entered  the  hospital  on  June  26  so  dyspnceic  that 
he  was  scarcely  able  to  speak.  The  signs  were  about  as  before.  He  did  not  improve 
as  before,  however,  in  spite  of  treatment,  and  remained  dyspnceic  throughout  the 
month,  subject  to  spells  of  intense  cardiac  asthma,  so  that  he  was  com- 
pelled to  seek  relief  by  being  propped  up  continually  in  a  wheel-chair  instead  of 
lying  in  bed.  During  this  period  his  maximal  pressure  remained  high  (15  0- 
17  0),  his  minimal  pressure  about  110  (Erlanger  apparatus).  During  the  after- 
noon of  August  1  the  cardiac  asthma  was  particularly  intense.  His  maximal  pressure  was 
150  mm.  Hg,  the  minimal  110.  Venesection  was  contemplated.  Before  this  could  be 
done,  however,  while  the  patient  was  being  examined  and  perfectly  conscious,  the  maximal 
blood-pr«ssure  suddenly  fell  to  110,  the  pulse  stopped  suddenly,  and 
the  patient  dropped  back  dead. 

At  autopsy  the  aortic  segments  were  found  to  be  thickened  at 
their  edges,  and  the  valve  was  clearly  incompetent.  The  aortic  orifice  meas- 
ured 8.5  cm.  in  circumference,  the  pulmonic  8.5  cm.  The  edge  of  the  mitral  valve  was 
slightly  thickened,  the  tricuspid  also;  but  there  was  no  stenosis  of  either.  The  tricuspid 
orifice,  on  the  contrary,  measured  14  cm.  There  was  much  dilatation  and  hy- 
pertrophy of  the  left  ventricle,  the  heart  weighing  760  Gm.  The  coro- 
nary arteries  were  clear.  There  were  numerous  thrombi  along  the  walls  of 
the  right  ventricle.  Corresponding  to  this  finding  there  were  numerous  areas  of 
embolism  of  the  branches  of  the  pulmonary  arteries,  evidently  from  the  loose- 
ening  of  such  thrombi.  Along  the  pericardium  there  were  numerous  raised  irregular  pearly 
fibrous  patches.  There  were  chronic  passive  congestion  and  cedema  of  the  lungs,  right- 
sided  hydrothorax,  chronic  passive  congestion  of  the  abdominal  viscera,  and  chronic 
gastritis. 


478  DISEASES   OF   THE   HEART   AND    AORTA. 

DIAGNOSIS. 

The  diagnosis  of  aortic  insufficiency  usually  presents  little  difficulty. 
The  following  conditions  may,  however,  give  rise  to  blowing  diastolic  mur- 
murs over  and  near  the  sternum  which  may  be  mistaken  for  aortic  insuf- 
ficiency (Cabot  and  Locke). 

1.  Dilatation  of  the  aorta. 

2.  Intense  anaemia. 

3.  Tuberculous  mediastinitis  and  similar  conditions  (murmur  is  cardio- 

respiratory, loudest  in  inspiration). 

4.  In  association  with  mitral  disease  and  dilatation  of  the  pulmonary 

artery  (functional  pulmonic  insufficiency). 

These  conditions  are,  as  a  rule,  easily  excluded,  and  do  not  frequently 
obscure  the  diagnosis. 

On  the  other  hand,  as  has  been  seen,  it  is  often  difficult  to  exclude 
complications  such  as  mitral  stenosis  in  the  presence  of  a  well-marked 
Flint  murmur,  or  of  aortic  stenosis  when  the  pulse  is  not  collapsing. 

The  dilatation  of  the  aorta,  which  often  follows  as  a  sequela  of  aortic 
insufficiency,  is  frequently  mistaken  for  aneurism.  It  may  be  accompanied 
by  very  marked  pulsation  in  the  second  right  interspace  and  even  of  the  upper 
portion  of  the  sternum,  with  dulness  in  these  regions.  Even  the  X-ray  when 
taken  in  the  anteroposterior  diameter  may  be  ambiguous,  and  oblique  illumi- 
nation may  be  necessary  to  remove  the  suspicion  of  aneurism  (Holzknecht). 

The  existence  of  a  functional  aortic  insufficiency  from  transitory 
dilatation  of  the  aortic  ring  can  only  be  definitely  diagnosed  when  an  aortic 
diastolic  murmur  and  an  abnormally  high  pulse-pressure  have  been  present 
and  have  passed  off.  This  is  indeed  a  rare  occurrence.  Other  complications 
are  few,  and  are  generally  those  of  arteriosclerosis.  Bronchial  features  may 
be  present,  as  in  any  other  form  of  cardiac  disease  when  the  pulmonary 
compensation  is  broken.  Anginal  attacks  and  coronary  sclerosis  may 
usually  be  regarded  as  a  feature  of  the  sclerotic  form  of  aortic  insufficiency 
rather  than  a  complication.  On  the  other  hand,  one  of  the  cases  under  the 
writer's  care  was  very  subject  to  severe  attacks  of  definitely  anginal  charac- 
ter, and  yet  at  autopsy  the  coronary  arteries  were  found  to  be  clear.  It  is 
possible  that  in  such  cases  the  pain  may  be  due  to  either  vasomotor  ischsemia 
or  ischsemia  due  to  the  low  mean  pressure  in  the  coronary  arteries. 

TREATMENT  AND  PROGNOSIS. 

For  purposes  of  prognosis  and  treatment  the  course  of  the  disease 
may  be  divided  into  three  stages. 

1.  Freedom  from  symptoms,  the  left  ventricle  performing 
its  work  perfectly  without  either  dilatation  or  pulmonary  stasis.  In  this 
stage  the  high  pulse-pressure,  low  diastolic  pressure,  and  collapsing  pulse 
and  throbbing  arteries  are,  nevertheless,  prominent.  The  only  indication 
is  to  aid  nature  by  avoidance  of  overstrain,  overeating,  alcohol,  coffee, 
tobacco,  unhygenic  surroundings,  and  exposure  to  infectious  diseases. 
When  hypertrophy  is  good,  the  lesion  may  persist  for  years  without  pro- 
ducing the  slightest  symptoms. 


AORTIC   INSUFFICIENCY.  479 

Three  years  ago  the  writer  examined  a  medical  student  twenty-five  years  old  who 
has  been  in  perfect  health  since  an  attack  of  rheumatic  endocarditis  at  the  age  of  ten. 
In  spite  of  his  lesion  he  has  become  an  athlete,  was  a  member  of  his  class  crew  at  Yale,  and 
excelled  in  long-distance  running;  he  smokes  and  takes  alcohol  in  moderation.  Cases 
like  this  may  persist  for  thirty-five  years  or  more  (Osier),  but  manifest  themselves  sooner 
or  later  after  infectious  diseases  or  with  the  onset  of  the  arteriosclerotic  period  of  life. 

In  cases  with  arteriosclerosis,  potassium  iodide,  0.3  Gm.  (gr.  v),  or 
sodium  nitrite,  0.2  Gm.  (gr.  iii),  three  times  a  day,  is  advisable,  to  help 
check  the  progress  of  the  arteriosclerosis  and  to  keep  down  the  blood-pres- 
sure. Occasional  Nauheim  baths,  warm  salt  baths,  or  even  ordinary  warm 
baths  are  useful  in  promoting  the  vasodilation.  Cardiac  tonicity  must  be 
maintained  at  all  costs  and  dilatation  must  be  prevented. 

2.  The  second  stage  is  that  of  dilatation  of  the  left 
ventricle.  This  is  the  stage  when  symptoms  appear,  some  arising 
in  the  sensory  nerves  of  the  ventricle  and  manifesting  themselves  in  the 
forms  described  above — palpitation,  referred  pain,  psychic  disturbances, 
anginal  attacks;  some  arising  in  the  pulmonary  circulation  as  a  result  of 
stasis,  presenting  the  various  forms  of  respiratory  disturbance.  According 
to  Head,  the  stage  of  cardiac  sensation  never  merges  into  the  stage  of  re- 
spiratory distress,  but  disappears  when  the  functional  mitral  insufficiency 
and  the  latter  symptoms  set  in.  There  is  a  "safety-valve"  action 
of  the  mitral  valve. 

As  has  been  seen,  the  important  factors  producing  distention  of  the 
ventricle  are  diminution  of  tone  and  high  peripheral  resistance.  Treatment 
should  therefore  be  directed  toward  counteracting  these  conditions.  The 
usual  cardiac  procedures,  rest,  light  diet,  free  purgation,  should  be  resorted 
to,  and,  when  improvement  warrants,  the  Nauheim  baths  and  gentle 
exercises  free  from  much  resistance. 

Digitalis  and  the  Nitrites. — The  use  of  digitalis  has  been  much  disputed. 
Corrigan  stated  that  "in  every  case  of  this  disease  in  which  digitalis  has 
been  administered  it  has  invariably  aggravated  the  patient's  sufferings." 
Broaclbent  believes  that  it  should  be  used  with  caution  and  that  it  may 
even  precipitate  sudden  death,  but  that  it  is  certainly  indicated  after  mitral 
insufficiency  has  set  in.  Romberg  thinks  it  should  always  be  used  with 
caution.  It  is  probable  that  any  deleterious  property  which  the  drug  may 
possess  lies  in  its  vasoconstrictor  action,  and  hence  from  a  priori  reasons 
it  should  be  combined  with  nitroglycerin  or  other  nitrites,  or  preferably 
strophanthus  substituted.  Indeed,  strophanthus  seems  to  be  the  drug  par 
excellence  in  these  conditions,  but  with  this  drug  it  is  well  to  give  nitro- 
glycerin. The  pharmacological  researches  of  Cameron  demonstrate  that 
the  nitrites  possess  the  two  properties  most  needed  in  aortic  insufficiency, 
— that  of  increasing  tone  and  of  dilating  the  peripheral  vessels;  and  the 
writer's  clinical  experience  bears  out  the  view  that,  either  alone  or  with 
strophanthus  or  digitalis,  they  furnish  great  relief  and  are  to  be  strongly 
recommended. 

A  beautiful  series  of  animal  experiments  recently  carried  out  by 
Cloetta  merits  consideration. 

Cloetta  found  that  the  administration  of  digitalis  over  prolonged  periods  caused  no 
changes  in  size  and  strength  of  normal  rabbits'  hearts.  If  aortic  insufficiency  were  pro- 
duced and  the  animals  left  untreated  for  a  year,  their  hearts  hypertrophied  and  gained 


480  DISEASES   OF   THE   HEART   AND    AORTA. 

80  per  cent,  of  their  original  heart  weight,  but  the  animals  lost  in  strength  and  endur- 
ance. If  they  were  treated  with  digitalis  immediately  after  producing  the  lesion,  and  the 
treatment  continued  throughout  the  year,  the  hearts  were  smaller  (hypertrophy  30  per 
cent.),  but  the  hearts  were  almost  as  strong  as  those  of  normal  rabbits.  The  aortas  of 
untreated  animals  had  widened  much  more  than  those  of  the  treated. 

Cloetta  claims  to  have  had  equally  good  results  in  patients  by  early 
and  continuous  treatment  with  digitalis,  but  the  matter  must  be  studied 
upon  a  larger  series  of  cases  before  attaining  general  acceptance.  It  is 
chiefly  applicable  to  early  rheumatic  cases,  though  it  seems  probable  that 
long-continued  administration  of  very  small  doses  of  digitalis  (0.3  c.c,  or 
5  minims,  of  the  tincture)  may  exert  this  beneficial  effect  without  pro- 
ducing the  harmful  effects  sometimes  met  with. 

For  the  extreme  palpitation  and  anginal  attacks,  little  can  be  done 
beyond  the  administration  of  amyl  nitrite  in  the  latter.  Ice-bags  to  the 
precordium  are  often  of  value,  as  is  the  Finsen  light  treatment,  galvanism 
of  the  vagus  (J.  O.  Hirschfelder) ,  etc.  Stewart  has  found  excellent  results 
after  a  lumbar  puncture,  even  when  the  cerebrospinal  pressure  was  low. 
It  is  not  unlikely  that  acupuncture  over  the  neural  segment  afflicted  might 
have  the  same  effect. 

3.  The  third  stage  is  the  stage  of  failure  of  the  right  ventricle, 
presenting  the  usual  signs  and  symptoms  except  that  anginal  attacks, 
spasms  of  cardiac  asthma,  and  Cheyne-Stokes  breathing  are  a  little  more 
common  than  in  other  diseases.  In  the  treatment  of  this  condition  the  aortic 
insufficiency  is  more  or  less  disregarded,  digitalis,  purgatives,  and  diuretics 
being  given  quite  freely.  The  administration  of  nitrites  is,  however,  still 
to  be  advised.    Ewart  recommends  C02  inhalations  (see  page  241). 

What  can  be  accomplished  occasionally  in  such  cases  is  shown  by  the  case  cited  on 
page  22,  a  farmer,  aged  33  years,  who  came  under  the  writer's  care  in  November,  1903, 
entering  the  hospital  after  a  year's  suffering  with  orthopnoea  so  great  that  he  had  been 
compelled  to  sleep  in  a  chair  for  six  months,  and  oedema  and  ulceration  of  the  legs,  as 
shown  in  Fig.  123.  Under  digitalis  and  free  purgation  improvement  set  in  rapidly,  and  in 
ten  weeks  he  left  the  hospital  free  from  cedema  and  almost  free  from  dyspnoea.  He  has 
remained  quite  well,  and  has  continued  his  work  as  a  farmer  during  the  past  five  years. 

On  the  other  hand,  failure  of  compensation  is  usually  a  more  serious 
event  than  in  mitral  insufficiency,  since  the  factors  producing  weakening 
of  the  ventricles  from  over-distention  are  more  intense  and  more  persistent. 
The  writer  has  found  in  several  instances  that  broken  compensation  in 
aortic  insufficiency  is  associated  with  a  high  diastolic  pressure  which  falls 
as  the  case  improves  in  many  cases  shortly  before  death.  It  is  probable 
that  this  is  due  to  asphyxial  vasoconstriction  and  furnishes  another  example 
of  the  vicious  circle : 

{Broken  compensation "} 
Slowed  circulation        >       N 
Medullary  asphyxia     J 

f  Increased  regurgitation  )  f  Vasoconstriction  ) 

\  Weakening  of  ventricle  J  (  Increased  peripheral  resistance  j 

Venesection  is  not  indicated  except  when  there  are  a  considerable 
grade  of  venous  stasis,  high  venous  pressure,  and  dilatation  of  the  right 
auricle;  but  in  the  writer's  experience  its  results  are  then  excellent. 


AORTIC  INSUFFICIENCY.  481 

In  the  anginal  attacks  and  the  spells  of  dyspnoea  or  for  insomnia,  codeine, 
.03  Gm.  (gr.  1),  or  morphine,  .0075  Gm.  to  .03  Gm.  (gr.  \  to  gr.  1),  hypo- 
dermically,  may  be  necessary,  but  should  always  be  used  as  sparingly  as 
possible,  since  the  habit  is  readily  formed  and  the  patient  injures  himself 
by  feigning  dyspncea  in  order  to  get  the  drug.  They  depress  the  respiratory 
centre  and  thus  predispose  to  Cheyne-Stokes  breathing  and  to  cardiac  asthma. 
Atropine  (0.5  to  1  mg.,  gr.  tyt  to  -gr)  should  be  given  simultaneously  to  inhibit 
the  effects  of  morphine  upon  the  respiratory  centre. 

BIBLIOGRAPHY. 
Aortic  Insufficiency. 

Cowper:  Phil.  Trans.,  1705,  No.  299.     Quoted  from  Osier  and  Gibson,  Diseases  of  the 

Valves  of  the  Heart,  Modern  Med.,  Phila.  and  N.  Y.,  1908,  iv,  205. 
Vieussens:  Nouvelles  decouvertes  sur  le  coeur,  1706.    Traite  nouveau  de  la  structure  et  des 

causes  du  mouvement  naturel  du  cceur,  Toulouse,  1705.    Quoted  from  Huchard,  Mai. 

du  coeur,  3d  ed.,  Paris,  1905,  iii. 
Morgagni:  also  quoted  from  Huchard. 

Hodgkin,  T.:    On  Retroversion  of  the  Valves  of  the  Aorta,  Lond.  M.  Gaz.,  1829,  iii,  433. 
Corrigan,  D.  J. :  On  Permanent  Patency  of  the  Mouth  of  the  Aorta  or  Inadequacy  of  the 

Aortic  Valves,  Edinb.  M.  and  S.  J.,  1832,  xxxvii,  225. 
Gillespie,  A.  L. :  An  Analysis  of  2368  Cases  Admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  Edinb.  Hosp.  Rep.,  1898,  v,  31. 
Hasenfeld,  A.,  and  Romberg,  E.:  Ueber  die  Reservekraft  des  hypertrophischen  Herz- 

muskels,  u.s.w.,  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1897,  xxxix,  333. 
Gibson,  G.  A.:  Jugular  and  Triscupid  Reflux,  Edinb.  M.  J.,  1880. 
Marey,  E.  J. :  La  circulation-  du  sang  a  1'etat  physiologique  et  dans  les  maladies,  Paris, 

1881. 
Cohnheim,  J. :  Vorlesungen  ueber  allgemeine  Pathologie,  Berl.,  1882,  i. 
Jaager:  Arch.  f.  d.  ges.  Physiol.,  Bonn,  xxxi. 

Rosenbach,  O.:  Arch.  f.  exper.  Pathol,  u.  Pharmakol.,  Leipz.,  1878,  ix,  1. 
Kornfeld,  S.:  Ueber  den  Mechanismus  der  Aorteninsufficienz,  Ztschr.  f.  klin.  Med.,  Berl., 

1896,  xxix,  91,  344. 
Moritz,  F. :  Ueber  ein  Kreislaufsmodell  als  Hilfsmittel  fur  Studium  und  Unterricht,  Deutsch. 

Arch.  f.  klin.  Med.,  Leipz.,  1899,  lxvi,  349. 
Stewart,  H.  A.:  Experimental  and  Clinical  Investigation  of  the  Pulse  and  Blood-pressure 

Changes  in  Aortic  Insufficiency,  Arch.  Int.  M.,  Chicago,  1908,  i,  102. 
Head,  H.:  On  Disturbances  of  Sensation,  with  Especial  Reference  to  the  Pain  of  Visceral 

Disease,  Brain,  Lond.,  1896,  xix,  153.     Certain  Mental  Changes  that  Accompany 

Visceral  Disease,  ibid,  1901,  xxiv,  345. 
Frankel:  Des  secousses  rhythmiques  de  la  tete  chex  les  aortiques,  Rev.  de  Med.,  Paris, 

1902,  664. 
M  tiller,  Fr.:  Pulsation  des  Gaumens  bei  Aorten  insumcienz,  Charite  Annalen,  Berl.,  1889, 

251. 
Becker:  Ueber  Retinalarterienpuls  bei   Insuffizienz   der  Aortenklappen,    Monatsschr.   f. 

Augenheilk.,  1870. 
Quincke,  H.:  Beobachtungen  ueber  Kapillar- und  Venenpuls,  Berl.  klin.  Wchnschr.,  1868. 
Lennhoff :  Ueber  Pseudoaorteninsuffizienz,  Diss.,  Berl.,  1893. 

V.  Weissmayer,  W. :  Insuffizienz  der  Aortenklappen  ohne  Gerausch  und  Pseudoaortenin- 
suffizienz, Ztschr.  f.  klin.  Med.,  Berl.,  1897,  xxxii,  29. 
Huber:  Ueber  Pseudoaorteninsuffizienz,  Berl.  klin.  Wchnschr.,  1898. 
Flint,  A.:  On  Cardiac  Murmurs,  Am.  J.  M.  Sc,  Phila.,  1862,  xliv,  29. 
Thayer,  W.  S.:  Observations  on  the  Frequency  and  Diagnosis  of  the  Flint  Murmur  in 

Aortic  Insufficiency,  Am.  J.  Med.  Sci.,  Phila.,  1901,  cxxii,  538. 
V.  Jurgensen,  Th. :  Valvular  Disease  of  the  Heart,  Nothnagel's  Encyclopaedia  of  Practical 

Medicine,  Amer.  edition,  trans,  by  G.  Dock,  Phila.,  1908. 
Gerhardt.    Quoted  from  v.  Jurgensen. 

31 


482  DISEASES  OF  THE  HEART  AND  AORTA. 

Romberg,  E. :  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart,  1906. 

Huchard,  1.  c,  Sibson,  quoted  from  Huchard. 

Broadbent,  W.  H. :  Heart  Disease  and  Aneurism  of  the  Aorta,  4th  ed.,  N.  Y.,  1906. 

Osier,  W.:  The  Principles  and  Practice  of  Medicine,  4th  ed.,  N.  Y.,  1901. 

Cole,  R.  I.,  and  Cecil,  A.:  The  Axillary  Diastolic  Murmur  in  Aortic  Insufficiency,  Johns 
Hopkins  Hosp.  Bull.,  Baltimore,  1908,  xix,  353. 

Foster,  B.:  Essays  on  Clinical  Medicine,  Lond.,  1874. 

Balfour,  G. :  Diseases  of  the  Heart,  Lond.,  1898. 

Grocco:  Arch.  ital.  riv.  clin.,  1888.  Also  Borgherini,  A.:  Ueber  das  Verhalten  des  riick- 
laufigen  Blutstroms  bei  Insuffizienz  der  Semilunarklappen  der  Aorta,  Deutsch.  Arch, 
f.  klin.  Med.,  Leipz.,  1898,  lx,  139. 

Eastman,  T.  J.  E.:  The  Diagnosis  of  Circulatory  Conditions  by  Temperature  Measure- 
ments, Bost.  M.  and  S.  J.,  1908,  clviii,  639. 

Holzknecht,  G.:  Die  roentgenologische  Diagnostik  der  Erkrankungen  der  Brusteinge- 
weide,  Hamb.,  1901. 

Cloetta,  M.:  Ueber  den  Einfluss  der  chronischen  Digitalisbehandlung  auf  das  normale  und 
pathologische  Herz,  Arch.  f.  exper.  Path.  u.  Pharmakol.,  Leipz.,  1908,  lix,  209. 


V. 


AORTIC  STENOSIS. 


PATHOLOGICAL    ANATOMY. 

In  a  certain  percentage  of  cases  (10  per  cent.)  in  which  the  aortic  valves 
are  diseased,  the  cusps  become  fused  into  a  ring  by  which  the  orifice  into 
the  aorta  is  narrowed  (aortic  stenosis) .  Owing  to  the  force  within  the  ven- 
tricle, this  ring  is  usually  pushed 
upward  into  the  lumen  of  the  aorta 
until  the  orifice  has  a  sort  of  dome- 
shaped  appearance  (Figs.  216  and 
217,  A). 

The  inflammatory  or  atheroma- 
tous changes  most  commonly  begin 
in  the  cusps  separately,  and  the 
process  extends  until  their  edges  be- 
come fused  with  an  organization  or 
atheroma  at  the  line  of  union.  Oc- 
casionally there  is  a  progressive 
uniform  diffuse  sclerosis  like  that 
which  often  occurs  in  mitral  lesions. 
The  condition  almost  always  arises 
from  the  same  conditions  as  aortic 
insufficiency,  but  in  rare  cases  may 
also  be  of  congenital  origin. 

Naturally  many  of  the  manifestations  depend  upon  the  degree  of 
stenosis,  which  is  sometimes  so  extreme  that  a  quill  can  barely  be  passed 

b  c 

A 


Fig.    216. 


-Specimen     showing     aortic     stenosis. 
Viewed  from  above. 


Fig.  217. — Forms  of  stenotic  aortic  orifices.  A.  Lateral  view  of  the  specimen  shown  in  Fig.  216.  B, 
b.  Aortic  stenosis,  with  edges  of  cusps  flexibly  fixed  at  ring  shown  by  broken  line,  but  capable  of  move- 
ment indicated  by  arrows.     C,  c.  Aortic  stenosis  with  rigid  cusps. 

through  the  orifice.  On  the  other  hand,  the  orifice  may  be,  relatively  speak- 
ing, wide,  and  the  valves  retain  sufficient  flexibility  to  close  it  during  dias- 
tole, so  that  a   pure    aortic   stenosis  occurs  without  any  insufficiency 

483 


484  DISEASES   OF   THE   HEART   AND    AORTA. 

whatever  (a  condition  present  in  about  60  per  cent,  of  the  cases).  In  the 
other  40  per  cent,  the  orifice  is  not  only  narrowed  but  the  cusps  are  so 
fused  and  rigid  that  they  do  not  close  the  aortic  orifice  during  diastole, 
and  an  aortic  insufficiency  is  present  along  with  the  ste- 
nosis  (double  aortic  lesion). 

OCCURRENCE    AND    ETIOLOGY. 

Aortic  stenosis  is  by  far  the  rarest  of  left-sided  valvular  lesions,  occur- 
ring in  only  5  per  cent,  of  the  1781  Johns  Hopkins  cases  and  in  2.73  per 
cent,  of  Romberg's  cases.  This  is  in  accordance  with  the  experience  of 
most  writers.  Gillespie's  statistics,  in  which  it  was  supposed  to  occur  in 
18  per  cent,  of  all  the  heart  cases  in  the  Edinburgh  Royal  Infirmary,  are 
unique  and  arouse  the  suspicion  that  the  fault  lay  in  the  diagnosis. 

The  etiological  factors  are  practically  the  same  as  in  aortic  insuffi- 
ciency. Syphilis  and  arteriosclerosis  play  a  relatively  important  role.  Con- 
genital stenosis  also  occurs  occasionally.  In  rare  cases  there  is  a  double 
stenosis, — one  at  the  aortic  orifice,  and  one  occurring  within  the  ventricle 
by  the  formation  of  a  fibrous  ring  from  the  septum  to  the  anterior  cusp  of 
the  mitral  valve.    The  disease  is  rare  among  women. 

PATHOLOGICAL    PHYSIOLOGY. 

The  changes  in  the  circulation  due  to  stenosis  of  the  aortic  orifice  were 
very  completely  shown  by  Liideritz  under  the  guidance  of  Prof.  Gad.  Liid- 
eritz  found  that  if  the  aortic  orifice  were  narrowed  by  the  tightening  of  a 
clamp,  the  aortic  blood-pressure  might  or  might  not  fall,  but  the  form  of  the 


Fig.  218. — Carotid  pulse  and  intraventricular  pressure  in  experimental  aortic  stenosis.  (After 
Liideritz,  Ztschr.  f.  klin.  Med.,  xx.)  |  St  marks  the  point  at  which  aortic  stenosis  was  produced.  The  carotid 
pulse  (CAR.)  shows  the  gradual  development  of  the  pulsus  tardus,  with  a  fall  in  blood-pressure,  while  the 
intraventricular  pressure  (INT.)  increases  tremendously. 

pulse-curve  changed.  The  upstroke  changed  from  sudden  to 
gradual  and  slanting,  ending  with  a  broad  rounded  top  whose  sum- 
mit was  reached  near  the  end  of  systole  (pulsus  tardus).  This  form  of 
pulse,  as  will  be  seen,  is  perfectly  typical  of  aortic  stenosis,  and  furnishes 
the  basis  for  the  diagnosis. 


AORTIC   STENOSIS. 


485 


AORTIC  STENOSIS 
LV 


Rise  of  Intraventricular  Pressure. — The  pressure  within  the  ventricle,  on  the  other 
hand,  rises  greatly,  often  as  much  at  100  per  cent.,  without  affecting  the  aortic  pres- 
sure; for  the  greater  part  of  the  contraction  is  unable  to  force  much  blood  into  the 
aorta.  The  excess  of  intraventricular  over  aortic  pressure  is  therefore  much  greater  than 
in  any  other  condition.  The  conditions  under  which  the  contraction  takes  place  conform 
more  or  less  to  those  for  the  execution  of  an  isometric  contraction,  and  the  curve  of  intra- 
ventricular pressure  comes  to  resemble  that  of  an  isometric  contraction,  the  summit 
changing  from  flat  to  the  dome-shaped,  as  is  typical  for  the  latter  (as  shown  by  Frank 
and  by  Huerthle).  That  is,  the  pres- 
sure does  not  at  once  reach  its  maxi-  NORMAL 
mum,  but  rises  gradually,  coinciding 
quite  well  with  the  rise  of  the  curve 
in  the  aorta.  It  is  the  direct  com- 
munication of  this  progressive  rise  of 
pressure  to  the  aorta  which  gives  rise 
to  the  pulsus  tardus,  as  well  as  the 
fact  that  the  volume  of  blood  flows 
into  the  aorta  more  slowly  than  usual. 
The  duration  of  systole  is  prolonged 
considerably,  seven  to  ten  per  cent. 
in  mild  grades  of  stenosis,  ten  to  fifty 
per  cent,  when  stenosis  is   extreme. 


Fig.  219. — Diagram  of  the  circulation  showing  the 
effect  of  aortic  stenosis.  The  broken  line  indicates  the 
intraventricular  pressure.  The  vertical  black  line  indicates 
the  volume  of  the  heart,  the  shaded  portion  representing 
the  amount  of  residual  blood.  (Compare  with  Fig.  26.) 


When  the  ventricle  is  not 
able  to  expel  its  quota  even  by 
the  end  of  systole,  extrasystoles 
are  likely  to  occur,  and  this  fre- 
quently assumes  the  form  of 
a  continuous  bigeminal  pulse. 
Such  overfilling  of  the  left  ventricle  naturally  leads  to  stasis  in  the  auricle 
and  pulmonary  veins,  with  rise  of  pressure  in  these  parts,  pulmonary  con- 
gestion, cardiac  dyspnoea  (v.  Basch),  oedema  of  the  lungs  (Welch),  and 
secondarily  also  of  the  right  ventricle.  These  in  turn  lead  to  dilatation 
and  hypertrophy  of  the  left  ventricle  and  left  auricle  and  hypertrophy  of 
the  right  ventricle,  which  are  usually  found  to  be  present  at  autopsy. 


SYMPTOMS    AND    CLINICAL    COURSE. 

Aortic  stenosis  is  probably  the  most  chronic  of  all  valvular  lesions,  and 
persists  for  years  without  affecting  the  duration  of  life.  However,  as  soon 
as  the  stenosis  becomes  marked,  so  that  the  left  ventricle  has  difficulty  in 
emptying  itself  completely,  slight  exertion,  excitement,  or  emotion  brings 
on  disagreeable  symptoms,  palpitation,  constriction,  substernal  pain  or 
anginal  attacks,  and  shortness  of  breath.  These  sensory  stimuli  probably 
arise  in  the  depressor  nerve  as  the  result  of  distention  of  the  ventricle,  for 
experiments  of  Sewall  and  Steiner  have  demonstrated  that  distention  has 
this  effect  in  animals.  The  symptoms  at  first  pass  off  when  the  patient 
rests  or  leads  a  quiet  and  hygienic  life,  but  as  the  disease  persists  they 
become  more  frequent  and  persistent.  Sudden  death  is  relatively  common, 
and  is  probably  due  to  acute  dilatation. 

Compensation. — As  in  mitral  stenosis,  compensation  is  dif- 
ficult. The  left  ventricle  may  by  increasing  its  power  continue  to  drive 
enough  blood  into  the  aorta  to  maintain  the  blood-pressure,  and  even  to 
cause  the  pulse  to  resume  the  normal  form  (Fig.  223),  but  this  is  done  at 


486 


DISEASES   OF   THE   HEART   AND    AORTA. 


an  enormous  waste  of  energy,  which  sooner  or  later  brings  on  heart  failure. 
Moreover,  the  lesion  itself  is  slowly  progressive,  and  this  constantly  increases 
the  difficulty  of  maintaining  the  circulation.  In  the  final  stage  broken 
compensation  sets  in  exactly  as  in  other  advanced  valvular  lesions. 

When  aortic  insufficiency  coexists  the  circulatory  difficulty  is  naturally 
increased,  since  the  ventricle  must  drive  an  even  excessive  amount  of  blood 
into  the  aorta  in  order  to  maintain  the  circulation,  in  spite  of  the  difficulty 
under  which  it  already  labors.  Moreover,  these  are  often  the  cases  with  the 
most  advanced  pathological  lesions,  so  that  the  coexistence  of  aortic  insuffi- 
ciency renders  the  prognosis  less  favorable  than  that  of  pure  aortic  stenosis. 

PHYSICAL    EXAMINATION. 

The  most  striking  feature  upon  general  physical  examination  in  aortic 
stenosis  is  the  presence  of  a  well-marked  systolic  thrill  and  bruit  over  the 
larger  arteries.  Over  the  chest  there  is  usually  a  certain  amount  of  pre-' 
cordial  bulging.  The  apex  impulse  is  sometimes  well  marked  and  heaving, 
situated  quite  outside  the  mammillary  line  in  the  fifth  or  sixth  interspace ; 
frequently,  however,  it  is  not  visible  nor  palpable.     Between  the  apex  and 

the  sternum  there  is  often  some 
systolic  retraction  of  the  inter- 
spaces from  the  contraction  of 
the  hypertrophied  right  ventri- 
cle. The  left  ventricle  hypertro- 
phies, increasing  in  size  along  its 
long  axis  (obliquely  downward) . 
Palpation.  —  Palpation  re- 
veals a  systolic  thrill  which  is 
usually  very  marked  and  felt 
over  the  whole  heart,  especially 
over  the  aortic  area.  It  is  pres- 
ent in  the  carotid  and  brachial 
arteries,  and  is  transmitted  in 
the  direction  of  the  blood  stream 
(see  page  156).  The  intensity 
of  this  thrill  is  often  the  most 
striking  feature  of  all  the  phys- 
ical signs,  and  may  far  exceed 
that  which  is  found  in  any  other 
condition.  The  shock  of  the  first  sound  is  usually  felt,  while  that  of  the 
second  is  often,  though  not  always,  absent. 

Percussion  and  X=ray  examination  reveal  no  peculiarities  other  than 
an  area  of  cardiac  dulness  enlarged  along  its  longitudinal  axis,  as  in  aortic 
insufficiency;  but,  owing  to  the  presence  of  functional  mitral  insufficiency 
and  dilatation  of  the  conus  arteriosus,  the  area  of  dulness  may  be  higher 
and  broader  than  in  aortic  insufficiency  and  resemble  that  found  in  organic 
mitral  insufficiency. 

Auscultation. — On  auscultation  one  is  immediately  struck  by  the  pres- 
ence of  a  loud  systolic  murmur  most  intense  over  the  aortic 
area,  and    transmitted   thence   to   the   first   right   inter- 


Fig.  220. — Diagram  showing  the  cardiac  outline  and 
distribution  of  the  murmur  in  aortic  stenosis.  The  par- 
allel shading  indicates  the  distribution  of  the  systolic 
murmur  and  thrill;  the  dot  indicates  the  point  at  which 
they  are  most  intense. 


AORTIC   STENOSIS. 


487 


CAROTID 


SOUNDS 


xJc  SEC. 


vv~Vtif|flft 


tfmmMmMwMMmmmimwwmmmwmwMwMwww 


1MUR 


1 


space  and  along  the  course  of  the  arteries,  where  it  is, 
as  a  rule,  still  loud  and  distinct.  It  is  also  heard  over  the  pulmonic  area, 
body  of  the  heart,  and  over  the  apex,  but  far  less  loudly  than  in  the  aortic 
area  and  the  arteries. 

This  murmur  is  usually  the  loudest  that  is  heard  in  any  form  of  valvular 
disease,  and  is  often  heard  several  feet  away  from  the  patient.  The  mechan- 
ism of  its  production  exemplifies  perfectly  the  simple  experiment  for  the 
production  of  thrills  and  murmurs  described  on  page  144.  Since  it  cannot 
be  produced  until  the  blood 
begins  to  flow  into  the  aorta, 
this  murmur  does  not  begin 
until  an  appreciable  in- 
terval after  the  begin- 
ning of  systole  (Boy- 
Teissier,  Romberg,  Weiss  and 
Joachim)  and  follows  the 
first  sound  in  that  region 
as  well  as  at  the  apex  (Fig. 
221).  Weiss  and  Joachim  have 
recorded  this  murmur  with  their 
phonoscope,  and  find  that  it 
sets  in  with  a  crescendo  char- 
acter at  the  very  end  of  the  first 
sound.   The  crescendo  continues 

until  the  crest  of  the  carotid  pulse,  after  which  it  changes  to  decrescendo 
throughout  the  rest  of  systole.  The  form  of  the  carotid  wave  portrays  the 
amplitude  of  the  vibrations  and  the  variations  in  loudness  of  the  murmur. 
When  mitral  insufficiency  (organic  or  functional)  is  present,  the  mitral 
murmur  may  enter  into  or  replace  the  first  sound. 

The  second  sound  may  vary  considerably  in  aortic  insufficiency. 
If  the  valves  are  fused  throughout  their  whole  extent,  it  will  be  entirely 
absent,  but  if  portions  of  the  cusps  remain  freely  movable  their  closure 
may  give  rise  to  a  sound.  Owing  to  the  small  excursion,  this  sound  may 
not  be  as  loud  as  it  would  be  if  no  stenosis  were  present,  but  this  factor 
may  be  more  than  balanced  by  the  presence  of  sclerotic  plaques  and  calcifi- 
cations whose  concussions  may  actually  render  the  second  sound  louder 
than  normal. 


Fig.  221. — Murmur  of  aortic  stenosis.  (After  Weiss 
and  Joachim.)  Upper  curve,  carotid  pulse;  middle  curve, 
heart  sounds;  lower  curve,  time;  one  vibration  equal 
to  1OT  second.  The  second  sound  is  practically  absent. 
The  murmur  is  composed  of  a  crescendo  followed  by  a 
decrescendo  character  loudest  with  the  upstroke  on 
the  pulse-wave. 


PULSE. 

Aortic  stenosis  may  be  said  to  be  the  only  disease  in  which  the  absolute 
diagnosis  is  determined  by  the  pulse-tracing.  The  pulse  is  small,  hard 
(high  diastolic  pressure),  and  in  typical  cases  rises  and  falls  very  slowly 
(pulsus  tardus).  Like  the  curves  in  experimental  aortic  stenosis  (Fig.  219), 
the  typical  radial  pulse-curve  (Fig.  222)  shows  a  very  oblique  ascent 
which  lasts  throughout  systole,  the  summit  of  the  curve  appearing  just  be- 
fore the  dicrotic  notch.  This  is  produced  by  the  slow,  gradual,  and  progres- 
sive filling  of  the  arteries  from  the  gradually  increasing  intraventricular 
pressure.  It  may  be  recalled  that  during  the  period  of  the  up-stroke  upon 
the  pulse-wave  blood  is  flowing  into  the  aorta  more  rapidly  than  onward 


488 


DISEASES    OF   THE    HEART    AND    AORTA. 


to  the  periphery;  that  during  the  period  of  the  plateau  the  inflow  and  out- 
flow are  equal;  and  during  the  period  of  fall  blood  is  flowing  onward  to  the 
periphery  more  rapidly  than  it  flows  into  the  aorta. 

The  pulse  of  aortic  stenosis,  there- 
fore, reflects  the  true  condition,  that 
blood  is  flowing  into  the  aorta  less 
rapidly  than  usual  and  out  of  it  also 
less  rapidly.  However,  it  must  be 
admitted  that  this  typical  form  of 
pulse  is  rather  rare.  Most  commonly, 
either  the  aortic  stenosis  does  not  reach 
this  stage  without  being  complicated 
by  an  insufficiency  which  changes  the 
pulse  form  or  death  intervenes  before 
these  signs  of  inability  of  the  heart 
to  empty  itself  have  set  in.  Indeed,  many  practitioners  may  pass  through 
long  lives  of  busy  practice  without  encountering  a  single  example  of  aortic 
insufficiency  with  pulsus  tardus.     The  anacrotic  pulse  is  so  much  more 


Fig.  222. — Diagram  showing  the  pulsus  tar- 
dus and  the  anacrotic  type.  Solid  line,  pulsus 
tardus,  showing  the  slow  gradual  rise;  broken 
line  snowing  the  anacrotic  form  with  sudden 
almost  vertical  rise  surmounted  by  a  plateau 
which  takes  up  the  greater  part  of  systole. 


Fig.  223. — Pulse  tracings  from  cases  of  aortic  stenosis.  The  heavily  shaded  curve  represents  the  sys- 
tolic portion  of  the  tracing.  I.  Anacrotic  pulse  from  a  case  of  tricuspid  insufficiency  but  no  aortic  stenosis, 
showing  quick  upstroke  with  only  the  summit  sloping.  II,  III.  Pulsus  tardus  from  a  case  of  aortic  ste- 
nosis (L.  S.).  IV.  Tracing  from  a  case  of  aortic  stenosis  and  insufficiency.  V,  VI,  VII.  Tracings  from 
another  case  of  aortic  stenosis  and  insufficiency.  V.  Taken  on  February  28  soon  after  admission;  symptoms 
of  cardiac  weakness  well  marked;  maximal  blood-pressure  130  mm.  Hg.  The  upstroke  is  gradual  and  slop- 
ing. VI.  From  same  patient  on  March  24  after  recovery  from  cardiac  symptoms.  Maximal  pressure  160. 
The  strong  heart  forces  blood  rapidly  through  the  stenosed  orifice  and  causes  a  sudden  upstroke.  VII. 
Pulse  tracing  taken  immediately  after  VI,  with  other  arm  raised.  The  increased  resistance  changes  the 
tracing  to  a  pulsus  bisferiens. 

common  in  aortic  stenosis  that  examples  of  it  are  given  in  many  text-books 
erroneously  labelled  pulsus  tardus.  A  pulse-curve  with  a  sud- 
den perpendicular  up-stroke,  however,  is  not  a  pulsus 
tardus,  but  an  anacrotic  pulse,  whatever  may  be  the  form  of  its  summit. 


AORTIC   STENOSIS.  489 

It  indicates  that  blood  is  flowing  into  the  aorta  from  the  heart  more  rapidly 
than  it  is  flowing  out  of  the  aorta  toward  the  periphery,  a  condition  which 
occurs  in  aortic  stenosis  only  (1)  when  the  orifice  is  so  slightly  narrowed 
that  the  hypertrophied  left  ventricle  is  able  to  drive  blood  through  it  with 
great  rapidity,  and  (2)  when  the  peripheral  vasoconstriction  is  so  great  that, 
in  spite  of  a  slow  inflow  into  the  aorta,  the  blood  still  enters  the  latter  much 
more  rapidly  than  it  can  leave  it.  The  former  is  the  more  common  condi- 
tion; and  it  would  appear  that  the  hypertrophy  of  the  ventricle  can  usually 
keep  pace  with  the  advancing  stenosis  until  a  very  late  stage  is  reached. 
The  pressure  within  the  ventricle  produced  under  these  conditions  is  prob- 
ably tremendous. 

These  facts  are  well  illustrated  in  Curves  V,  VI,  VII  (Fig.  223).  The  first  (V)  was 
taken  when  the  patient's  heart  was  weak,  and  the  blood-pressure  shows  a  gradual  up-stroke 
and  is  fairly  typical  of  aortic  stenosis.  The  other  curves  (VI  and  VII),  taken  after  his 
heart  had  improved,  have  taken  on  the  characters  of  aortic  insufficiency  and  have  lost  those 
of  aortic  stenosis. 

Arrhythmia. — The  rhythm  of  the  heart  in  man,  as  in  animal  experi- 
ments, is  frequently  irregular;  small  beats  and  dropped  beats  being 
frequent,  due  to  the  occurrence  of  a  pulsus  alternans  or  to  extrasys- 
toles  arising  in  the  left  ventricle  when  that  chamber  is  unable  to  empty 
itself  sufficiently.  Exercise,  emotion,  or  any  other  form  of  cardiac  over- 
strain, on  the  one  hand,  or  of  cardiac  weakening,  on  the  other,  precipitates 
this  irregularity. 

BIood=pressure.  —  The  blood-pressure  in  aortic  stenosis  is  usually 
slightly  elevated  (maximal  pressure  130  to  160  mm.),  due  in  part  to  the 
accompanying  arteriosclerosis,  in  part  to  the  increase  in  the  intraventricular 
pressure,  especially  when  the  heart  hypertrophies. 

DIAGNOSIS. 

In  typical  cases  the  diagnosis  of  aortic  stenosis  is  extremely  simple. 
The  presence  of  slow,  gradual  pulse,  the  pulse-tracings,  the  enlarged  heart, 
the  very  intense  systolic  thrill,  the  thrill  and  murmur  over  the  aortic  area 
and  arteries,  and  the  absence  or  marked  diminution  of  the  aortic  second 
sound,  present  a  perfectly  characteristic  picture.  In  certain  cases,  however, 
and  especially  when  there  is  arteriosclerosis  or  aortic  insufficiency,  it  may 
become  extremely  difficult  to  decide  whether  a  mild  grade  of  stenosis  is 
present. 

Case  op  Aortic  Stenosis. 

Mrs.  L.  S.,  housewife,  aged  58,  entered  the  Johns  Hopkins  Hospital,  April  29,  1904, 
complaining  of  heart  trouble.  She  has  always  been  healthy;  has  had  no  infectious  diseases 
and  never  had  rheumatism,  but  occasionally  has  had  sore  throat.  She  has  occasionally 
had  fainting  spells  and  palpitation  after  mental  excitement,  and  during 
the  past  year  has  had  to  void  three  or  four  times  a  night.  Except  for  these  symptoms  she 
was  quite  well  until  a  year  before  admission,  when  one  night  after  a  heavy  meal  she  awoke 
with  extreme  dyspnoea,  palpitation,  and  a  feeling  of  extreme  weakness.  She  had  no  pain, 
but  felt  considerably  alarmed.  Immediately  after  this  her  feet  became  swollen 
and  in  spite  of  a  sojourn  in  bed  she  became  subject  to  attacks  of  extreme  dyspnoea.  The 
oedema  of  the  feet  subsided,  however,  but  reappeared  after  exertion. 

At  the  time  of  examination  the  patient  was  propped  up  in  bed,  with  slight 
dyspnoea.      She  was  fairly  nourished,  pale,  sallow,  lips    very   cyanotic.      Lungs 


490  DISEASES   OF   THE   HEART   AND    AORTA. 

clear  on  percussion  and  auscultation,  except  at  both  bases,  where  the  note  is  impaired  and 
the  breath  sounds  are  accompanied  by  crackling  rales. 

Heart.  —  The  apex  impulse  is  barely  visible  in  the  sixth  left  interspace 
13  cm.  from  the  midline,  from  which  point  dulness  extends  upward  to  the  third  rib, 
as  well  as  3  cm.  to  the  right  of  the  midline.  There  is  slight  impairment  of  the  percussion 
note  over  the  sternum.  A  soft  systolic  murmur  is  heard  at  the  apex  and  in  the 
axilla,  becoming  louder,  however,  as  the  sternum  is  approached,  and  m  a  x  i  nra  1  over 
the  second  right  interspace,  where  it  becomes  rough  in  character.  It  is 
transmitted  to  the  carotids  but  not  to  the  subclavians.  The  second  pul- 
monic sound  is  louder  than  the  second  aortic.  There  is  a  well-marked  thrill 
over  the  base  and  manubrium,  most  marked  in  the  second  right  interspace. 
Slight  pulsation  over  the  manubrium.  No  tracheal  tug.  The  pulse  is  small, 
regular,  100  per  minute.  The  left  radial  pulse  is  a  trifle  larger  than  the  right.  Tracing 
shows  a  well-marked  pulsus  tardus  (Fig.  I  and  II) .  Blood-pressure  150 
m  m  .   Hg. 

The  abdomen  is  distended  but  does  not  contain  fluid.    The  legs  are  very  cedematous. 

Urine  is  reddish;  specific  gravity  1030;  acid,  and  contains  a  large  number  of 
hyaline   casts. 

Red  blood-corpuscles  5,300,000;   haemoglobin  85  per  cent.;  leucocytes  10,000. 

During  the  first  week  she  improved  under  rest,  purgation,  and  digi- 
talis; but  on  May  8  had  a  severe  spell  of  dyspnoea  not  controlled  by  morphine 
or  nitroglycerin,  but  somewhat  relieved  by  strychnine,  3  mg.  (^  gr.  hypo.).  During  the 
attack  the  aortic  murmur  was  much  less  marked  than  it  had  been  before. 
The  cardiac  outlines  were  unchanged.  There  was  very  slight  development  of  fresh 
rales,  indicative  of  pulmonary  oedema.  After  the  attack  and  the  nitroglyc- 
erin there  was  unequal  dilatation  of  the  peripheral  venules.  Cheyne-Stokes  respiration 
developed  during  the  night.  A  few  purpuric  areas  were  seen  over  the  extremi- 
ties and  the  sacrum. 

On  the  next  day  she  had  another  attack  of  dyspnoea,  aft-er  which  cyanosis  deepened, 
respiration  became  labored,  the  pulse  weakened,  and  the  blood-pressure  fell  gradually 
until  the  patient  died  in  the  early  evening. 

At  autopsy  the  three  aortic  cusps  were  found  to  be  fused  together 
by  a  calcareous  cement,  leaving  an  orifice  not  more  than  3  mm.  in 
diameter.  The  left  ventricle  was  markedly  hypertrophic,  the  right 
less  so.  Both  were  dilated.  The  heart  weighed  600  Gm.  There  were  slight  atheroma  of 
the  aorta  below  the  transverse  arch,  infarction  and  oedema  of  the  lungs,  left  hydrothorax, 
left  pleural  adhesions,  chronic  passive  congestion  of  the  liver  (nutmeg),  spleen,  and  kid- 
neys; general  anasarca. 

TREATMENT. 

As  regards  treatment  there  is  little  to  be  said.  Fortunately,  the  disease 
is  very  chronic  in  its  course,  especially  when  it  begins  after  the  period  of 
adolescence  has  passed.  A  quiet  life  under  the  best  possible  hygienic  con- 
ditions, with  avoidance  of  infections,  excitement,  and  all  forms  of  stimulants 
and  overstrain,  usually  serves  to  stave  off  the  onset  of  symptoms  for  many 
years.  When,  these  once  appear  in  spite  of  quiet,  the  case  is  practically 
hopeless.  Absolute  rest,  light  diet,  moderate  purgation,  and  lessening  of 
the  peripheral  resistance  by  means  of  the  nitrites  and  the  Nauheim  baths 
constitute  the  most  important  means  of  treatment.  Digitalis  is  of 
value  until  the  heart  reaches  its  limit  of  hypertrophy,  after  which  it  merely 
precipitates  overwork  and  irregularity  of  the  heart. 

In  the  acute  attacks  of  acute  heart  failure,  venesection  should  be 
resorted  to  promptly,  in  order  to  lessen  the  residual  blood  in  the  left  ven- 
tricle by  diminishing  the  inflow  into  it. 


AORTIC   STENOSIS.  491 

BIBLIOGRAPHY. 

Aortic  Stenosis. 

Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
Gillespie,  A.  L.:    An  Analysis  of  2368  Cases  Admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  during  the  Five  Years  1891-1896,  Edinb.  Hosp.  Rep.,  1898, 

v,  31. 
Liideritz,  C:  Versuche  ueber  den  Ablauf  des  Blutdrucks  bei  Aortenstenose,  Ztschr.  f, 

klin.  Med.,  Berl.,  1892,  xx,  373. 
Welch,  W.  H.:  Zur  Pathologie  des  Lungenoedems,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1878, 

lxxii,  375. 
Sewall,  H.,  and  Steiner,  D.  W.:  A  Study  of  the  Action  of  the  Depressor  Nerve,  etc.,  J. 

Physiol.,  Camb.,  1885,  vi,  162. 
Boy-Teissier:  L'auscultation  retrosternale,  Rev.  de  Med.,  Par.,  1892,  xii,  169. 


VI. 

PULMONARY  INSUFFICIENCY. 

Insufficiency  of  the  pulmonary  orifice  usually  occurs  either  as  a  con- 
genital lesion  or  as  a  result  of  a  severe  endocarditis  in  which  other  valves 
are  involved.  Even  as  such  it  is  a  very  rare  disease,  only  3  cases  having 
been  seen  among  24,000  admitted  to  the  medical  service  of  the  Johns  Hop- 
kins Hospital. 

Lesions  of  the  pulmonary  valves  had  been  described  by  Morgagni,  but 
the  first  clinical  cases  of  pulmonary  insufficiency  were  described  by  Norman 
Chevers  in  1846,  and  after  him  by  Frerichs,  Benedikt,  Walshe,  and  Stokes. 
Barie  in  1891  was  able  to  collect  detailed  records  of  58  cases  with  24 
autopsies. 

PATHOLOGICAL    ANATOMY. 

The  conditions  leading  to  regurgitation  at  the  pulmonary  orifice  may 
be  divided  into  six  groups: 

I.  Congenital  malformations  of  the  valve  resulting  in 
atrophy  and  deformity.  The  presence  of  only  two,  or,  on  the  other  hand, 
of  four  cusps  does  not  usually  bring  about  any  leakage.  In  this  category 
may  also  be  mentioned  stenosis  of  the  orifice. 

II.  Endocarditic  vegetations  upon  the  valves,  especially 
arising  in  very  acute  attacks  of  endocarditis  with  lesions  of  other  valves. 

III.  Arteriosclerotic  changes  in  the  cusps,  often  associated 
with  dilatation  and  arteriosclerosis  of  the  pulmonary  artery. 

IV.  Aneurisms   of    the    cusps. 

V.  Ruptures  of  the  cusps  during  coughing  or  strain,  especially  of 
cusps  already  diseased. 

VI.  Dilatation  of  the  pulmonary  artery  and  conus  arteriosus  lead- 
ing to  a  functional    insufficiency  of  the  valves. 

According  to  many  writers,  especially  Gibson,  a  functional  insuffi- 
ciency of  the  pulmonary  valve  of  more  or  less  transitory  duration  takes 
place  as  a  result  of  dilatation  of  the  artery  and  of  the  right  ventricle. 
This  would  naturally  occur  most  frequently  in  cases  of  mitral  stenosis 
with  broken  pulmonary  compensation,  and  would  account  for  the  blow- 
ing diastolic  murmur  which  is  sometimes  heard  to  the  left  of  the  sternum 
in  these  cases. 

The  experimental  data  upon  this  subject  are  more  or  less  uncertain.  G.  A.  Gibson  has 
shown  upon  the  dead  heart  that  the  pulmonary  valves  become  insufficient  under  much  lower 
pressures  than  are  necessaay  to  cause  leaks  at  the  aortic.  He  has  also  shown  that  these 
leaks  can  be  prevented  from  occurring  in  the  dead  heart  if  the  pulmonary  orifice  be  pre- 
vented from  dilating  (as  by  surrounding  it  with  a  string).  His  studies  would  therefore 
lead  one  to  believe  that  such  regurgitations  would  occur  readily  in  hearts  whose  tonicity 
was  diminished  and  in  which  the  fibres  about  the  pulmonary  orifice  stretched  accordingly. 

492 


PULMONARY   INSUFFICIENCY. 


493 


On  the  other  hand  Sollman  has  shown  in  the  living  excised  cat's  heart  perfused  with  Ringer's 
solution  and  other  salt  mixtures  that  the  pulmonary  orifice  can  withstand  tremendous 
pressure  without  leaking. 

However,  Stokes,  Kolisko,  Bristowe,  Coupland,  Litten,  Chauffard, 
Gouget  and  Preble,  have  reported  cases  of  relative  pulmonary  insufficiency, 
supported  by  autopsy.  In  all  these  cases  there  was  dilatation  of  the  right 
ventricle,  and  in  three  of  them  a  mitral  lesion  with  pulmonary  stasis.  It 
seems  quite  likely,  moreover,  that  such  a  pulmonary  insufficiency  was 
present  in  cases  W.  H.  (page  504)  and  B.  I.  (page  519),  though  the  water 
test  was  not  applied  to  the  valves  at  autopsy. 


ETIOLOGICAL   FACTORS. 

Barie's  statistics  collected  from  50  cases  of  organic  pulmonary  insuf- 
ficiency show  that  the  two  sexes  are  affected  with  equal  frequency.  It  was 
found  in  patients  of  all  ages  from  birth  to  75  years,  but  37  out  of  46  cases 
(80  per  cent.)  occurred  between  the  ages  of  18  and  34  years.  In  40  per  cent, 
the  disease  was  congenital,  but  in  these  it  never  occurred  as  the  sole  lesion, 
being  usually  associated  with  stenosis.  Rheumatism  was  the  etiological 
factor  in  16  per  cent,  of  the  cases.  Puerperal  infection,  gonorrhoea,  and 
the  other  infectious  diseases  rank  next  in  frequency.  There  is  also  an 
arteriosclerotic  group  due  to 
syphilis,  alcohol,  and  other 
affections  especially  associated 
with  mitral  stenosis  and  scle- 
rosis of  the  pulmonary  artery. 

PATHOLOGICAL    PHYSIOLOGY. 

Pulmonary  insufficiency 
bears  the  same  relation  to  the 
lesser  circulation  that  aortic 
insufficiency  bears  to  the  sys-> 
temic  circulation.  The  effect 
of  the  leak  is  to  bring  about  a 
lowered  diastolic  pressure  and 
an  increased  pulse-pres- 
sure in  the  pulmonary 
artery,  accompanied  by  a 
somewhat  greater  systolic  out- 
put from  the  right  ventricle  to  compensate  for  the  leak.  The  increased 
intraventricular  pressure  in  the  right  ventricle  during  diastole  gives  rise  to 
hypertrophy  when  the  strain  is  compensated,  and  dilatation  when  the 
strain  becomes  too  great.  As  a  result  of  this  dilatation,  functional 
insufficiency    of    the    tricuspid    valve  very  readily  sets  in. 

The  results  of  these  secondary  changes  are,  therefore: 

1.  To  slow  the  circulation  through  the  lungs. 

2.  To  cause  a  marked  rise  of  pressure  and  stasis  in  the  systemic  veins. 

3.  When  this  occurs  less  blood  enters  the  left  ventricle  than  before.     This  would 
naturally  lead  to  a  fall  in  blood-pressure;  but,  just  as  in  mitral  stenosis,  it  is  compensated 


NORMAL 

PULMONARY 
INSUFFICIENCY 

, 

AO 

AO 

M*k           i 

™i           1 

MIMM                                               I 

m,n^           i 

n    rA 

H   , 

\    Ik. 

v~it 

V  /^  ' 

t^ 

\a/ 

LA 

i     t  ^j 

fkO                  RA 

.14 

AO.     __     RA             __          LA 

Fig.  224. — Diagram  of  the  circulation  in  pulmonary- 
insufficiency.  I.  Normal.  II.  Moderate  grade  of  pul- 
monic insufficiency,  showing  a  rise  of  pressure  in  the  sys- 
temic veins  and  a  large  pulse  amplitude  in  the  pulmonary 
artery.      (Compare  with  Fig.  25.) 


494 


DISEASES   OF   THE   HEART   AND    AORTA. 


by  constriction  of  the  peripheral  vessels  and  the  blood-pressure  maintained.  The  vaso- 
constriction, however,  manifests  itself  in  the  smallness  of  the  arteries  and  of  the  pulse,  which 
thus  presents  a  striking  contrast  to  the  pulse  of  aortic  insufficiency.  The  pulse-pressure 
also  is  never  increased,  as  is  the  rule  in  the  latter  condition. 


SYMPTOMS. 

The  symptoms  and  complications  are  chiefly  respiratory  in  origin: 
dyspnoea,  especially  in  intense  paroxysms  which  are  brought 
about  by  slight  exertion;  cough  and  bronchitis,  resulting  from  the  poor 
circulation  through  the  lungs.  The  intense  pulsation  of  the  pulmonary 
vessels  weakens  their  walls  and  predisposes  to  haemoptysis  and  the 
expectoration  of  blood-tinged  sputum.    Phthisis  is  a  common  complication. 

Palpitation  is  sometimes  noted. 
Anginoid  attacks  and  pressure 
at  the  base  of  the  sternum  are 
frequently  met  with;  also  pain, 
which,  in  contrast  to  that  aris- 
ing in  aortic  insufficiency,  is 
more  commonly  referred  to  the 
right  shoulder  and  down  the 
right    arm. 

Sudden  death  is  rela- 
tively common,  sometimes  re- 
sulting from  over-distention  of 
the  right  ventricle,  sometimes 
from  embolism  in  the  pulmo- 
nary artery. 


Fig.  225. — Distribution  of  the  murmur  in  pulmo- 
nary insufficiency.  The  parallel  shading  indicates  the 
area  over  which  the  murmur  is  heard.  The  dot  indicates 
the  point  at  which  it  is  loudest;  the  diagram  at  the  right 
indicates  its  position  in  the  cardiac  cycle.  The  diagrams 
over  the  shaded  area  represent  the  pulsations,  i.  e.  the 
systolic  impulse  over  the  pulmonary  area  and  the  systolic 
retraction  over  the  right  ventricle. 


PHYSICAL    SIGNS. 


Cyanosis,   as  a  result  of 

the    slowed    circulation    in    the 

lungs,  is  one  of  the  earliest  signs. 

It  is  usually  very  marked  and 

is    liable    to    occur    in    paroxysms.      Signs    of    bronchitis    or    often    of 

bronchopneumonia    are   found    in    the    chest. 

Examination  of  the  heart  shows,  as  a  rule,  some  precordial  bulging, 
with  well-marked  pulsation  of  the  conus  arteriosus  in  the  second 
left  interspace,  and  a  systolic  retraction  in  the  third,  fourth,  and  fifth  left 
interspaces  and  epigastrium,  due  to  the  vigorous  beating  of  the  right  ven- 
tricle. The  area  of  cardiac  dulness  is  increased  to  the  right  in  the  trans- 
verse diameter,  owing  to  dilatation  of  the  right  auricle.  Very  often  it 
extends  upwards  in  the  second  left  interspace  as  well  (dilated  conus  arterio- 
sus), where  it  extends  5-6  cm.  to  the  left  of  the  midline.  The  area  of 
cardiac  flatness  is  increased  to  both  left  and  right,  and  forms  a  scalene 
triangle  extending  to  the  right  border  of  the  sternum.  On  palpation  the 
vigorous  beating  of  the  conus  arteriosus  may  be  felt  in  the  second  left 
interspace,  also  a  diastolic  or  systolic  and  diastolic  thrill  in  this  region  and 
over  the  right  ventricle.  On  auscultation  the  sounds  at  the  apex  may  be 
clear.    The  characteristic  feature  is  the  presence  of  a  very  superficial  dias- 


PULMONARY   INSUFFICIENCY.  495 

tolic  murmur  maximal  over  the  pulmonary  area,  varying  from  short  and 
soft  to  loud,  rough  and  hissing  in  character  and  not  infrequently  musical. 
It  is  also  heard  along  the  left  sternal  margin,  but  less  distinctly  over  the 
aorta.  The  difference  is  accentuated  on  coughing.  Owing  to  the  presence 
of  other  lesions  in  the  pulmonary  artery,  there  may  also  be  a  loud  systolic 
murmur  at  the  base,  while  over  the  base  of  the  sternum  a  systolic  mur- 
mur, due  to  the  secondary  tricuspid  insufficiency,  may  also  be  present. 

The  pulse,  in  contrast  to  aortic  insufficiency,  with  which  this  con- 
dition may  be  confounded,  is  small  and  weak;  the  blood-pressure  is  prob- 
ably but  little  affected.  Marked  systolic  pulsation  of  the  veins  and  liver 
(positive  venous  pulse)  is  frequently  present,  due  to  the  secondary  tricus- 
pid insufficiency.  In  the  extremities  cedema  sets  in  readily,  and  there  is 
often  clubbing  of  the  fingers  and  toes  even  in  cases  which  are  not 
congenital. 

The  following  notes  are  taken  from  the  records  of  the  medical  service  of  the  Johns 
Hopkins  Hospital: 

Case  of  Pulmonary  Insufficiency. 

R.  R.,  a  colored  laborer,  aged  48,  was  admitted  on  Feb.  8,  1900,  complaining  of 
pain   in  the  stomach  and  chest. 

He  had  measles  and  whooping-cough  as  a  child,  several  attacks  of  tertian  malaria, 
syphilis  in  1897,  rheumatism  in  1899,  and  several  attacks  of  gonorrhoea. 
He  uses  alcohol  and  tobacco  in  moderation. 

Present  illness  began  two  years  ago,  coincident  with  the  onset  of  urethral 
discharge  and  an  attack  of  rheumatism  (gonorrhceal ?) .  This  caused  him  to 
stop  work.  Since  then  the  rheumatism  has  become  better,  but  he  has  been  troubled  with 
shortness   of  breath   and   palpitation,   though  these  are  not  very  severe. 

Note  by  Dr.  Henry  Harris  states  that  the  patient  is  a  well-nourished  man,  not  dys- 
pnceic  nor  cyanotic.    Lungs  clear  except  for  a  few  moist  rales  over  the  upper  fronts. 

The  note  on  the  heart  by  Dr.  Osier  on  Feb.  10,  1900,  is  as  follows:  "Chief 
impulse  is  in  the  fourth  left  interspace  just  at  the  nipple,  also  a  little 
impulse  above.  The  impulse  in  the  second  left  interspace  extends  5-6 
cm.  outside  of  the  left  sternal  border.  No  impulse  in  the  aortic  area;  no 
dilated  veins;  no  visible  pulsation  of  the  arteries.  On  palpation  there  is  no 
thrill.  There  is  not  a  very  large  area  of  cardiac  dulness.  The  pulse  is  easily  com- 
pressed and  not  collapsing.  In  the  fifth  interspace,  at  the  apex,  and  over 
the  aortic  area  the  sounds  are  practically  normal.  In  the  fourth  left 
interspace  and  at  the  nipple  itself  both  sounds  are  loud.  There  is  a  short,  distant,  slightly 
rumbling  murmur  before'  the  first  sound,  becoming  distinct  on  moving  towards 
the  sternum. 

" At  the  third  interspace  5  cm.  from  the  left  sternal  border  a  short, 
loud  diastolic  murmur  is  heard,  much  louder  as  the  left  sternal  border  is 
approached,  maximal  at  the  left  sternal  border.  There  is  also  a  roughness  of 
the  first  sound.  The  diastolic  murmur  disappears  in  the  sternum,  being  very 
circumscribed.  At  the  second  left  interspace  5  cm.  from  the  left 
sternal  border  the  diastolic  is  louder.  At  the  left  sternal  border  it  has 
a  maximal  intensity.  There  is  a  short  systolic,  and  a  loud  somewhat  booming  dia- 
stolic, with  a  rough  somewhat  vibratory  quality.  In  the  first  interspace  the  murmur 
diminishes,  being  just  feebly  heard.  In  the  second  interspace  the  murmur  practically 
abolishes  the  second  sound,  which  is  clearly  heard  at  the  aortic  area. 

"No  thrill  after  walking  about.  No  evidence  of  congenital  heart 
disease . 

"The  condition  is  most  likely  pulmonary  insufficiency. 
There  is  a  possibility  of  aneurism,  but  firm  pressure  with  the  stethoscope 
far  out  in  the  second  left  interspace  gives  no  sense  of  lifting  and  no  diastolic 
shock.    There  is  no  tracheal  tugging  and  no  diastolic  shock." 


496  DISEASES   OF  THE   HEART   AND   AORTA. 


DIAGNOSIS. 

The  diagnosis  of  pulmonary  insufficiency  is  rarely  made  during  life. 
The  history  of  very  severe  endocarditis  or  evidence  of  affection  of  several 
valves  or  of  a  lesion  dating  from  birth  leads  to  the  suspicion  of  right-sided 
valvular  disease.  It  is  always  difficult  to  exclude  aortic  insufficiency  or 
the  presence  of  the  two  lesions  at  once.  The  small  size  of  the  pulse, 
the  absence  of  visible  pulsation  of  the  large  arteries,  the  small  pulse-pres- 
sure, the  marked  pulsation  of  the  conus  arteriosus  (both  against  the  chest 
wall  and  as  shown  by  the  fluoroscope),  the  retraction  of  the  interspaces 
over  the  right  ventricle,  the  increase  in  the  horizontal  diameter  of  dulness 
to  the  right  and  not  to  the  left,  and  especially  the  dulness  in  the  second 
left  interspace  furnish  the  basis  for  the  diagnosis.  This  is  also  confirmed 
when  there  is  pain  down  the  right  arm  instead  of  the  left.  On  the  other 
hand,  the  congenital  heart  lesions — open  ductus  Botalli,  open  septum 
auriculorum  or  ventriculorum,  etc. — are  very  difficult  to  exclude,  and  will 
be  dealt  with  in  connection  with  congenital  heart  diseases. 

The  diagnosis  of  functional  pulmonary  insufficiency  is  based  upon  the 
presence  of  a  transitory  diastolic  murmur  along  the  left  sternal  border 
during  periods  of  pulmonary  stasis,  in  the  absence  of  other  signs  of  aortic 
insufficiency.  No  doubt  this  diagnosis  may  sometimes  be  made  correctly 
especially  in  cases  of  mitral  stenosis,  but  it  is  one  of  which  even  Gibson 
cannot  feel  certain  in  any  individual  case. 

TREATMENT. 

Treatment  is  the  usual  procedure  for  cardiac  overstrain  of  any  sort,— 
rest,  light  diet,  purgation,  and  digitalis.  Venesection,  by  relieving  the 
distention  of  the  right  auricle  and  ventricle,  is  particularly  useful,  arrd,  as 
stated  by  Alexander  Morison,  yields  remarkably  good  results  in  this 
condition. 

The  main  hope,  however,  lies  in  bringing  about  the  hypertrophy 
of  the  right  ventricle  and  in  preserving  the  balance  between  the  strength 
of  the  right  ventricle  and  the  strain  put  upon  it.  Symptomatic  treatment 
of  the  bronchitis  and  pulmonary  complications  may  do  much  to  relieve 
the  patient. 

The  Prognosis  is  bad  when  pulmonary  stenosis  is  present,  but  in  the 
presence  of  a  pure  insufficiency  depends  greatly  upon  the  condition  of  the 
right  ventricles  and  the  amount  of  cardiac  embarrassment  caused  by  the 
lesion.  As  seen  from  Barie's  cases,  patients  may  reach  the  age  of 
seventy-five  in  spite  of  the  lesion.    These  cases  are,  however,  rare. 

BIBLIOGRAPHY. 

Pulmonary  Insufficiency. 

Chevers,  N.:  A  Collection  of  Facts  Illustrating  the  Morbid  Conditions  of  the  Pulmonary 

Artery,  Lond.  M.  Gaz.,  1846. 
Frerichs:   Insufficientia  valvularum  arteriae  pulmonae,  Wien.  med.  Wchnschr.,  1853,  hi, 

817  and  833. 


PULMONARY   INSUFFICIENCY.  497 

Benedikt,  J.:  Ein  Fall  von  insufficientia  valvularum  semilunararum  arteriae  pulmonae, 

ibid.,  1854,  iv,  547. 
Walshe:  A  Practical  Treatise  on  Diseases  of  the  Lungs,  Heart,  and  Aorta,  Lond.,  1854. 
Barie,  E.:  Recherches  sur  l'insuffisance  des  valvules  de  l'artere  pulmonaire,  Arch,  de  med. 

gen.,  Paris,  1891,  i  (vol.  xxvii),  650,  and  1891,  ii  (vol.  xxviii),  30  and  183. 
Gibson,  G.  A.:  Jugular  Reflux  and  Tricuspid  Regurgitation,  Edinb.  M.  J.,  1880,  xxv,  978. 
Preble,  R.  B.:  Relative  Insufficiency  of  the  Pulmonary  Valves,  J.  Am.  M.  Asso.,  Chicago, 

1897,  xxviii,  1012. 
Morison,  A.:  On  Dextral  Valvular  Disease  of  the  Heart,  Edinb.  M.  J.,  1880,  xxv,  102,  439, 

515,  619,  748. 


VII. 
TRICUSPID  INSUFFICIENCY. 

ORGANIC    AND    FUNCTIONAL   TRICUSPID    INSUFFICIENCY. 

Insufficiency  of  the  tricuspid  valve  occupies  a  unique  position  among 
the  valvular  lesions.  In  the  functional  form,  due  to  dilatation  of  the  right 
ventricle,  it  is  extremely  common,  and  indeed  probably  occurs  at  some 
stage  in  every  dying  or  failing  heart.  In  the  organic  form,  on  the  other 
hand,  it  is  rare,  occurring  only  16  times  in  1781  cases  of  valvular  disease  at 
the  Johns  Hopkins  Hospital  (0.85  per  cent.)  and  in  less  than  0.7  per  cent, 
of  Gillespie's  cases  at  Edinburgh. 

The  organic  forms  occur  more  frequently  in  severe  or  malignant  endo- 
carditis, as  is  indicated  by  the  fact  that  in  none  of  the  Johns  Hopkins 
cases  was  it  the  only  valve  affected,  mitral  stenosis  being  present  in  10, 
aortic  insufficiency  in  7  of  the  cases.  Three  valves,  the  aortic,  mitral,  and 
tricuspid,  were  involved  in  7  of  these  cases,  the  pulmonary  orifice  once. 
Although  severe  rheumatic  fever  is  perhaps  the  most  frequent  cause, 
streptococcus  and  gonococcus  infections  are  relatively  common  etiological 
factors  (see  Chapter  I),  more  so  than  in  the  milder  valvular  affections. 
Occasionally  it  occurs  as  a  congenital  lesion,  the  result  of  endocarditis 
during  fetal  life. 

Anatomically  the  lesions  of  the  tricuspid  valve  exactly  resemble  those 
of  the  mitral,  with  which  they  are  so  frequently  associated,  being  due  to 
vegetations,  thickenings,  ulcerations,  hemorrhages,  and  occasionally  tumors 
or  malformations  upon  the  valves. 

Functional  Tricuspid  Insufficiency. — Our  knowledge  of  functional  tri- 
cuspid insufficiency  dates  from  the  remarkable  anatomical  and  physiolog- 
ical studies  of  T.  W.  King  in  1837. 

King  stated  that  "  the  right  ventricle  is  liable  to  dilatation  and  that  the  dilatation 
deranges  its  valves. 

"The  last  proposition  is  thus  explained.  The  cavity  is  formed  by  the  solid  septum 
of  the  heart  for  its  inner  wall,  and  by  a  thinner,  more  extensive  and  yielding  layer  of  muscle 
for  its  outer  or  right  wall;  whilst  each  of  these  walls  affords  points  of  attachment  to  the 
cords  of  the  valves.  ...  In  the  progress  of  post-mortem  examinations,  I  have  found  in 
hearts  thus  dilated,  or  only  greatly  distended  by  the  final  congestion,  that  upon  injecting 
the  ventricle  by  the  pulmonary  artery  the  tricuspid  curtains  when  stretched  out  were  under 
all  circumstances  a  great  deal  too  small  to  close  the  opening,  ....  and  it  appears  from 
careful  examination  that  the  united  areas  of  these  valvular  portions  are  scarcely  more  than 

equal  to  the  mean  extent  of  the  oval  opening I  have  shown  that  upon  injecting 

fluids  into  the  ventricles  by  their  respective  arteries  (the  semilunar  valves  destroyed)  the 
left  or  bicuspid  valve  (human  heart)  was  always  seen  to  close  completely  and  firmly,  the 
curtains  being  so  extensive  as  to  fold  together  in  the  form  of  a  cone  or  wedge  within  the 
ventricle,  whilst  the  tricuspid  valve  was  constantly  found  in  its  ordinary  state  incapable 
of  preventing  a  considerable  reflux.  With  every  attempt  to  induce  an  accurate  closure 
of  this  valve,  its  scanty  and  divided  curtains  united  imperfectly  or 
scarcely  met,  and  were  only  sufficient  at  the  best  to  form  a  plane 
498 


TRICUSPID   INSUFFICIENCY. 


499 


Fig.  226. — The  outline  of  a  normal  heart  super- 
posed upon  that  of  a  dilated  heart,  showing  the 
enlargement  of  the  tricuspid  orifice.  Normal  heart 
shown  in  light  shading,  dilated  heart  shown  in 
black,  the  diameter  of  the  orifices  in  white  and 
black  bars,  respectively. 


equal    to     the    area    of     the    opening No    position    in    or    out 

of  water,  no  degree  of  gentleness  or  force,  no  state  in  anywise 
natural  to  the  organ  that  I  was  able  to  induce,  would  prevent 
a  considerable  riband-like  stream  of  regurgitation  between  the 
ill-apposed  edges  of  the  valve... 
The  only  possible  means  of  obtaining  a  nice, 
though  weak,  adjustment  of  the  tricuspid 
curtains  was  to  compress  the  ventricle,  and 
by  the  same  means  to  lessen  the  extent  of 
the  valvular  aperture.  ...  I  have  twice 
had  an  opportunity  of  experimenting  on  the 
human  heart  at  the  earliest  period  that 
propriety  could  admit  of.  In  one  of  the 
cases  (of  which  I  have  not  hitherto  spoken), 
after  performing  the  experiment  and  eliciting 
results  similar  to  those  related,  the  heart 
was  set  aside,  with  the  expectation  that  its 
tonicity  wTould  gradually  contract  the 
ventricles  and  fleshy  pillars,  which  accord- 
ingly occurred.  The  first  trial  of  this  heart 
was  made  with  warm  water,  and  the  fluid 
was  thrown  in  at  first  gently,  and  after- 
wards pretty  forcibly;  but  the  regurgitation 
at  this  time  was  always  considerable.  Now 
upon  repeating  this  experiment  on  the  same 

heart  when  contracted  after  the  lapse  of  a  few  hours,  the  tricuspid  valve  was  still  found 
to  be  much  less  incomplete;  still  in  this  case  there  was  some  refluent  stream.  In  the 
second  case,  however,  under  precisely  similar  circumstances,  I  obtained  at  least  an 
almost  perfect  valvular  action." 

King  also  confirmed  these  observations  by  extended  experiments 
upon  the  hearts  of  a  great  variety  of  mammals  and  birds  during  life  as  well 
as  after  death.  His  experiments  were  repeated  and  substantiated  by  G.  A. 
Gibson  in  1880,  who  showed  that  merely  narrowing  the  orifices  by 
constricting  them  with  a  cord  was  sufficient  to  prevent  the  reflux.  Fran- 
cois-Franck  in  1882  was  able  to  demonstrate  the  production  of  tricuspid 
insufficiency  in  the  living  animal  under  conditions  which  led  to  cardiac 
dilatation,  and  to  demonstrate  its  disappearance  under  digitalis.  The 
frequency  with  which  such  functional  insufficiencies  occur  in  heart  failure 
during  life  was  shown  by  Friedreich,  Mahot,  Riegel,  Mackenzie,  Hirsch- 
felder,  and  a  host  of  other  writers.  In  hearts  which  have  been  dilated 
for  a  long  period  there  is  a  considerable  stretching  of  the  valvular  orifice, 
as  was  already  noted  by  King.  This  has  lately  been  very  clearly  shown 
by  Keith's  figures  of  the  hearts  of  Mackenzie's  patients,  in  which  the 
stretching  was  so  great  that  the  usual  narrowing  at  the  auriculoventricular 
opening  had  completely  disappeared  (Fig.  226). 


PATHOLOGICAL    PHYSIOLOGY. 

As  Rosenbach  has  shown,  the  production  of  tricuspid  insufficiency 
has  in  itself  little  effect  upon  the  systemic  circulation.  Blood-pressure 
in  the  arteries  remains  unchanged,  and  there  is  no  characteristic  change 
in  the  pulse.  In  the  pulmonary  circulation  there  may  be  a  slight  fall  of 
pressure  as  a  result  of  the  regurgitation.  On  the  other  hand,  this  may  be 
compensated  by  a  slight  increase  in  the  systolic  output  of  the  right  ventricle 
and  no  change  may  occur. 


500 


DISEASES   OF   THE   HEART   AND    AORTA. 


The  principal  effect  of  tricuspid  regurgitation  is 
exerted  upon  the  circulation  in  the  systemic  veins. 
The  blood  thrown  back  into  them  at  each  systole  causes  the  pressure  to 
rise,  so  that  in  such  cases  the  pressure  may  reach  as  high  as  26  cm.  H20 
(20  mm.  Hg)  (Hooker  and  Eyster).  The  stasis  thus  occurring  also  affects 
the  peripheral  circulation  of  the  limbs  and  body,  giving  rise  to  oedema  and 
ascites;  stasis  in  the  kidneys  causing  diminished  excretion  of  a  concen- 
trated urine  rich  in  albumen  and  casts,  also  stasis  in  the  medulla  oblongata 
where  the  accumulation  of  C02  causes  a  general  reflex  vasoconstriction. 
The  secondary  effect  of  this  vasoconstriction  is  rise  of  general  blood-pres- 
sure, further  increase  of  the  work  of  the  heart,  and  increased  heart  failure— 
the  vicious  circle  of  asphyxia  (see  page  38). 


NORMAL 


TRICUSPID 
INSUFFICIENCY 


Fig.  227. — Diagram  showing  the  changes  in  the  circulation  in  tricuspid  insufficiency.  The  arrows 
show  the  rise  in  pressure  in  the  right  auricle  (RA)  and  vena  cava,  and  the  fall  of  pressure  in  the  pulmonary 
artery  (PA).  The  white  curves  represent  the  pulse-waves,  that  above  RA  showing  the  ventricular  type 
of  the  venous  pulse.  (Compare  with  Fig.  26.) 

Venous  Pulse  in  Tricuspid  Insufficiency. — In  contrast  to  the  normal 
(negative,  presystolic,  diastolic,  "double")  venous  pulse,  the  typical  pulsa- 
tion in  tricuspid  insufficiency  is  synchronous  with  and  of  the  same  frequency 
as  ventricular  systole  (single  venous  pulse)  (Friedreich,  Riegel,  Mackenzie, 
Hirschfelder) .  Since  there  is  a  free  communication  between  auricle  and 
ventricle,  the  jugular  pulse-wave  (Fig.  228)  closely  resem- 
bles the  curve  of  intraventricular  pressure,  with  its 
up-stroke  and  plateau  during  systole  and  its  fall  during  diastole.  In  the 
advanced  stages  the  wave  (a)  due  to  auricular  systole  is  absent,  since  the 
auricles  are  paralyzed  (Mackenzie) . 

Mackenzie  states,  however,  that,  contrary  to  preconceived  notions, 
all  cases  with  tricuspid  insufficiency  do  not  necessarily  show  a  positive 
venous  pulse,  and  in  a  number  of  his  cases  which  at  autopsy  showed  both 
organic  and  functional  insufficiencies  the  positive  venous  pulse  was  absent. 
Mackenzie  finds  in  these  cases  that  the  up-stroke  of  the  wave  (v),  which  is 
due  to  stagnation  in  the  ventricle,  begins  earlier  than  usual.  As  the  lesion 
increases,  this  wave  (reflux)  begins  sooner  and  sooner  after  the  beginning 
of  systole,  until  finally  it  takes  up  the  entire  systolic  period,  and  the  posi- 


TRICUSPID   INSUFFICIENCY. 


501 


JUG. 


BRACH. 


tive  or  ventricular  type  is  assumed.  These  observations  have  been  con- 
firmed in  man  by  Gibson  and  Sewall,  and  in  animals  with  tricuspid  lesions 
by  J.  Rihl,  who  found  that  as  long  as  the  regurgitation  was  slight  the 
auricular  type  of  venous  pulse  persisted,  but  when  it  became  severe  this 
gave  way  to  the  ventricular  type.  As  Sewall  states,  "among  patients  pre- 
senting themselves  for  examination  on  account  of  a  wide  range  of  func- 
tional disorders,  I  have  been 
struck  with  the  uniformity 
with  which  evidences  of  cardiac 
insufficiency  could  be  distin- 
guished, based  upon  the  nature 
of  the  symptoms  and  the  char- 
acter of  the  venous  pulse  .  .  . 
The  v  wave  has  a  double  crest; 
or  rather,  the  wave  v,  which 
begins  just  at  the  moment  of 
closure  of  the  aortic  valves,  as 
determined  by  the  dicrotic 
notch  in  the  lower  tracing,  is 
immediately  preceded  by  a  wave 
which  is  completed  during  the 
last  moments  of  ventricular 
outflow."  He  believes  that 
this  last-mentioned  wave  (the 
t  wave  of  Bard)  is  produced  by 
a  slight  regurgitation  due  to 
weakness  of  the  papillary  mus- 
cles, and  is  indicative  of  such 

regurgitation,  but  he  does  not  take  into  account  the  fact  that  it  may 
be  present  without  any  other  signs  of  tricuspid  insufficiency.  On  the  other 
hand,  as  shown  by  Theopold,  Hewlett,  and  others,  the  positive  venous  pulse 
may  be  present  without  any  regurgitation  at  the  tricuspid. 


SEC. 


Fig.  228. — Venous  pulse  of  patients  with  tricuspid 
insufficiency  (positive  venous  pulse).  JUG.,  pulsation 
over  the  jugular  vein;  BRACH.,  pulse  in  the  brachial 
artery;  c,  moment  of  onset  of  the  pulse-wave  in  the 
carotid  artery.  The  tracing  shows  an  elevation  through- 
out systole,  with  a  very  slight  depression  (perhaps  due  to 
fling)  immediately  following  the  upstroke.  The  curve 
corresponds  almost  exactly  to  the  curve  of  pressure  in 
the  right  ventricle. 


Fig.  229. —  Venous  pulse  of  another  patient.  VJD,  right  jugular  pulse;  ACS,  left  carotid  artery. 
The  slow  slanting  upstroke  indicates  a  slightly  less  smaller  leak  than  in  the  preceding  case.  There  is  no 
fling,  and  hence  no  midsystolic  depression. 


SYMPTOMS. 

The  condition  of  patients  with  tricuspid  insufficiency  well  illustrates 
the  fact  that  this  is  one  lesion  which  is  not  often  compensated,  though  com- 
pensation can  take  place  through  increased  suction-pump  action  of  the 
right  ventricle.  They  are  usually  markedly  clyspnceic  or  orthopnceic,  weak 
and  readily  exhausted  by  the  slightest  effort,  often  drowsy  and  somnolent. 


502       J        DISEASES   OF   THE   HEART    AND    AORTA. 

Palpitation  may  be  extreme.  One  of  the  early  symptoms  is  pain  in  the 
region  of  the  liver,  from  the  stretching  of  the  capsule.  This  is  often  accom- 
panied by  slight  jaundice;  and  the  appearance  of  an  icteroid  hue  is  one  of 
the  unfavorable  signs  in  tricuspid  insufficiency,  since  it  marks  an  intense 
hepatic  stasis.  Gastric  disturbances,  loss  of  appetite,  and  indigestion  are 
the  rule  and  vomiting  is  frequent. 

PHYSICAL    EXAMINATION. 

The  patients  are  usually  quite  pale  and  deeply  cyanotic.  When 
secondary  renal  changes  have  set  in,  the  face  may  be  puffy.  Emaciation 
and  slight  jaundice,  the  result  of  catarrhal  cholangitis  from  stasis  in  the 
portal  system,  are  among  the  most  suggestive  signs  that  tell  the  onset  of 
tricuspid  insufficiency.  The  veins  are  full  and  show  well-marked  pulsation, 
systolic  in  time  and  synchronous  with  the  carotid  pulse.  There  is  often 
cedema  of  the  extremities,  genitalia,  and  back,  and  large  ecchymoses  are 
not  uncommon.  Ascites  and  right-sided  hydrothorax  are  seen  in  the  last 
stages  of  almost  every  case.  Examination  of  the  eye-grounds  usually  shows 
distention  of  the  retinal  veins  (Black).  The  urine  is  usually  scant  and 
concentrated,  and  contains  a  large  amount  of  albumen  and  casts  in  large 
numbers. 

Heart. — The  precordium  often  bulges,  and  the  very  vigorous  beating 
of  the  hypertrophied  right  ventricle  is  seen  in  the  retraction  of  the  inter- 
spaces between  the  parasternal  line  and  sternal  margin.  In  the  epigastrium 
and  over  the  liver  a  systolic  pulsation  is  seen  and  felt.  Percussion 
shows  a  marked  extension  of  the  cardiac  dulness  to  the  right  of  the  sternum, 
due  to  dilatation  of  the  right  auricle.  It  often  reaches  5-6  cm.  from  the  mid- 
line, but  the  cardiohepatic  angle  remains  acute.  If  the  left  ventricle  also 
weakens,  dulness  may  extend  to  the  left  of  the  mammillary  line.  Character- 
istic of  tricuspid  insufficiency  is  a  murmur  lasting  throughout 
systole,  usually  loudest  over  the  right  ventricle,  in  the  fourth  and  fifth 
left  interspaces  between  the  parasternal  and  the  midline,  and  over  the  ensi- 
form  cartilage.  To  these  areas  it  is  probably  conducted  along  the  papillary 
muscle.  To  the  right  of  the  sternum  the  murmur  is  of  different  character, 
caused  by  the  direct  impact  of  the  regurgitant  stream.  Occasionally,  as  in 
Case  J.  D.,  this  murmur  cannot  be  heard  when  the  patient  is  lying  on  his 
back  or  even  standing,  but  can  be  elicited  by  causing  him  to  bend  for- 
ward to  an  angle  of  45°.  This  does  not  increase  the  accidental  murmur 
which  is  often  heard  over  the  entire  right  ventricle,  nor  does  it  augment 
cardiopulmonary  murmurs  over  this  area. 

The  murmur  is  often  accompanied  by  a  systolic  thrill  over  the  lower 
sternum  and  neighboring  portions  of  the  chest  wall.  The  distribution  to 
the  right  of  and  behind  the  sternum  corresponds  to  the  wall  of  the  right 
auricle,  the  chamber  into  which  the  regurgitant  stream  is  conducted  (see 
Figs.  230  and  231).  The  area  to  the  left  of  the  sternum  over  which  the 
murmur  is  loudly  heard  corresponds  to  the  wall  of  the  right  ventricle.  As 
in  mitral  insufficiency,  it  is  difficult  to  explain  the  loud  transmission  of  this 
murmur  in  a  direction  opposite  to  that  of  the  leakage,  but  it  seems  possible 
that  the  vibrations  of  the  valve  may  be  communicated  to  the  ventricular 
wall  along  the  tense  chordae  tendinese.    The  murmur  is  rarely  transmitted 


TRICUSPID   INSUFFICIENCY. 


503 


Fig.  230. — Distribution  of  the  murmur  and  cardiac 
outline  in  tricuspid  insufficiency.  The  shaded  area  indi- 
cates the  region  over  which  the  systolic  murmur  is  heard, 
the  diagram  at  the  left  indicates  its  relation  to  the  cardiac 
cycle.  The  heart  is  seen  to  be  enlarged  to  the  right.  The 
systolic  pulsation  of  the  liver  is  indicated  by  the  small 
diagram  and  the  arrows. 


as  far  as  the  pulmonary  area,  though  a  systolic  murmur  of  different  origin 
(accidental  murmur)  is  often  heard  in  the  latter  area  in  cases  with  tricuspid 
insufficiency  as  well  as  in  others.  The  tricuspid  murmur  is,  as  a  rule,  not 
transmitted  to  the  apex.  Most  frequently  in  dilated  hearts  there  is  also  a 
functional  mitral  insufficiency 
coexisting,  and  it  is  this  which 
gives  rise  to  a  systolic  murmur 
at  the  apex  and  in  the  axilla,  but 
this  is  usually  less  superficial 
than  the  tricuspid  murmur  and 
it  can  usually  be  differentiated 
from  the  latter.  Moreover,  there 
is,  between  the  two  areas  at 
which  each  murmur  has  its 
maximum,  a  zone,  correspond- 
ing to  the  interventricular  sep- 
tum, at  which  both  murmurs 
diminish  in  intensity. 

As  Hering  and  others  have 
shown,  a  systolic  murmur  is 
not  heard  in  all  cases  of  tricus- 
pid insufficiency,  especially  in 
those  in  which  the  heart  is  too 
weak  to  give  rise  to  a  loud 
sound  or  in  which  the  aperture 

of  leakage  is  too  large  to  produce  one  (large  leaks).  Sometimes  the  murmur 
has  a  musical  character.  Occasionally,  as  in  Case  W.  H.,  in  which  the  pres- 
ence of  tricuspid  insufficiency  was  demonstrated  conclusively  by  venous 
and  liver  tracings  during  life  and  by  autopsy,  peculiar  diastolic  murmurs 

are  heard  over  the  right  ventricle, 
especially  along  the  left  sternal  mar- 
gin. They  are  sometimes  blowing  and 
sometimes  rumbling  (mid-diastolic  in 
character) ,  and  may  perhaps  be  caused 
by  functional  insufficiency  of  the  pul- 
monic valves  due  to  the  dilatation  of 
the  right  ventricle. 

Organic  murmurs  are  frequently 
rough,  while  those  due  to  functional 
insufficiency  are  usually  soft  and  blow- 
ing, and  sometimes  barely  audible. 
Hering  states,  as  the  result  of  pro- 
longed experimental  investigation, 
that  functional  insufficiency  which  gives,  rise  to  distinct  murmurs  is 
usually  of  slight  grade,  but  when  the  orifice  is  much  dilated  and  the  leak 
is  a  large  one  no  murmur  is  heard.  This  aphony  of  the  valves  corre- 
sponds to  the  condition  described  on  page  176. 

Except  for  the  accompanying  murmur  which  often  replaces  the  first 
sound,  the  cardiac  sounds  are  not  greatly  modified.     The  sounds  at  the 


Fig.  231. — Cross  section  of  the  body,  show- 
ing the  paths  of  propagation  of  the  murmur  of 
tricuspid  insufficiency. 


504 


DISEASES   OF   THE   HEART   AND    AORTA. 


base  are  very  considerably  dependent  upon  the  pulmonary  and  aortic  pres- 
sures and  on  the  degree  of  arteriosclerosis,  and  hence  their  relative  loudness 
varies  considerably. 

Pulse. — The  radial  pulse  in  tricuspid  insufficiency  is  usually  small  and 
weak  and  often  irregular.  The  arrhythmia  usually  assumes  the  character 
of  permanent  absolute  irregularity  (pulsus  irregularis  perpetuus)  (see  page 
118)  and  is  accompanied  by  paralysis  of  the  auricles. 

Blood=pressure. — The  blood-pressure  is  usually  normal  or  a  little  below 
normal;  but  there  are  no  characteristic  features,  and  secondary  rises  of 
blood-pressure  from  medullary  asphyxia  are  common. 

The  liver  is  usually  enlarged  and  may  extend  far  below  the  costal 
margin  or  even  below  the  umbilicus.  It  is  usually  hard  and  its  edge  smooth, 
and  often  shows  a  distinct  systolic  pulsation  (Fig.  232). 


SYSTOLIC   PULSATION 


II 
SYSTOLIC  RETRACTION 


Fig.  232. — Tracings  of  liver  pulsation.  I.  Systolic  pulsation  of  the  liver  in  tricuspid  insufficiency. 
LIV,  tracing  from  the  liver;  BRACH,  tracing  from  the  brachial  artery;  b,  pulse- wave  in  the  brachial  ar- 
tery; c  and  d  have  their  usual  significance.  The  upstroke  of  the  arrow  indicates  a  protrusion,  the  downstroke 
a  retraction.  II.  Systolic  retraction  over  the  liver  from  a  case  of  marked  hypertrophy  of  the  right  heart. 
CAR,  tracing  from  the  carotid  artery. 


Ascites  and  oedema  of  varying  grades  may  be  but  are  not 
always  present,  dependent  upon  the  patient's  condition.  "Broken  com- 
pensation" does  not  always  indicate  "tricuspid  insufficiency/'  nor  vice 
versa. 

CASES  OF  TRICUSPID  INSUFFICIENCY. 

Myocarditis  with  Tricuspid  Insufficiency  and  probably  also  Pulmonary  • 

Insufficiency. 

W.  H.,  colored  driver,  aged  48,  first  admitted  to  the  Johns  Hopkins  Hospital  on  May 
12,  1896,  complaining  of  swelling  of  the  feet  and  shortness  of  breath.  He 
had  always  been  healthy  except  for  measles  and  chicken-pox  in  childhood  and  malaria  in 
1861.    Gonorrhoea  at  33  but  no  lues.    Drinks  and  smokes  in  moderation. 

Present  illness  began  during  the  past  winter,  with  gradually  developing  shortness 
of  breath,  especially  on  exertion.  After  such  attacks  the  extremities  would  swell  very 
much.    A  few  days  before  admission  his  testicle  also  began  to  swell. 

On  examination  by  Dr.  Thayer  at  this  time  he  was  found  to  be  a  well-formed  colored 
man,  mucous  membranes  of  good  color.  Lungs  clear  except  for  moist  rales  over  the  right 
front.  The  a p e x  was  then  in  the  sixth  interspace  at  the  mammillary 
line.  The  first  sound  was  feeble,  but  no  murmurs  were  heard.  The  abdomen  was  full; 
liver  and  spleen  not  palpable.  Slight  oedema  of  the  extremities.  The  cedema  dis- 
appeared under  rest  and  digitalis.  The  patient  gained  in  strength  and  was  discharged  in 
three  weeks.  He  returned  again  three  years  later,  with  similar  symptoms,  and  again 
made  a  rapid  recovery.  On  this  admission  the  liver  was  felt  by  Dr.  McCrae. 
He  was  treated  in  the  hospital  repeatedly  during  the  next  few  years,  always  presenting 


TRICUSPID   INSUFFICIENCY.  505 

about  the  same  clinical  picture.  On  Dec.  9,  1903,  the  apex  was  14.5  cm.  to  the 
left  of  the  midline,  and  Dr.  Thayer  noted  that  the  sounds  were  clear  in  the  tricuspid  area. 
There  was,  however,  a  soft  diastolic  and  a  rumbling  presystolic  murmur 
heard  over  the  heart  between  the  left  parasternal  line  and  the  sternal  margin  (pulmonary 
insufficiency).  When  he  first  came  under  the  writer's  care  in  July,  1904,  during  a  similar 
attack  of  cardiac  failure,  this  diastolic  murmur,  and  indeed  all  the  other  murmurs, 
had  disappeared,  the  heart  sounds  were  very  feeble  and  the  heart  action 
irregular.  As  his  condition  improved  under  treatment,  the  former  murmur 
reappeared  and  increased  to  about  the 
previous  intensity,  though  heard  only  with  the 
larger  beats.  During  the  next  admission  a  few 
months  later  the  rumble  was  definitely  mid-dias- 
tolic  and  very  rough. 

Blood-pressure     during     these      admissions 
ranged  from  130  to  160  mm.  Hg. 

He   was    readmitted  for   the    last    time    in 
October,  1905,  the  sounds  being  about  as  before, 

the  cedema  somewhat  greater.     There  was  severe 

•     i_  ^        •  j     j     i.      j         a  i.  it  iic  233. — bystolic  pulsation  of  the  liver 

right-sided    h  y  d  ro  t  h  o  r  a  x  .       Venous      of   patient  W.  H.     Car.,  carotid  arterial 
tracings    showed    a    positive    venous    pulse    of       pulse;  s,  onset  of  ventricular  systole, 
the     ventricular     type,     and     there     was 

systolic  pulsation  of  the  liver  (tricuspid  insufficiency)  (Fig.  233). 
The  blood-pressure  during  this  admission  was  110  mm.,  but  rose  to  130 
mm.    on   the   day  before   death. 

Autopsy  showed  dilatation  of  the  right  auricle  and  ventricle, 
dilatation  of  the  pulmonary  artery,  marked  sclerosis  of  the  cor- 
onary arteries,  very  marked  chronic  fibrous  myocarditis  (cardiosclerosis), 
and  relative  tricuspid  insufficiency.  There  was  marked  cardiac  hyper- 
trophy, the  heart  weighing  620  Gm.  There  were  also  chronic  passive  congestion  of  the 
viscera,  cirrhosis  of  the  liver,  chronic  interstitial  nephritis,  chronic  fibrous  pleurisy,  and 
acute  gastritis.  There  were  no  valvular  lesions  and  there  was  no  tricuspid  steno- 
sis to  account  for  the  middiastolic  rumble.  It  is  quite  probable  that  there  was  during  life 
a  functional   pulmonary  insufficiency. 

Case  of  Mitral  and  Tricuspid  Insufficiency. 

J.  D.,  painter,  aged  69,  came  to  Johns  Hopkins  Dispensary  complaining  of  swell- 
ing of  the  limbs.  He  has  always  been  healthy  except  for  inflammatory  rheu- 
matism off  and  on  during  the  last  twenty  years.  Denies  venereal  disease.  Has  not 
worked  during  the  past  twenty  years. 

He  has  had  swelling  of  the  feet  and  legs  after  exertion  during  the  past  four  years, 
some  shortness  of  breath,  but  can  always  sleep  without  a  pillow.  His  legs 
and  penis  have  been   swollen  for  the  past  month. 

The  patient  is  a  well-nourished  man,  looking  much  younger  than  he  acutally  is. 
His  color  is  a  trifle  sallow  but  not  icteroid.  Pupils  equal.  No  glandular  enlargement. 
No  lead  fine  on  the  gums,  in  spite  of  his  occupation.  The  chest  is  clear  on  percussion 
and  auscultation  except  for  a  few  wheezing  rales  at  the  bases. 

The  heart  is  markedly  enlarged,  d  u  1  n  e  s  s  extending  to  the  anterior  ax- 
il 1  ar  y  fine  in  the  fifth  left  interspace,  above  to  the  middle  of  the  second  left  interspace 
and  5  cm.  to  the  right  of  the  midline.  At  the  apex  the  first  sound  is 
replaced  by  a  blowing  systolic  murmur  heard  distinctly  throughout  the  entire 
left  axilla,  this  diminishes  in  intensity  to  the  right  of  the  mammillary  line.  When  the 
patient  is  standing  and  bending  forward  at  an  angle  of  45°,  a  loud 
blowing  systolic  murmur  of  different  character  is  heard  over  the  entire  tri- 
cuspid area,  but  this  is  not  evident  in  any  other  position.  In  the  pulmonic  area 
there  is  a  loud  blowing  mesosystolic  murmur,  also  heard  in  the  second  right  interspace, 
but  not  transmitted  to  the  carotid  arteries.  The  heart's  action  is  somewhat  irregular; 
the  jugular  veins  are  distended  but  do  not  pulsate;  the  venous  pressure,  as  shown 
by  Gaertner's  method,  is  high.  (The  veins  of  the  back  of  the  hand  and  wrist 
do  not  empty  until  the  hand  is  about  20  cm.  above  the  level  of  the  heart.) 


506  DISEASES   OF  THE   HEART   AND   AORTA. 

The  liver  is  not  palpable.  There  is  little  if  any  fluid  in  the  abdominal  cavity.  The 
6erotum  and  penis  are  markedly  oedematous,  as  are  also  the  legs  and  thighs. 

The  patient  entered  the  hospital,  where  he  died  of  heart  failure  a  few  days  later. 

DIAGNOSIS. 

The  absolute  diagnosis  of  tricuspid  insufficiency  depends  upon  the 
presence  of  a  dilatation  of  the  right  auricle  (increased  dulness  to  the  right), 
a  systolic  murmur  loudest  at  and  about  the  base  of  the  sternum,  a  positive 
venous  pulse  of  the  ventricular  type,  and  an  enlarged  liver  with  systolic 
pulsation. 

As  has  been  seen  above,  these  features  are  not  always  present.  Hering  has  summed 
up  the  whole  question  in  the  following  conclusions: 

1.  A  large  tricuspid  insufficiency  may  give  no  murmur,  but  small  regurgitations 
usually  give  distinct  murmurs. 

2.  A  small  tricuspid  regurgitation  may  cause  no  change  in  the  venous  pulse,  but  a 
large  leakage  gives  rise  to  a  positive  venous  pulse  of  the  ventricular  type.    Hence, 

I.  Loud  murmur  +  auricular  (presystolic,  diastolic,  double,  physiological)  venous 
pulse  =  slight  tricuspid  regurgitation. 

II.  No  murmur  +  positive  ventricular  venous  pulse  +  systolic  pulsation  of  liver  = 
severe  tricuspid  regurgitation, 

TREATMENT. 

Francois-Franck  showed,  in  his  experiments  upon  functional  tricuspid 
insufficiency,  that  the  administration  of  digitalis  caused  the  signs  of  insuffi- 
ciency to  disappear.  This  is  in  perfect  harmony  with  the  clinical  experience 
that  "broken  compensation"  (and  tricuspid  insufficiency)  is  in  general 
the  signal  for  digitalis,  and  the  administration  of  this  drug  furnishes  the 
main  therapeutic  measure.  Absolute  rest  is  necessary  for  prolonged  periods; 
but  after  the  tricuspid  insufficiency  has  persisted  for  months  in  spite  of  it, 
it  is  useless  to  reduce  the  patient  to  a  permanently  bedridden  condition 
in  the  hope  of  final  recovery.  It  is  better  to  render  his  life  as  pleasant  as 
possible  under  the  conditions,  to  let  him  sit  up  and  move  quietly  about  the 
house,  go  driving,  or  indulge  in  other  pleasant  diversions  which  do  not 
entail  exercise,  effort,  or  excitement.  It  must  not  be  forgotten  that  worry 
and  nervousness  bring  on  palpitation  and  cardiac  overstrain  almost  as 
readily  as  does  exercise;  and,  conversely,  mental  diversion  and  cheerfulness 
assist  in  re-establishing  conditions  favorable  for  cardiac  recovery.  The 
important  feature  in  this  phase  in  the  management  of  the  case  is  the  avoid- 
ance of  dyspncea.  The  simple  methods  of  counting  between  steps  on  a 
staircase  or  of  taking  for  one's  gait  one  step  for  each  inspiration  may  give 
the  patient  considerable  latitude  for  accomplishment  without  strain  or 
injury. 

Diet  should  always  be  light,  partly  to  avoid  the  strain  on  the  heart, 
partly  on  account  of  the  disordered  digestion,  gastritis,  and  catarrhal 
jaundice,  which  are  entailed  by  portal  stasis. 

The  bowels  should  be  kept  open  with  saline  purgatives  and  several 
movements  a  day  should  be  secured. 

In  stages  of  acute  heart  failure  when  the  venous  pressure  is  high  and 
the  right  auricle  much  distended,  venesection  should  be  resorted 
to  promptly  and  continued  until  the  right  border  of  the  heart  has  receded. 


TRICUSPID  INSUFFICIENCY.  507 

In  such  cases  digitalis  should  be  administered  in  the  large  doses  recommended 
by  Cary  Eggleston  (see  page  257),  or  at  least  in  the  somewhat  smaller  doses 
(50  minims  of  the  tincture)  administered  by  J.  O.  Hirschfelder.  Intravenous 
injections  of  strophanthin  gr.  -§V  (1  nig.)  may  also  be  used. 

BIBLIOGRAPHY. 
Tricuspid  Insufficiency. 

Gillespie,  A.  L.:  An  Analysis  of  2368  Cases  admitted  with  Cardiac  Lesions  into  the  Royal 

Infirmary,  Edinburgh,  Edinb.  Hosp.  Rep.,  1897,  v,  31. 
King,  T.  W. :  An  Essay  on  the  Safety-valve  Function  in  the  Right  Ventricle  of  the  Human 

Heart,  Guy's  Hosp.  Rep.,  Lond.,  1837,  ii,  104.    Part  II.  On  the  Safety-valve  Action 

in  the  Mammalia,  ibid.,  142.    Part  III.  Of  the  Safety-valve  in  Birds,  ibid. 
Gibson,  G.  A.:  Jugular  Reflux  and  Tricuspid  Regurgitation,  Edinb.  M.  J.,  1880,  xxv,  979. 
Francois-Franck:  Sur  la  part  importante  qui  revient  a  l'etat  du  muscle  cardiaque  dans  la 

production   des  insuffisances   tricuspidiennes   transitoires,   Compt.-rend.   Soc.    Biol., 

Paris,  1882,  xxxiv,  88. 
Friedreich,  N.:  Ueber  den  Venenpuls,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1866,  i,  241. 
Mahot:  Des  battements  du  foie  dans  l'insufhsance  tricuspide,  These,  Paris,  1869. 
Riegel,  F.:  Ueber  den  normalen  und  pathologischen  Venenpuls,  Deutsch.  Arch.  f.  klin. 

Med.,  1882,  xxxi,  26. 
Mackenzie,  J. :  The  Venous  and  Liver  Pulses,  and  Arrhythmic  Contractions  of  the  Cardiac 

Cavities,  J.  Path,  and  Bacterid.,  Edinb.  and  Lond.,  1894,  ii,  84,  273.    The  Study  of 

the  Pulse  and  Movements  of  the  Heart,  Lond.,  1903.    The  Interpretation  of  Pulsa- 
tions in  the  Jugular  Veins,  Am.  J.  M.  Sci.,  Phila.,  1907,  cxxxiv,  12. 
Hirschfelder,  A.  D.:  Graphic  Methods  in  the  Study  of  Cardiac  Diseases,  ibid.,  1906,  cxxxii, 

378.     Inspection  of  the  Jugular  Vein;    its  Value  and  its  Limitations  in  Functional 

Diagnosis,  J.  Am.  M.  Asso.,  Chicago,  1907,  xlviii,  1105. 
Keith,  A.:  An  Account  of  the  Structures  concerned  in  the  Production  of  the  Jugular  Pulse, 

J.  Anat.  and  Physiol.,  Lond.,  1907,  xliii,  1. 
Rosenbach,  O.:  Ueber  artifizielle  Herzklappenfehlern,  Arch.  f.  exper.  Path.  u.  Pharmakol., 

Leipz.,  1878,  ix,  1. 
Hooker,  D.  R.,  and  Eyster,  J.  A.  E.:  An  Instrument  for  the  Determination  of  Venous 

Blood-pressure  in  Man,  Bull.  J.  Hopkins  Hosp.,  Balto.,  1908,  xix,  274. 
Gibson,  G.  A.:  Our  Debt  to  Ireland  in  the  Study  of  the  Circulation,  Reprint  from  the 

Dublin  J.  M.  Sci.,  1907. 
Rihl,  J.:  Ueber  den  Venenpuls  nach  experimenteller  Lasion  der  Trikuspidalklappe,  Ver- 

handl.  d.  Kong.  f.  innere  Med.,  Wiesbaden,  1907,  xxiv. 
Sewall,  H.:  Safeguards  of  the  Heart-beat,  Am.  J.  M.  Sci.,  Phila.,  1908,  cxxxvi,  32. 
Hering,  H.  E.:  Ueber  pulsus  irregularis  perpetuus,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz., 

1908,  xciv,  185. 


VIII. 
TRICUSPID  STENOSIS. 

OCCURRENCE    AND    ETIOLOGY. 

Stenosis  of  the  tricuspid  orifice  belongs  to  the  rarer  valvular  lesions, 
and  also  to  the  group  which  rarely  occurs  alone.  In  the  24,000  cases  which 
have  been  admitted  to  the  Medical  Service  of  the  Johns  Hopkins  Hospital 
tricuspid  stenosis  has  been  found  in  only  seven  cases,  in  all  of  which  other 
lesions  were  present.  W.  W.  Herrick  has  recently  given  the  following 
statistics  from  187  cases  collected  from  the  literature: 

SUMMAKY   OF   REPORTED   CASES. 

Sex. 

Male 38 

Female 133 

Sex  not  known 16 

Age. 

10  to  20  years 16 

20  to  30  years 59 

30  to  40  years , 38 

40  to  50  years 28 

50  to  60  years 10 

60  to  70  years 6 

Not  known , 30 

187 

Previous  History. 

Rheumatism 61 

Doubtful  rheumatism  or  chorea 11 

No  rheumatism .    . .  33 

Not  known .  , ! 82 

Association  of  Valvular  Lesions. 

Tricuspid  alone 14 

Tricuspid  and  mitral 102 

Tricuspid  and  aortic 64 

Tricuspid  and  aortic  and  pulmonary , 1 

Tricuspid  and  endocardium  of  left  auricle 1 

Tricuspid,  mitral,  and  pulmonary 2 

Total  cases 184 

Cases  showing  adherent  pericardium 12 

In  Leudet's  series  rheumatism  was  an  etiological  factor  in  over  50  per 
cent.,  puerperal  fever  in  5  per  cent.  Syphilis  has  also  been  assigned  as  a 
causal  factor. 

508 


TRICUSPID   STENOSIS.  509 

In  the  cases  in  which  the  tricuspid  stenosis  follows  the  mitral  stenosis 
the  same  etiological  factors  are  concerned  as  for  the  single  lesion.  In  view 
of  the  work  of  Goodhart,  Roy  and  Adami,  and  Weber  and  Deguy  quoted 
above  (page  441),  it  is  not  unlikely  that  the  overstrain  of  the  right  ventricle, 
brought  about  by  the  latter  conditions,  leads  to  cedema  and  hemorrhage 
into  the  tricuspid  valve,  and  that  these  processes  usher  in  the  fibrosis.  In 
other  words,  the  mitral  stenosis  itself  becomes  an  etiological  factor  in  the 
tricuspid  lesion,  and  the  pathological  process  completed  in  the  mitral  is 
now  transferred  back  one  step  in  the  circulation  and  repeats  itself  in  the 
tricuspid. 

Occasionally,  as  in  a  case  reported  by  Gairdner,  a  fibrinous  ball,  a 
tumor,  or  a  hemorrhage  into  the  valve  may  assist  in  producing  the  stenosis. 

A  certain  percentage  of  the  cases  are  congenital  in  origin. 

PATHOLOGICAL    ANATOMY. 

The  anatomical  changes  in  the  valve  are  exactly  similar  to  those 
which  occur  upon  the  mitral  in  stenosis  of  that  orifice:  a  progressive  fibro- 
sis accompanied  by  fusion  of  the  cusps  along  their  line  of  closure,  and 
gradual  web-like  extension  of  the  valvular  membrane,  which  grows  down- 
ward between  the  shrunken  chordae  tendinese  forming  an  elongated  funnel 
with  narrow  outlet. 

The  liver  is  usually  enlarged,  though  in  some  cases  it  may  be  smaller 
than  usual,  owing  to  the  cirrhotic  changes  and  perihepatitis  which  result 
from  the  prolonged  stasis. 

PATHOLOGICAL    PHYSIOLOGY. 

The  changes  which  tricuspid  stenosis  produces  are  exactly  similar 
to  those  already  seen  in  mitral  stenosis,  except  that  they  affect  the  systemic 
veins  instead  of  the  pulmonic.  The  filling  of  the  right 
ventricle  is  retarded.  The  amount  of  blood  which  enters  it 
passively  in  early  diastole  is  diminished,  and  the  amount  driven  in  by  the 
auricle  is  increased.  The  auricle  thus  begins  to  hypertrophy.1  Its  strength 
increases,  and  the  presystolic  wave  which  it  produces  in  the  venous  pulse 
increases  in  size.  In  well-marked  cases  the  force  of  auricular  contraction 
may  be  great  enough  to  produce  a  definite  presystolic  pulsation  in  the 
liver  with  a  wave  exactly  similar  to  that  found  in  the  vein  (Mackenzie) . 

When  the  tricuspid  orifice  is  narrowed  to  such  an  extent  that  the 
increased  force  of  the  auricle  no  longer  empties  the  latter,  the  auricular 
contraction  begins  to  drive  the  blood  back  into  the  veins  and  to  increase 
the  already  high  venous  pressure,  thus  still  further  impeding  the  circula- 
tion through  the  heart  and  lungs,  so  that  the  aeration  of  the  blood  is  greatly 
interfered  with  and  marked  cyanosis  produced.  This  in  turn  gradually 
predisposes  to  polycythemia  (red  blood  count  8,000,000  to  9,000,000). 
The  latter  condition  causes  increased  viscosity  of  the  blood,  and  still 
further  increases  the  burden  upon  the  heart.     On  the  other  hand,  the 

1  The  right  ventricle  is  almost  always  hypertrophied  in  tricuspid  stenosis,  owing  to 
the  presence  of  mitral  stenosis  and  tricuspid  insufficiency. 


510 


DISEASES   OF   THE   HEART    AND    AORTA. 


hypertrophy  of  the  right  auricle  gradually  reaches  its  limit,  and  when 
the  venous  pressure  becomes  too  high  from  exercise  or 
other  cause,  this  chamber  becomes  dilated  and  paralyzed,  and  the  pre- 
systolic wave  disappears  from  the  jugular  and  liver  pulse  (Mackenzie). 
Unlike  lesions  of  other  valves,  no  further  compensation  is  now 
possible,    and  only  rest  of  the  heart  can  prevent  the  over-distention  of 

the  veins.  Consequently  slight 
I  tricuspid  stenosis  overstrain  results  at  once  in 
venous  stasis,  oedema,  etc., 
which  may  pass  off  readily 
when  the  patient  is  at  rest. 

The  liver  is  often,  though 
not  always,  enlarged;  and  a 
pulsation  presystolic  in  time 
may  be  felt  in  it  as  long  as 
the  right  auricle  is  beating 
strongly  (Mackenzie) .  (Edema, 
ascites,  and  hydrothorax  may 
be  present  as  in  other  cardiac 
diseases. 

The  pulse  is  usually 
small  because  the  peripheral 
arteries  are  constricted  in  or- 
der to  maintain  the  blood- 
pressure,  which  may  be  per- 
fectly normal.  The  rhythm 
may  continue  regular  or  may  become  irregular  as  the  disease  advances. 
Still  more  common  are  attacks  of  heart  failure  and  dropsy. 
In  many  cases,  notably  those  of  Shattuck  and  Mackenzie,  such  attacks 
may  recur  at  intervals  during  a  decade  or  more.  At  first  the  condition 
yields  readily  to  rest  and  treatment,  but  later  the  attacks  become  more 
and  more  frequent  and  persistent. 


Fig.  234. — Diagram  showing  the  changes  in  the  circu- 
lation in  tricuspid  stenosis.  The  arrows  indicate  the  rise 
in  venous  pressure  in  the  right  auricle  (RA)  and  the  vena 
cava,  and  the  fall  in  pressure  in  the  pulmonary  artery 
{PA).  The  pressure  in  the  left  auricle  and  ventricle  may 
remain  unchanged  or  may  fall.  (Compare  with  Fig.  26.) 


SYMPTOMS. 

Fortunately  for  the  patients,  the  course  of  tricuspid  stenosis  is  usually 
a  chronic  one,  the  development  of  the  lesion  generally  lagging  behind  the 
concomitant  stenosis  of  the  mitral  or  the  other  lesions  that  may  be  present. 
As  a  consequence,  the  lesion  may  be  present  for  a  number  of  years  without 
manifesting  any  signs  other  than  cyanosis,  and  no  symptoms  whatever. 
Osier  quotes  a  case  reported  by  Hirtz  and  Lemaire  who  was  known  as 
"l'homme  bleu"  for  two  years  before  he  developed  any  symptoms.  On 
the  other  hand,  in  the  case  mentioned  by  Shattuck  there  was  said  to  be  "no 
cyanosis." 

There  is  nothing  pathognomonic  about  the  symptoms.  Dyspnoea  on 
the  slightest  exertion  sets  in  and  becomes  progressively  worse.  Pain 
down  either  arm  is  relatively  common,  occasionally  pain  about  the  right 
side  and  abdomen  due  to  distention  of  the  auricle  or  of  the  liver.  Sudden 
death  is  quite  common. 


TRICUSPID   STENOSIS. 


511 


PHYSICAL    SIGNS. 

On  inspection  the  extreme  cyanosis  is  striking,  and  there  may  be  dila- 
tation and  accentuated  pulsation  of  the  veins.  When  carefully  timed  this 
pulsation  is  seen  to  be  presystolic,  and  is  often  a  "double"  pulse  of  the 
physiological  type.  Those  characteristics  are  brought  out  more  clearly 
by  a  venous  tracing.    In  long-standing  cases  the  fingers  may  be  clubbed. 

The  lungs  usually  show  signs  of  bronchitis,  oedema,  or  often  of  tuber- 
culosis. Pulmonary  infarction,  with  the  presence  of  areas  of  consolidation 
and  the  expectoration  of  dark  red  or  "prune-juice"  sputum,  is  relatively 
common.  In  the  physical  exam- 
ination of  the  heart  the  real 
lesion  is  often  overlooked.  Ex- 
cept for  the  systoliG  retraction 
over  the  right  ventricle,  there 
may  be  nothing  abnormal  on 
inspection.  The  area  of  cardiac 
clulness  is  increased  to  the  right, 
corresponding  to  the  dilated 
right  auricle;  occasionally  also 
to  the  left,  as  a  result  of  con- 
comitant lesions  other  than  the 
tricuspid  stenosis. 

Palpation  sometimes  re- 
veals a  presystolic  thrill  over 
the  lower  part  of  the  sternum 
and  just  to  the  left  of  the  latter, 
but  it  is  rarely  as  distinct  in 
the  former  situation  as  in  the 

latter  (due  to  concomitant  mitral  stenosis).  The  shock  accompanying  the 
first  sound  over  the  right  ventricle  may  be  tapping.  The  second  pul- 
monic shock  is  usually  less  marked  than  might  be  expected  to  result  from 
the  lesions  present. 

The  characteristic  sign  on  auscultation  is  the  pres- 
ence of  a  short  presystolic  rumble,  which  is  maximum  over  the 
base  of  the  sternum  and  different  in  character  from  the  presystolic  rumble 
heard  at  the  apex.  There  is  also  a  snapping  character  to  the  first  sound  in 
this  area,  and  it  may  be  accompanied  by  a  tricuspid  systolic  murmur. 
This  murmur  is,  however,  often  absent,  indistinct,  or  merges  so  gradually 
into  the  mitral  murmur  that  its  existence  is  not  noted.  Except  when  other 
lesions  are  present  the  second  aortic  and  pulmonic  sounds  are  not  as  loud 
as  might  be  expected. 


Fig.  235.  —  Cardiac  outline  and  distribution  of  the 
presystolic  rumble  and  snapping  first  sound  in  tricuspid 

stenosis. 


DIAGNOSIS. 


So  indistinct  are  the  murmurs  due  to  the  tricuspid  lesion  and  so  com- 
pletely are  they  overshadowed  by  those  of  the  mitral  or  other  orifices  that 
the  diagnosis  before  death  was  made  in  only  six  of  Leudet's  114  cases.  The 
correct  diagnosis  has  been  almost  equally  rare  since  then.  It  may  be  made 
with  certainty  in  the  presence  of  marked  cyanosis,  dilatation  of  the  right 


512  DISEASES   OF  THE   HEART   AND   AORTA. 

auricle  (increase  of  dulness  to  the  right) ,  presystolic  thrill  and  rumble,  and 
presystolic  liver  pulsation.  But  these  signs  disappear  as  the  auricle  begins 
to  weaken,  and  in  very  many  cases  the  existence  of  the  lesion  is  one  that 
can  be  suspected  rather  than  proved. 

Case  of  Tricuspid  Stenosis. 

The  following  notes  are  from  one  of  the  rare  cases  in  which  the  diagnosis 
was  made  during  life.  This  diagnosis  was  made  by  Professor  T.  B.  Futcher, 
who  has  kindly  permitted  the  writer  to  make  use  of  the  notes. 

Mrs.  A.  J.,  aged  37,  entered  the  private  wards  of  the  Johns  Hopkins  Hospital  on 
April  30,  1909.  The  family  history  was  negative.  She  was  not  a  blue  baby; 
has  been  healthy  since  childhood,  but  subject  to  occasional  sore  throat.  She  has  never 
had  acute  articular  rheumatism.  At  the  age  of  nineteen  she  had  an  obscure  fever  lasting 
several  weeks. 

She  has  been  somewhat  short  of  breath  for  the  past  nineteen  years,  and  since  an 
attack  of  grippe  about  twelve  years  ago  has  complained  of  palpitation  on 
exertion  or  after  eating.  These  symptoms  became  much  more  marked  four  years  ago, 
when  oedema  of  the  feet  and  ankles  and  cyanosis  appeared  for  the  first  time. 
This  condition  passed  off  under  treatment,  but  returned  again  two  years  later,  again  pass- 
ing off,  only  to  return  with  increased  severity  eight  weeks  before  admission.  During  this 
attack  she  has  been  blue  and  has  had    severe   orthopnoea. 

Note  by  Dr.  Futcher,  May  1,  1909:  "Patient  is  of  short  stature,  a  little  overstout; 
very  marked  cyanosis  of  ears,  lips,  cheeks,  and  finger-nails,  although  this  is 
nothing  as  compared  with  the  day  she  reached  Baltimore.  There  is  a  distinct  jaun- 
diced tint  to  the  face  and  sclerotics.  Propped  up  in  bed;  considerable  dyspnoea.  Tongue 
moist,  only  a  trifle  coated;  pupils  normal  size  and  equal,  react  to  light  and  accommodation. 

"  Still  impossible  to  count  pulse  at  wrist,  although  very  faint  beats  are  occa- 
sionally appreciable.  Thorax  well  formed,  expansion  good  and  equal  on  both  sides. 
Lower  left  axillary  region  expands  slightly  less  than  right.  Lungs  :  Right  side  clear 
throughout  front  and  axilla  on  percussion.  There  is  an  occasional  crackling  rale  heard  at 
the  base.  Fairly  numerous  fine  moist  rales  audible  throughout  whole  back.  Left  lung 
(in  semi-recumbent  posture)  flatness  reaches  to  level  of  fourth  interspace  in  anterior  axil- 
lary line.  In  midaxillary  line  it  reaches  nearly  to  apex  of  axilla,  and  in  posterior  scapular 
line  to  a  point  about  3  cm.  above  left  scapula.  Slight  movable  dulness  in 
front  with  change  of  position.  On  auscultation,  breath  sounds  are  harsh  above  and  below 
clavicle,  as  in  compensatory  breathing.  Below  level  of  flatness  there  is  absence  of  vocal 
fremitus  and  distant  tubular  breathing  and  distant  nasal  quality  of  the  voice  sound. 

"  Heart. — Point  of  maximal  impulse  seen  and  felt  in  fifth  interspace  11  cm.  to 
the  left  of  the  midsternal  line  and  just  in  the  mammillary  line.  There  is  very  slight  pre- 
cordial bulging,  but  practically  no  pulsation  or  heaving.  Systolic  shock  distinctly  tap- 
ping at  apex;  no  definite  thrill.  Relative  cardiac  dulness  commences  at  the  upper 
border  of  the  third  rib,  in  fourth  right  interspace,  extends  8.5  cm.  from 
midsternal  line,  and  merges  into  the  fluid  flatness  to  left,  but  apparently  dulness  extends 
considerably  outside  of  midline.  There  is  no  apparent  Rotch's  sign  to  the  right.  The 
absolute  cardiac  dulness  begins  at  the  upper  border  of  the  fourth  rib  at  the  left  sternal 
margin,  extends  to  right  sternal  margin  at  level  of  fourth  rib  and  to  point  of  maximal 
impulse  in  fifth  left  interspace.  On  auscultation,  the  first  sound  is  very  snap- 
ping at  apex.  There  is  as  yet  no  definite  presystolic  murmur,  but  there  is  a  slight  echo- 
ing rumble  in  diastole.  There  is  no  systolic  bruit  at  the  apex.  The  second  sound  is 
not  audible  here.  In  the  fourth  and  fifth  interspace  at  the  left  ster- 
n a  1  border  the  snapping  quality  of  the  first  sound  is  even  more  marked 
than  at  the  apex  and  the  tapping  systolic  shock  is  very  striking  here. 
The  second  sound  is  audible  and  there  is  definitely  reduplicated.  There  is  no 
rumbling  presystolic  murmur  here.  In  diastole,  however,  there  is,  on 
very  careful  auscultation,  a  faint,  soft,  prolonged,  blowing  diastolic 
murmur.  At  the  aortic  area  yesterday  there  was  a  faint  systolic  thrill. 
It  is  just  perceptible  this  morning.  The  first  sound  is  audible  and  is  accompanied 
by  a  very  rough  systolic  bruit  transmitted  upwards  to  stenoclavicu« 


TRICUSPID   STENOSIS.  513 

I  a  r  articulation.  The  second  aortic  is  quite  loud  and,  if  anything, 
accentuated.  There  is  no  aortic  diastolic  bruit  heard  here.  Pulmonic  sounds  clear, 
second  pulmonic  accentuated.    The  external  jugulars  are  only  slightly  distended. 

''Liver. ; — Absolute  flatness  extends  from  sixth  rib  to  a  point  apparently  on  a 
level  with  the  costal  margin  in  right  mammillary  line.  In  median  line  it  reaches  only  to 
tip  of  ensiform.  Owing  to  cedematous  abdominal  walls,  it  is  not  possible  to  palpate  for 
liver  edge.     No  visible   or  palpable  liver  pulsation. 

"Abdomen  moderately  distended,  walls  cedematous,  tympanitic  in  elevated  and  flat 
in  dependent  portions.  Undoubtedly  some  ascites.  There  is  very  marked  cedema  of 
dependent  portions  of  trunk,  moderate  of  arms  and  hands,  very  marked  of  thighs  and  legs. 

" Over  dorsal  surfaces  of  both  wrists  there  are  quite  numerous  pin-head 
sized   petechias." 

The  urine  was  very  scant  (300  c.c),  of  orange  color,  specific  gravity  1015,  acid,  con- 
tains a  trace  of  albumin  and  many  hyaline  and  finely  granular  casts. 

Her  chest  was  aspirated  by  Dr.  Henry  on  May  1,  and  500  c.c.  of  dark  straw- 
colored  clear  fluid  removed.  She  became  worse,  however,  and  her  kidneys  refused  to  act. 
On  May  3  her  pulse  became  irregular,  cyanosis  increased,  and  the 
petechial  eruption  on  the  dorsum  of  wrists  became  more  extensive.  She  died  at 
3.15  p.m. 

Intra  vitam  diagnosis  by  Dr.  Futcher:  Aortic  stenosis  and  insuffi- 
ciency,  mitral   stenosis,   probable   tricuspid  stenosis. 

Autopsy  showed  tricuspid,  mitral,  and  aortic  stenosis,  dila- 
tation and  hypertrophy  of  the  auricles,  contraction  and  atrophy  of  the 
ventricles,  chronic  passive  congestion  of  all  the  tissues  except  the 
lungs,  generalized  cedema,  pleural  and  pericardial  effusion,  compression  and  atelectasis 
and  cedema  of  the  lungs,  hemorrhagic  infarctions  of  lungs,  acute  diphtheritic  hemorrhagic 
colitis,  generalized  narrowing  of  arteries  and  thickening  of  veins. 

TREATMENT. 

Except  for  rest,  purgation,  and  palliative  treatment,  little  can  be  said 
in  this  condition.  Digitalis  is  sometimes  of  value  to  restore  tone  to  the 
auricle  and  increase  the  force  of  the  ventricular  contraction,  but  it  very 
frequently  fails.  In  the  spells  of  acute  heart  failure  a  free  venesection 
may  ward  off  impending  death  by  lowering  the  venous  pressure,  relieving 
the  heart  failure;  and  by  diminishing  the  viscosity  of  the  blood  may  afford 
more  lasting  relief.  Free  purgation  is  often  also  of  great  benefit,  because  it 
may  lower  the  pressure  in  the  veins. 

PROGNOSIS. 

The  prognosis  depends  entirely  upon  the  degree  of  stenosis  and  the 
rapidity  of  its  progress.  As  has  been  said,  this  is  frequently  very  chronic. 
Mackenzie's  famous  case,  which  is  typical,  was  a  woman  whose  lesion 
probably  dated  from  an  attack  of  rheumatism  in  1880,  at  the  age  of  twenty- 
nine.  In  1892  she  complained  of  weakness  and  shortness  of  breath,  and 
at  that  time  the  liver  showed  a  presystolic  pulsation.  She  was  subject  to 
numerous  temporary  attacks  of  extreme  heart  failure  and  died  in  1899. 
However,  this  woman  was  under  excellent  care  during  the  last  seven  years 
of  her  life,  and  lived  a  tolerably  discreet  and  hygienic  existence.  Had  she 
been  compelled  to  do  heavy  work  her  life  would  probably  have  been  much 
shorter. 

33 


514  DISEASES   OF  THE   HEART   AND   AORTA. 

BIBLIOGRAPHY. 
Tricuspid  Stenosis. 

Herrick,  W.  W.:  Tricuspid  Stenosis,  with  Report  of  a  Cure,1  Arch.  Int.  Med.,  Chicago, 
1908,  ii,  295. 

Huchard,  H.:  Maladies  du  coeur,  tome  hi,  Paris,  1905;  based  upon  statistics  of  Leudet, 
R.:  Essai  sur  le  retrecissement  tricuspidien,  Paris,  1888. 

Herrick.  J.  B.:  Tricuspid  Stenosis,  with  Report  of  Three  Cases  with  Autopsies,  etc.,  Bost. 
M.  and  S.  J.,  1897,  cxxxvi,  245.  " 

Goodhart,  Roy  and  Adami,  Weber  and  Deguy.     See  page  449. 

Gairdner.     Quoted  from  Herrick. 

Mackenzie,  J.:  Notes  on  a  Case  Presenting  some  Novel  Features  in  Cardiac  Symptoma- 
tology, Edinb.  Hosp.  Rep.,  1897,  v,  22.  Studies  on  the  Pulse  and  Movements  of  the 
Heart,  N.  Y.,  Edinb.,  and  Lond.,  1902. 

1  Probably  intended  to  be,  "  with  Report  of  a  Case." 


IX. 


MARRIAGE,   PREGNANCY   AND   LABOR   IN   CASES   OF   HEART 

DISEASE. 

PULSE-RATE    AND    BLOOD-PRESSURE. 

The  effect  of  pregnancy  upon  the  heart  is  influenced  by  several  factors. 
The  gradual  pushing  of  the  diaphragm  as  the  uterus  grows  causes  the  heart 
to  assume  a  more  transverse  position  (raising  the  apex  to  the  fourth  inter- 
space in  28  out  of  35  cases  observed  by  Stengel  and  Stanton),  and  thus  plac- 
ing it  in  a  position  which  embarrasses  its  action.  Moreover,  a  reflex  vagus 
inhibition  is  often  present,  which  causes  the  pulse-rate  to  become  slowed. 
Blot  has  reported  a  pulse-rate  as  low  as  36;  40  per  cent,  of  Vegas's  cases 
were  slow,  but  only  26  per  cent,  of  Skabo's  cases  were  below  75  per  minute. 
There  is  also  an  increase  in  the  width  of  the  blood  channel  through  the 
uterine  vessels,  which  is  manifested  by  the  presence  of  a  dicrotic  pulse. 
In  order  to  overcome  these  factors  and  to  keep  up  the  equilibrium  of  the 
circulation,  the  heart  is  compelled  to  put  forth  increased  efforts.  Slemons 
and  Goldsborough  in  a  most  careful  series  of  observations  have  found  the 
following  figures,  which  accord  well  with  the  previous  findings  of  O.  Fellner, 
Stengel  and  Stanton,  and  Vogeler. 

They  found  the  following  figures  : * 


Blood-pressures. 

Pulse- 
rate. 

Cardiac 

output 

P.P.  x  P.R. 

Work  of  heart. 
Mean  pi.  x  pulse- 
rate. 

Max. 

Min. 

Pulse- 
pressure. 

Mean   pressure 
(min.+^  P.  P.) 

Normal 

(Erlanger) 
Pregnancy . . . 

Puerperium . . 

110 
127 

115 

65 
74 

72.5 

45 

53 

49 
in  primig. 

60 
in  multip. 

42.5 

80 

91.6 
86.5 

72 
80.5 

70.5 

.     3240 

3325 
(primig.) 

5332 
(multip.) 

3000 

259,000 

Primig. 
195,000  to  429,000 

Multip. 
42l,000to  1,065,000 

Primig. 
290,000  to  327,000 

Multip. 
156,000  to  337,000 

H 

YPERTROPH 

y. 

This  prolonged  increase  in  work  was  supposed  by  Larcher  to  bring 
about  hypertrophy  of  the  heart,  a  fact  which  has  found  some  support  in 
the  weighings  of  certain  observers;  but  the  more  careful  work  of  W.  Muller 
and  of  later  observers  (average  weight  of  heart  during  pregnancy  227  Gm.) 

1  While  this  method  of  calculation  is  not  intended  to  be  regarded  as  quantitatively 
accurate  (see  p.  36),  it  shows  the  qualitative  changes  fairly  well. 

515 


516  DISEASES  OF  THE  HEART  AND  AORTA. 

fails  to  substantiate  this  view.  The  increase  in  size  supposed  to  represent 
hypertrophy  is  probably  due  in  part  to  dilatation  of  the  heart,  and  in  part 
to  the  apparent  increase  in  cardiac  area  which  occurs  when  the  heart  lies 
in  a  more  transverse  position.  However,  a  very  slight  hypertrophy,  like 
that  of  the  athlete's  heart,  may  occur  during  pregnancy.  During  labor  an 
additional  strain  of  short  duration  is  thrown  on  the  heart. 

FUNCTIONAL     TRICUSPID     INSUFFICIENCY     AND     OVERSTRAIN     DURING     LABOR. 

James  Mackenzie  has  shown,  moreover,  that  the  dilatation  during 
pregnancy  affects  the  right  heart  particularly,  and  that  in  very  many  cases 
even  of  otherwise  normal  women  a  definite  insufficiency 
of  the  tricuspid  valve  may  appear,  disappear,  and  reappear  accord- 
ing to  the  condition  of  the  patient.  The  presence  of  this  insufficiency  is 
shown  by  both  the  positive  venous  pulse  and  the  systolic  murmur  in  the 
tricuspid  area. 

THE   EFFECTS   DURING   THE   LABOR   PAINS. 

Moreover,  J.  C.  Litzenberg  (Am.  Journ.  Obstetrics,  1916,  Ixxiii,  228)  has 
found  urobilin  is  present  in  the  urine  of  25  per  cent,  of  normal  pregnant  women, 
especially  in  the  later  stages.  This  indicates  diminished  liver  function  which 
is  really  brought  about  by  stasis;  and  is  perhaps  one  of  the  signs  of  cardiac 
overstrains  in  late  pregnancy. 

Dr.  Slemons  informs  the  writer  that  Muring  the  labor  pains  there  is  often 
a  rise  of  fifty  millimetres  of  mercury  in  the  maximal  pressure,  though  these 
elevations  are  of  short  duration.  It  is  therefore  not  surprising  that  some 
hearts  should  fail  and  that  pulmonary  oedema  should  be  an  occasional  com- 
plication, especially  in  mitral  stenosis  where  the  pulmonary  circulation  is 
already  engorged.  It  is  perhaps  surprising,  however,  that  so  few  cases  actu- 
ally succumb  during  the  strains  of  labor.  Schlayer's  results  typify  the  gen- 
eral experience  in  this  regard.  He  lost  eight  out  of  twenty-five  cases  (32  per 
cent.)  of  severe  heart  disease,  but  only  two  of  these  (8  per  cent.)  died  during 
labor.  The  act  of  labor  itself  does  not  impose  a  much  more  severe  strain 
upon  the  organism  than  that  arising  during  the  course  of  pregnancy. 

CAUSE  AND  FREQUENCY  OF  DEATH  FROM  LABOR. 

The  immediate  cause  of  death  during  labor  is  usually  pulmonary 
oedema  from  failure  of  the  left  ventricle.  However,  as  above  stated,  only 
about  one-fourth  of  the  fatal  cases  die  during  labor,  the  greater  number 
surviving  some  days,  weeks,  or  months.  In  the  cases  of  mitral  stenosis, 
apoplexy  or  cerebral  embolism  is  not  uncommon,  owing  to  loosening  of 
thrombi  which  form  in  the  left  auricle  during  the  periods  of  stasis. 

As  regards  the  results  obtained  by  different  writers  in  cases  with  heart 
lesions  the  greatest  divergence  is  found.  The  following  represent  the  mor- 
tality reported  by  various  writers:  Macdonald  61  per  cent.,  v.  Guerard 
34  per  cent.,  Lublinsky  60  per  cent.,  v.  Leyden  55  per  cent.,  Schlayer  48 
per  cent.,  Wessner  49.3  per  cent.,  Lwoff  12  per  cent.,  Gusserow  6  per  cent., 
Jess  31.5  per  cent.,  Wiesenthal  12.5  per  cent.,  Schneider  7.1  per  cent.,  Mtiller 
3  per  cent. 


PREGNANCY  AND  LABOR  IN  HEART  DISEASE. 


517 


A  very  careful  study  of  these  conditions  has  been  made  by  O.  Fellner  in 
Schauta's  clinic  in  Vienna.  Fellner  noted  that  the  percentage  of  heart  cases 
reported  in  obstetrical  clinics  was  far  too  low  for  the  general  prevalence  of 
cardiac  disease,  and  upon  careful  routine  examination  found  that  about  six 
cases  out  of  seven  of  compensated  heart  diseases  were  actu- 
ally escaping  detection  in  the  clinics.  So  little  effect  had  heart 
disease  made  upon  the  course  of  pregnancy  and  labor!  Of  the  cases  that  had 
been  recognized  in  the  obstetrical  clinic  in  ten  years  he  found  the  following:1 


Cases. 


Mother 
died. 


Child 
died. 


Mitral  insufficiency, 

Compensated 

Uncompensated 

Mitral  stenosis, 

Compensated 

Uncompensated 

Mitral  stenosis  plus  insufficiency, 

Compensated 

Uncompensated 

Aortic  insufficiency, 

Uncompensated 

Aortic  insufficiency  plus  mitral  insufficiency, 

Compensated 

Uncompensated 

Total 


26 
14 


10 
17 


2 
10 


81 


26 


In  the  900  cases  occurring  since  his  own  routine  examinations  of  the 
heart  were  instituted,  he  found: 


Mitral  insufficiency, 

Compensated 

Uncompensated 

Mitral  stenosis  plus  insufficiency, 

Compensated 

Uncompensated 

Aortic  insufficiency  plus  mitral  insufficiency, 
Compensated 


FACTORS   INFLUENCING   PROGNOSIS. 

These  statistics  from  unselected  cases  are  much  more  favorable  than 
the  previous  reports  would  indicate,  and  are  in  accordance  with  the  con- 
clusions of  Hicks  and  French  that  few  women  with  heart  disease  are  sterile, 
that  they  are  not  particularly  liable  to  abort,  and  that  most  of  them  bear 

1  Jaschke  (Arch.  f.  Gynaekol.,  xcii,  466)  reports  similar  findings  in  546  heart  cases 
among  37,014  women. 


Cases. 

Mother 
died. 

14 

0 

1 

0 

3 

0 

1 

1 

1 

0 

Child 
died. 


518  DISEASES   OF   THE   HEART   AND   AORTA. 

children  well.  Blacker,  in  a  most  excellent  resume  of  the  subject,  coin- 
cides with  these  opinions,  but  finds  53  deaths  (12  per  cent.)  in  453  cases  of 
heart  disease  taken  from  the  literature. 

Most  writers  believe  that  the  variety  in  the  results  is  due  to  the  severity 
of  the  cases  which  happen  to  be  encountered,  or  at  least  recognized;  but 
the  excellent  statistics  from  Schauta's  clinic  would  indicate  that  skill  in. 
the  management  of  the  case  plays  a  considerable  role.  It  must  not  be 
forgotten  that  the  recognition  of  an  organic  valvular  lesion  in  a  pregnant 
woman  may  be  by  no  means  easy,  for  the  functional  or  accidental  systolic 
murmurs  at  the  apex,  occurring  during  pregnancy,  may  closely  simulate 
those  from  an  organic  mitral  insufficiency;  and,  unless  their  disappearance 
is  noted  by  the  end  of  the  puerperium,  this  discrepancy  may  not  be  noted. 
The  constancy  of  the  murmur,  its  roughness,  its  transmission  to  the  axilla 
and  the  increase  rather  than  decrease  in  intensity  at  times  when  the  condi- 
tion of  the  heart  improves  favor  the  diagnosis  of  an  organic  mitral  insuffi- 
ciency; while  in  the  presence  of  a  soft  murmur  occurring  with  a  dilated  heart, 
a  rapid  pulse,  and  a  break  in  compensation  the  presumption  is  temporarily 
in  favor  of  the  more  common  functional  insufficiency.  The  diagnoses  of 
mitral  stenosis  and  of  aortic  insufficiency  are  probably  more  uniformly' 
correct  and  present  less  difficulty. 

Broken  Compensation  in  Pregnancy. — On  the  other  hand,  it  may  be 
difficult  to  judge  when  compensation  should  be  considered  broken.  The  push- 
ing up  of  the  diaphragm  by  the  pregnant  uterus  and  the  increased  volume  of  the 
blood  all  tend  to  overwork  the  heart,  and,  on  the  other  hand,  the  pressure  of 
the  uterus  on  the  pelvic  veins  may  cause  oedema  of  the  legs  which  may  simu- 
late a  heart  failure  that  may  not  be  present.  And,  moreover,  a  relative  tricus- 
pid insufficiency  of  muscular  origin  may  be  present  as  a  result  of  the  pregnancy 
without  organic  lesion,  but  may  nevertheless  give  rise  to  the  same  signs  and 
practical  effects  as  the  latter. 

The  diagnosis  of  broken  compensation  in  pregnancy  therefore  depends 
upon  signs  which  are  relative  rather  than  absolute,  since,  as  Mackenzie  shows, 
a  certain  degree  of  broken  compensation  is  an  almost  normal  phenomenon  in 
the  later  months  of  pregnancy.  This  again  is  relative,  for  some  women  are 
almost  as  active  throughout  pregnancy  as  at  other  times,  while  other  quite 
normal  women  may  be  almost  invalids  throughout  the  entire  period.  Due 
attention  should  be  paid  to  Litzenberg's  sign  of  urobilinuria  (see  page  516). 
Dyspnoea  and  cyanosis  on  very  slight  exertion,  such  as  quietly  walking  a 
distance  of  a  few  hundred  yards  or  less,  walking  up  a  few  stairs,  etc.,  and 
the  presence  of  a  small  rapid  pulse,  persistent  cough,  enlargement  of  the  liver 
and  oedema  of  the  feet  and  legs  may  be  regarded  as  the  most  important 
symptoms.  The  earlier  in  pregnancy  they  occur  the  more  alarming  they  are. 
Persistent  dyspnoea  or  orthopnoea  and  cyanosis  alone,  especially  in  the  pres- 
ence of  a  valvular  lesion,  are  in  themselves  most  significant  and  should  warrant 
immediate  attention. 

MANAGEMENT   OF    CASES   OP   HEART   LESIONS   IN   PREGNANCY. 

The  correct  management  of  a  case  of  heart  lesion  complicated  by  preg- 
nancy is,  as  stated  by  Blacker,  to  treat  the  heart  disease  with- 
out   regard     to    the     pregnancy    until    the    break    in 


PREGNANCY  AND    LABOR   IN   HEART   DISEASE.         519 

compensation  is  seen  to  persist,  and  then  to  termi- 
nate the  pregnancy.  In  other  words,  as  long  as  compensation  is 
good  the  patient  should  merely  be  carefully  watched  but  no  medication 
need  be  resorted  to.  At  the  first  signs  of  cardiac  weakening  and  dilatation 
(dyspnoea  and  cyanosis,  etc.,  on  slight  exertion)  absolute  rest  should  be 
insisted  on  and  digitalis  or  strophanthus  should  be  given.  This  procedure 
should  be  insisted  on  even  if  the  diagnosis  of  organic  valvular  lesion  is  not 
definite,  for  these  procedures  will  afford  quite  as  much  relief  in  cases  of 
functional  tricuspid  insufficiency.  Moreover,  they  should  be  repeated  at 
the  slightest  indication  (see  page  252),  especially  toward  the  end  of  pregnancy. 
It  is  advisable  in  such  cases  to  give  a  few  prophylactic  doses  of  digitalis 
when  labor  seems  imminent,  or  a  few  doses  of  strophanthus  at  the  begin- 
ning of  labor  pains,  so  as  to  have  the  tonus  of  the  heart  muscle  at  its  opti- 
mum by  the  time  the  strain  of  the  second  stage  is  imposed  upon  it.  At 
periods  of  acute  dilatation,  and  especially  when  pulmonary  oedema  sets 
in,  venesection  affords  the  greatest  relief. 

If  cardiac  symptoms  disappear  the  patient  may  be  gradually  allowed 
up  and  around,  but  she  must  be  more  careful  than  before,  and  if 
signs  of  a  second  break  in  compensation  occur,  terminating  the  pregnancy 
should  be  seriously  considered.  This  is  especially  true  in  cases  of  mitral 
stenosis,  in  which  the  cardiac  accidents  of  pregnancy  are  particularly  fre- 
quent. Women  with  compensated  mitral  stenosis  may  pass  through  five, 
six,  or  seven  pregnancies  without  appearing  to  be  injured  by  them  (Len- 
hartz),  but  when  cardiac  symptoms  appear  in  a  case  of  this  disease  during 
the  course  of  a  pregnancy  it  is  nearing  the  danger  line,  and  if  these  persist 
in  spite  of  rest  and  treatment  or  when  compensation  is  once  broken,  the 
danger  becomes  great. 

Fellner's  low  mortality  (21  cases  with  1  death)  is  probably  due  to  the 
careful  practice  of  Schauta's  clinic,  which  he  summarizes  in  the  advice  to 
"terminate  pregnancy  in  cases  of  mitral  stenosis  as  soon  as  the  slightest 
signs  of  broken  compensation  appear,"  or  in  cases  in  which  signs  of  danger 
had  been  present  in  previous  pregnancies. 

Case  of  Mitral  Stenosis  with  Pregnancy  and  Labor. 

The  danger  of  disregarding  this  advice  was  well  illustrated  by  a  patient  under  the 
writer's  care  during  the  past  year.  She  was  a  young  married  woman  of  twenty-six,  and 
was  seen  in  November,  1907,  in  the  sixth  month  of  pregnancy,  complaining  of 
shortness  of  breath  and  was  quite  cyanotic.  Her  trouble  dated  from 
the  birth  of  her  first  child  nine  months  before,  at  which  time  she  had 
evidently  received  a  mild  puerperal  infection.  The  veins  were  rather  full; 
her  heart  was  not  enlarged,  and  at  the  apex  the  first  sound  was  snapping 
and  preceded  by  a  slight  presystolic  rumble.  This  varied  in  intensity  from  time 
to  time.  Occasionally  a  blowing  diastolic  murmur  wras  heard  along  the  left 
border  of  cardiac  dulness,  but  not  over  the  aortic  area.  The  pulse  was  small 
and  weak,  not  collapsing,  usually  regular.  There  was  slight  oedema  of  the 
shins  and  ankles.  The  patient  was  placed  in  the  hospital,  and  her  condition  improved  at 
once,  so  that  within  two  weeks  she  was  allowed  to  enter  the  waiting  ward  of  the  obstet- 
rical department.  It  was  then  proposed  that  labor  should  be  induced,  but  the  obstetrical 
house  staff  did  not  regard  the  case  as  imperative.  She  left  the  hospital  contrary  to  advice, 
and  on  January  1,  1908,  in  the  seventh  month  of  pregnancy,  she  was  delivered  of  a 
healthy  premature  child.  The  labor  was  easy.  She  insisted  upon  giv- 
ing the  infant  the  breast  for  a  couple  of  weeks,  but  remained  in  bed  and  quiet,  suffering 


520  DISEASES   OF   THE   HEART   AND    AORTA. 

from  orthopnoea.  This  continued  in  spite  of  digitalis.  Her  liver  was  enlarged,  and 
oedema  of  the  legs  gradually  set  in.  She  finally  returned  to  the  hospital,  but  never  recu- 
perated, and  died  in  June,  1908.  The  child,  which  had  always  been  under  the 
care  of  a  district  nurse  and  later  in  the  Thomas  Wilson  Hospital,  a  l's  o  died  dur- 
ing the  same  month. 

Termination  of  Pregnancy. — In  an  almost  exactly  similar  case  Hellendal 
performed  an  abortion  as  soon  as  the  signs  of  broken  compensation  were 
definite,  and  eight  days  later  resected  both  tubes  to  prevent  subsequent 
pregnancy.  The  patient  made  a  perfect  recovery  and  her  life  is  no  longer 
endangered. 

In  deciding  the  question  of  terminating  pregnancy,  it  must  be  borne 
in  mind  that  in  from  2  5  to  40  per  cent,  of  patients  with 
severe  heart  lesions  the  pregnancy  does  not  reach 
term,  but  premature  labor  occurs  spontaneously  owing  to  partial  asphyxia 
of  the  foetus.  The  placental  circulation  is  slowed,  the  aeration  is  poor,  and, 
as  Fellner  has  shown,  there  is  often  a  large  necrotic  border  about  the  pla- 
centa. This  probably  results  from  thrombosis.  Moreover,  the  statistics 
of  the  obstetrical  clinics,  even  of  Schauta's,  are  far  more  favorable  than  the 
end  results  would  show.  Our  own  case  above  mentioned  would  be  classed 
in  such  statistics  as  "improved"  at  the  end  of  the  puerperium  and  the 
child  as  "  living " ;  while,  as  a  matter  of  fact,  both  died  within  six  months 
after  the  labor.  Since  most  statistics  are  compiled  from  the  histories  of 
hospitals,  where  the  cases  are  subsequently  lost  sight  of,  it  is  probable  that 
this  represents  a  very  large  class  of  cases.  The  children  are  especially  deli- 
cate, and,  even  if  they  survive,  succumb  more  easily  to  pulmonary  and  gastro- 
intestinal infections  during  the  first  or  second  year  than  do  other  children. 

The  inevitably  high  child  mortality  and  the  danger  to  the  mother, 
especially  in  mitral  stenosis,  somewhat  lessen  the  moral  responsibility  of 
terminating  pregnancy.  Moreover,  as  Weber  and  Deguy  have  shown, 
pregnancy  and  labor  are  in  themselves  causal  factors  in  valvular  disease, 
and  especially  mitral  stenosis,  through  the  occurrence  of  hemorrhages  into 
the  substance  of  the  valves  (see  Chapter  III),  or,  as  in  the  case  of  our 
patient,  bring  about  the  recurrence  of  a  slumbering  endocarditis,  and  thus 
leave  the  patient  worse  than  before,  often  with  a  progressive  lesion.  When 
it  has  been  decided  to  terminate  pregnancy,  this  should  be  done  as  soon  as 
possible.  The  procedure  of  choice  depends  upon  the  severity  of  the  symp- 
toms and  the  necessity  for  immediate  emptying  of  the  uterus.  They  have 
been  summed  up  by  Fellner  in  the  following  scale:  (1)  Induction  of 
labor  with  de  Ribes  bag  or  packing  the  cervix;  (2)  craniotomy;  (3)  forceps; 
(4)  version  and  extraction;  (5)  Csesarean  section.  In  general  it  must  be 
said  that  the  less  the  operative  interference  with  the  physiological  course 
of  each  stage,  the  less  shock  to  the  patient  and  the  better  the  end  result. 
On  the  other  hand,  each  stage  of  labor  is  likely  to  be  prolonged  in  such 
cases  and  this  must  be  avoided.  When  the  condition  is  alarming,  the 
relief  should  be  rapid.  Pulmonary  oedema  is  often  at  once  relieved  by 
tapping  the  fetal  membranes,  removing  the  amniotic  fluid,  and  allowing 
the  diaphragm  to  descend;  although  the  labor  then  becomes  much  harder. 
The  patients  usually  stand  the  operative  interference  well.  As  in  other 
conditions,  ether  is  preferable  to  chloroform  where  the  heart  is  diseased. 


PREGNANCY  AND    LABOR   IN   HEART    DISEASE.         521 


AORTIC    DISEASE    IN    PREGNANCY. 

As  aortic  disease  is  comparatively  rare  in  women,  it  usually  receives 
little  mention.  It  is  significant,  however,  that  in  Fellner's  series  there  was 
a  very  high  mortality  (60  per  cent.)  in  the  fcetus.  Newell  reports  a  case 
in  which  there  was  little  cardiac  discomfort  throughout  pregnancy,  but  a 
hard  labor  set  in.  Forceps  were  used.  Collapse  and  pulmonary  oedema 
ensued,  and  the  mother  died  four  hours  after  labor.  The  child  died  also. 
This  is  simply  an  example  of  the  acute  heart  failure  (probably  acute  dila- 
tation of  the  left  ventricle  with  sudden  onset  of  functional  mitral  insuffi- 
ciency) so  characteristic  of  aortic  insufficiency.  Mitral  lesions  are  usually 
more  dangerous  than  aortic,  but  they  usually  give  signs  of  gradual  progres- 
sion. The  danger  in  aortic  insufficiency  may,  as  in  Ne well's  case,  come  on 
very  rapidly  and  result  in  the  death  of  the  patient. 

SUBSEQUENT    PRECAUTIONS. 

In  cases  in  which  dangerous  breaks  in  compensation  occur  during  the 
course  of  pregnancy  and  termination  of  the  latter  becomes  necessary,  as 
well  as  in  those  which  reach  a  natural  termination  under  conditions  in  which 
the  life  of  the  mother  is  endangered,  measures  must  be  taken  to  prevent 
subsequent  conception.  As  Feis  points  out,  the  physician's  advice  to  a 
married  woman  to  absolutely  avoid  coitus  is  so  rarely  followed  that  for 
practical  purposes  it  is  scarcely  worth  giving.  To  rely  entirely  upon  it 
therefore  savors  of  hypocrisy.  Feis  believes  that  in  these  cases  prophylactic 
measures  against  conception  should  be  advised.  Fellner  and  Hellendal 
go  one  step  further.  They  both  advise  and  practise  sterilization  of  the 
mother  by  resection  of  the  tubes,  an  operation  which  is  not  fraught  with 
much  danger,  and  which  then  relieves  her  from  the  sword  of  Damocles 
that  otherwise  hangs  over  her  head. 

MATRIMONY    AND    HEART    DISEASE. 

The  question  also  arises  under  what  condition  may  women  with  heart 
disease  be  permitted  to  marry.  As  Fellner's  statistics  show,  the  danger 
is  not  very  great.  Blacker  sums  up  the  facts  in  the  statement  that  all 
women  with  heart  lesions  will  suffer  from  them  sooner  or  later,  and  that 
this  period  need  not  be  much  accelerated  by  pregnancies.  Some  writers 
even  go  so  far  as  to  state  that  pregnancies  do  not  alter  the  duration  of  life 
at  all,  but  this  view  is  much  too  optimistic.  The  best  proof,  however, 
that  the  compensated  heart  lesion  should  not  be  a  bar  to  matrimony  is 
shown  by  Fellner's  statistical  proof  that  six  out  of  every  seven  heart  lesions 
are  not  even  suspected  in  the  average  obstetrical  clinic.  On  the  other  hand, 
if  compensation  is  poor,  marriage,  like  any  other  strain,  should  of  course 
be  forbidden.  This  again,  as  Fellner  points  out,  depends  as  much  on  socio- 
logical as  on  physical  factors,  for  a  woman  in  poor  circumstances  may  be 
able  to  live  more  quietly  and  avoid  cardiac  strain  more  readily  in  married 
life  than  when  supporting  herself  by  her  own  work.  Under  such  circum- 
stances the  patient  should  be  made  fully  aware  of  the  dangers  of  conception 
and  coitus.    All  things  being  considered,  compensated  mitral  stenosis  cannot 


522  DISEASES  OF  THE  HEART  AND  AORTA. 

be  made  an  exception  to  these  rules,  although  its  presence  warrants  a  cer- 
tain foreboding  in  the  physician  consulted,  and  should  direct  his  advice 
toward  the  side  of  caution.  If  compensation  has  once  been  broken  in  a  case  of 
mitral  stenosis,  conception  should  be  forbidden  and  marriage  strongly  advised 
against.  The  same  applies  to  well-marked  chronic  myocarditis 
or  nephritic  cardiopathy  when  these  can  be  diagnosed  with 
probability,  since  they  run  a  more  unfavorable  course  for  both  mother  and 
foetus  than  do  the  cases  of  valvular  lesions. 

MARRIAGE   IN   MEN   SUFFERING   FROM   HEART  DISEASE. 

In  men  with  cardiac  disease  the  problem  of  marriage  is,  as  a  rule,  less 
serious  than  in  women,  owing  to  the  less  severe  physical  strain  imposed 
upon  the  patient;  but,  nevertheless,  it  entails  certain  dangers.  These  may 
be  divided  into  two  groups,  the  purely  physical  strain  of  coitus  and  the 
mental  strains  incident  to  providing  for  a  family,  as  well  as  those  of  domestic 
arguments  and  disagreements. 

Whether  the  effects  of  coitus  will  be  deleterious  depends  upon  many 
factors.  As  long  as  compensation  is  good  and  sexual  indulgence  is  moderate 
no  ill  effects  need  be  feared,  but  in  patients  whose  compensation  is  poor  or 
uncertain,  the  effect  will  depend  largely  upon  the  frequency  and  the  intensity 
of  the  sexual  excitement.  It  is  by  no  means  rare  to  find  heart  failure  begin- 
ning shortly  after  marriage  in  men  whose  compensation,  though  otherwise 
maintained,  was  never  very  good.  This  is  especially  true  of  old  men  married 
to  young  and  passionate  wives. 

Coitus  raises  the  blood-pressure  more  in  men  than  in  women,  and  also 
increases  the  force  of  the  heart-beat,  apparently  in  proportion  to  the  degree 
of  sexual  excitement,  and  therefore  differently  with  different  people  and 
under  different  conditions.  When  repeated  several  times  during  the  same 
night  it  is  especially  deleterious,  since  the  fatigue  is  far  greater  and  the  after- 
effects are  of  longer  duration  than  from  a  single  coitus,  and  sudden  death 
during  coitus  is  far  from  rare,  especially  in  patients  with  aortic  insufficiency 
or  diseased  coronary  arteries. 

On  the  other  hand,  the  worries  and  psychic  excitements  entailed  by 
marriage  are  equally  important.  In  all  but  the  most  well-to-do  it  becomes 
necessary  for  the  man  to  earn  more  money  than  would  suffice  him  if  unmar- 
ried, and  as  his  whole  life  becomes  more  strenuous  the  wear  and  tear  on  the 
body,  and  especially  upon  the  heart,  increases.  He  may,  for  the  sake  of  his 
family,  take  greater  chances,  endure  greater  exposure,  which  in  itself  may 
bring  on  rheumatism  and  bronchopneumonia!  infections,  and  these  in  turn 
react  unfavorably  on  the  heart. 

Among  the  individual  valvular  lesions  the  greatest  danger  is  encountered 
in  aortic  insufficiency,  for  the  act  of  coitus  imposes  a  sudden  strain  which,  in 
the  weaker  hearts,  may  lead  to  an  increase  in  the  amount  of  blood  regurgitat- 
ing and  bring  on  acute  dilatation  immediately.  It  is  not  surprising,  therefore, 
that  in  this  form  of  disease  particularly  death  during  the  act  of  coitus  is  not 
infrequent;  though  severe  heart  failure  resulting  in  death  subsequently  is,  of 
course,  much  more  common.  Such  failures  naturally  occur  in  persons  whose 
hearts  are  in  a  much  weakened  condition  before  the  coitus.  In  hearts  whose 
tonicity  is  low  this  balance  is  readily  overthrown  and  dilatation  sets  in  on 


PREGNANCY  AND  LABOR  IN  HEART  DISEASE.  523 

relatively  slight  provocation;  so  that  all  influences  which  tend  to  lower  cardiac 
tonicity  such  as  recent  febrile  or  gastrointestinal  diseases  or  even  severe  fatigue 
constitute  definite  contraindications  to  sexual  intercourse  in  this  class  of  cases. 

On  the  other  hand,  the  greater  number  of  patients  with  aortic  insuffi- 
ciency which  is  well  compensated  may,  with  perfect  safety,  marry  without 
misgivings;  but  the  necessity  of  heeding  the  above-mentioned  danger  signals 
must  be  impressed  upon  them.  One  point  worthy  of  consideration  in  all 
cases  of  aortic  insufficiency,  except  those  upon  a  definitely  rheumatic  basis, 
is  the  frequency  with  which  this  lesion  is  the  result  of  syphilitic  aortitis,  and 
this  question  ought  to  be  carefully  investigated  before  the  patient  is  permitted 
to  marry.  In  all  cases  of  possible  doubt  a  Wassermann  reaction  should  be 
resorted  to;  and  if  this  is  positive  antisyphilitic  treatment  should  be  instituted 
promptly. 

In  cases  of  mitral  disease  the  contraindications  to  matrimony  are  a  little 
less  urgent,  since,  from  the  nature  of  the  lesion,  sudden  heart  failure  results  in 
oedema  and  congestion  of  the  lungs  rather  than  in  extreme  dilatation  of  the 
ventricles,  and  the  patient's  chances  of  recovery  from  an  acute  heart  strain  are 
therefore  greater  than  in  the  aortic  cases.  The  same  general  principles  and 
precautions,  however,  in  the  management  of  the  patient  should  be  followed. 

In  cases  of  arrhythmia,  the  advisability  of  matrimony  depends  upon  the 
severity  of  the  condition.  The  sinus  arrhythmias  and  paroxysmal  tachy- 
cardia, when  the  attacks  are  not  severe  and  are  unaccompanied  by  valvular 
lesions  or  signs  of  coronary  sclerosis,  are  in  themselves  no  bar  to  marriage. 
Occasional  extrasystoles  also  fall  into  this  category,  particularly  those  asso- 
ciated with  flatulence  and  gastrointestinal  disturbance,  but  not  with  muscular 
effort.  If  their  frequency  is  increased  on  exertion  or  they  are  associated  with 
the  presence  of  severe  valvular  lesion  or  chronic  hypertension,  however,  they 
should  be  regarded  much  more  seriously  and  the  question  of  marriage  be- 
comes a  much  more  dubious  one. 

Heart-block  is  in  most  cases,  of  course,  a  definite  bar  to  marriage.  This 
is  particularly  the  case  in  persons  with  partial  heart-block,  and  especially 
those  who  are  subject  to  attacks  of  weakness,  giddiness  or  syncope,  or  in 
persons  with  complete  block,  unless  the  latter  condition  has  shown  a  tendency 
to  remain  complete  and  the  ventricle  has  demonstrated  its  ability  to  main- 
tain an  adequate  circulation  over  a  long  period  of  time.  However,  one  occa- 
sionally encounters  persons  who,  in  spite  of  long-continued  complete  heart- 
block,  retain  their  cardiac  compensation,  reserve  force  and  bodily  vigor;  and 
in  these  persons  the  case  is  different.  This  was  strikingly  exemplified  by  a 
gentleman  (cited  on  page  571)  whose  pulse-rate  had  remained  at  about  half 
the  normal  (about  32  per  minute)  since  some  time  before  his  marriage,  which 
had  occurred  35  years  previous  to  his  examination.  During  this  time  he  had 
enjoyed  perfect  health  and  had  led  an  extremely  active  life,  and  not  until  old 
age  was  upon  him  had  any  symptoms  referable  to  the  circulatory  system  set 
in.  During  this  period  he  had  led  a  normal  married  life  and  had  been  the 
father  of  several  healthy  children.  Such  cases  are  unfortunately  extremely 
rare;  and  before  marriage  is  permitted  in  heart-block  the  greatest  precaution 
should  be  exercised,  and  the  patient  should  be  subjected  to  a  variety  of  ex- 
ercise and  exertion  tests  to  demonstrate  that  he  is  thoroughly  able  to  accom- 
modate himself  to  new  taxes  upon  his  system. 


521  DISEASES  OF  THE  HEART  AND  AORTA. 

The  same  restrictions  apply  also  to  absolute  arrhythmia  with  auricular 
fibrillation.  Here,  also,  occasional  cases  are  met  with  in  which  the  arrhythmia 
exists  for  years  without  signs  of  cardiac  weakness  or  any  symptoms  referable 
to  the  circulation.  In  these  cases  the  heart  has  accommodated  itself  to  the 
abnormal  rhythm  and  may  be  fairly  expected  to  do  so  for  some  time  to  come. 
In  the  great  majority  of  cases  auricular  fibrillation  entails  not  only  persistent 
arrhythmia  but  persistent  inability  to  withstand  exertion,  and  for  most  of 
these  marriage  is  out  of  the  question.  Should  the  patient  insist  upon  marry- 
ing against  the  physician's  advice,  the  prospective  bride  should  be  cautioned 
that  she  must  assume  more  or  less  the  role  of  nurse  toward  her  husband  and 
she  must  be  informed  that  his  chances  of  life  rest  largely  in  her  hands. 

In  chronic  hypertension  the  same  general  rules  apply,  though  this  con- 
dition is  perhaps  a  little  more  likely  to  be  insidiously  progressing  and  the 
patient  may  pass  into  the  danger  zone  without  realizing  the  transition.  The 
degree  of  renal  function  and  the  presence  or  absence  of  dyspnoea  or  presence 
of  extrasystoles  on  mild  exertion  constitute  the  main  criteria.  In  cases  in 
which  the  condition  is  progressive,  the  prospective  bride  should  be  informed 
that  her  husband's  life  is  probably  of  limited  duration. 


BIBLIOGRAPHY. 

Stengel,  A.,  and  Stanton:  Heart  and  Circulation  in  Pregnancy  and  the  Puerperium,  Trans. 
Asso.  Am.  Phys.,  Phila.,  1904,  xix,  520. 

Vejas:  Mittheilungen  ueber  den  Puis  und  die  vitale  Lungencapacitat,  etc.,  Samml.  klin. 
Vortr.,  Leipz.,  1886,  No.  269. 

Szabo:  Ueber  die  Bradykardie  im  Wochenbette,  FrommePs  Jahresb.,  1910,  700. 

Slemons,  J.  M.,  and  Goldsborough,  F.  C:  The  Obstetrical  Significance  of  the  Blood-pres- 
sures and  their  Relation  to  the  Work  of  the  Heart,  Johns  Hopkins  Hosp.  Bull.,  Bait., 
1908,  xix,  194. 

Fellner,  O.:  Herz  und  Schwangerschaft,  Monatschr.  f.  Geburtsh.  u.  Gynakol.,  Berl.,  1901, 
xvi,  370. 

Vogeler,  W.:  The  Blood-pressure  during  Pregnancy  and  the  Puerperium,  Am.  J.  Obstetr., 
1907,  lv,  490. 

Macdonald,  A.:  The  Bearings  of  Chronic  Diseases  of  the  Heart  upon  Pregnancy,  Parturi- 
tion, and  Childbed,  Lond.,  1878. 

Leyden:  Ueber  die  Complication  der  Schwangerschaft  mit  chronischer  Herzkrankheit, 
Ztschr.  f.  klin.  Med.,  Berl.,  1893,  xxiii,  1. 

Schlayer,  Schneider,  and  Vinay.     Quoted  from  Feis. 

Miiller,  W.:  Die  Massenverhaltnisse  des  menschlichen  Herzens,  Berl.,  1878. 

Mackenzie,  J. :  Pulsations  in  the  Veins,  with  the  Description  of  a  Method  for  Graphically 
Recording  Them,  J.  Path.  u.  Bacterid.,  Edinb.  and  Lond.,  1893,  i,  53. 

Schlayer.     Quoted  from  Fellner.     Hicks  and  French.    Quoted  from  Blacker. 

Blacker,  G.  F.:  Heart  Diseases  in  Relation  to  Pregnancy  and  Labor,  Brit.  M.  J.,  Lond., 

1907,  i,  1225. 

Hellendal,  H. :  Herzfehler  in  der  Schwangerschaft  und  operative  Sterilisation,  Med.  Klinik, 

Berl.,  1907,  763. 
Newell,  F.  S.:  Valvular  Diseases  of  the  Heart  Complicating  Pregnancy,  Surg.,  Gynecol., 

and  Obstet.,  Chicago,  1907,  iv,  610. 
Feis,  O.:  Ueber  Komplication  von  Schwangerschaft,  Geburt,  und  Wochenbett  mit  chroni- 

schem  Herzfehler,  Samml.  klin.  Vortr.,  Leipz.,  Gynakol.  No.  78. 
The  articles  by  v.  Rosthorn  and  by  Lenhartz,  H.,  Die  Beziehungen  der  weiblichen  Ge- 

schlechtsorgane  zu  innere  Erkrankungen,  Verhandl.  d.  Kong.  f.  inn.  Med.,  Wiesb., 

1908,  xxv,  29;  Tuszkai,  Uterus,  Graviditat  und  Herz,  ibid.,  1908,  xxv,  118,  and  the 
subsequent  discussion  contain  much  valuable  information. 


X. 
CONGENITAL  HEART  DISEASE. 

DEVELOPMENT  OF  THE  HEART. 

In  the  human  heart,  as  in  all  other  complex  anatomical  structures, 
there  are  many  portions  whose  form  and  function  are  obscure  and  difficult 
of  comprehension  when  considered  only  in  the  light  of  conditions  pres- 
ent in  the  adult,  but  which  become 
quite  clear  when  seen  in  the  various 
stages  of  their  development.  A 
brief  consideration  of  the  embryol- 
ogy of  the  heart  will  therefore  greatly 
simplify  the  study  of  the  anatomy. 
Moreover,  it  must  be  borne  in  mind 
that  occasionally  some  portion  of 
the  adult  heart  fails  to  develop 
beyond  the  embryonic  stage,  giving 
rise  to  the  signs  and  symptoms  of 
congenital  heart  disease;  and  there- 
fore a  knowledge  of  the  embryologi- 
cal  development  is  necessary  for  pur- 


,— —      -»> 

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Fig  236. — Very  early  stage  in  the  development  of  the  human  circulatory  system.  (Drawn  from 
a  model  of  a  human  embryo  2.5  mm.  long,  about  two  weeks  after  fertilization.  From  Prof.  F.  P.  Mall's 
collection.  The  model  was  prepared  by  Mr.  W.  E.  Dandy.)  The  specimen  shows  the  two  aorta?  (AO)  leading 
the  blood  to  the  chorionic  villi,  and  the  two  umbilical  veins  (UMB  V)  leading  it  back  to  the  primitive 
heart  (H).  The  five  branchial  or  aortic  arches  (A  A)  which  connect  the  heart  with  the  aortse  are  shown 
also.     A.  Dorsal  aspect.     B.   Lateral  aspect  of  the  head  end  of  the  same  embryo. 


poses  of  practical  diagnosis  and  prognosis  as  well  as  for  anatomical  study. 

The  earliest  stage  of  the  circulatory  system  in  the  mammalian  embryo 

consists  in  the  formation  of  a  number  of  small  blood-vessels  and  capillary 

525 


526 


DISEASES    OF   THE   HEART    AND    AORTA. 


'TRA 


plexuses,  which  arise  from  the  mesoblast  over  the  surface  of  the  yolk-sac. 
These  soon  unite  to  form  a  definite  symmetrical  vascular  system. 

Eternod  has  carefully  described  the  earliest  development  of  the  circu- 
latory system  in  a  human  embryo  1.2  mm.  long,  estimated  at  about  eleven 
days  after  fertilization.  Another  embryo  of  almost  the  same  age  (Fig.  236) 
has  recently  been  discovered  by  Dr.  Mall  and  modelled  by  Mr.  W.  E.  Dandy. 
In  this  embryo  the  venous  system  is  represented  almost  entirely  by  the 
umbilical  veins  (JJmb  V),  which  carry  the  blood  that  has  been  aerated  in  the 
placenta  back  to  the  heart.  They  follow  the  border  between  the  embry- 
onic area  and  the  yolk-sac  and  pass  forward  to  the 
head  end  of  the  embryo.  Here  (H)  the  two  veins 
unite,  and  at  the  union  there  are  given  off  a  second 
set  of  vessels  consisting  of  a  group  of  four  upon 
each  side,  the  aortic  arches  (A  A),  which  pass 
backward  more  or  less  parallel  to  the  midline 
and  soon  reunite  to  form  a  single  vessel  on  each 
side,  the  primitive  aortse  (AO).  These  two 
aortse  carry  the  blood  from  the  embryo  proper 
back  on  each  side  of  the  midline  to  the  numer- 
ous ramifications  in  the  placenta,  whence,  as 
we  have  seen,  it  is  returned  through  the  umbil- 
ical veins.  At  this  stage  the  heart  is  simply  a 
small  dilatation  of  the  venous  tube,  and  the 
blood  is  propelled  by  the  pulsations  of  the  ves- 
sels throughout  their  entire  lengths.  There  is 
scarcely  a  widening  of  the  lumen  to  mark  the 
site  at  which  the  heart  will  develop, — namely, 
at  the  point  of  union  of  the  two  umbilical 
veins  just  behind  the  place  where  the  aortic  arches 
are  given  off. 

At  a  little  later  stage  (Fig.  237)  we  find 
the  heart  the  form  of  an  S-shaped  tube  just 
ventral  to  the  pharynx  of  the  embryo  to  which 
it  is  fixed,  and  already  two  dilatations  have 
taken  place  in  the  lumen,  forming  the  primitive 
sacs  of  the  ventricle  (V)  and  the  auricle  (atrium) 
(A).  The  point  of  union  of  the  veins  (sinus 
reuniens,  S  R)  has  been  pushed  further  backward.  The  umbilical  veins 
have  received  veins  entering  from  the  yolk-sac  (vitelline  veins)  as  well 
as  a  branch  (duct  of  Cuvier,  D  Cuv)  from  the  body  wall  on  each  side. 
The  duct  of  Cuvier  is  in  turn  formed  by  the  union  of  a  branch  to  the 
head  (jugular  vein,  Jug)  and  a  branch  (cardinal  vein,  Card)  extending 
downward  along  each  side  of  the  body  wall  and  giving  off  branches  to 
the  muscle  segments.  The  veins  to  the  intestine  arise  from  the  vitelline 
vein,  while  the  umbilical  or  omphalomesaraic  veins  continue  as  before 
to  carry  the  blood  back  to  the  placenta  and  yolk-sac. 

Anteriorly  the  arterial  portion  of  the  circulatory  system  may  now  be 
observed  to  be  composed  of  the  truncus  arteriosus  (TV  A),  a  continuation 
of  the  ventricle,  and  four  aortic  arches  each  now  corresponding  to  a  definite 


Fig.  237. — Human  embryo  4 
mm.  long  (about  the  fourth  week 
after  fertilization),  showing  the 
further  development  of  the  heart 
and  of  the  branchial  or  aortic 
arches  (A  A).  (Modified  from 
His.)  The  heart  has  assumed 
an  S  shape,  and  is  divided  into 
a  truncus  arteriosus  (TR  A),  a 
single  ventricle  (V),  and  a  single 
auricle  (AUR).  The  inner  en- 
dothelial cardiac  tube  (shaded 
light)  is  much  narrower  than  the 
outer  muscular  tube  (MUS). 
On  each  side  the  jugular  veins 
(JUG)  from  the  head  unite  with 
the  cardinal  veins  (CARD)  from 
the  trunk  to  form  the  duct  of 
Cuvier  (D  CUV)  which  empties 
into  the  sinus  reuniens  (S  R). 


CONGENITAL    HEART    DISEASE. 


527 


visceral  (or  gill)  arch  of  the  embryo  (V  A).  These  branches  of  the  aorta 

are  of  great  importance,  for  from  them  the  carotid,  axillary,  innominate, 
and  pulmonary  vessels  will  develop. 
As  the  embryo  grows  older  (Fig. 

240)  the  heart  is  still  more  S-shaped,  '    ^.r  ( — A< 


Sept.V. 
'  "V    Oav. 

^^- Pa 


Fig.  238. — Heart  of  an  embryo  slightly  older 
than  that  shown  in  Fig.  237,  showing  the  earliest 
stages  in  the  formation  of  two  auricular  and  two 
ventricular  pouches.     (Drawn  from  a  His  model.) 


5.R. 


Fig.  239. — A  diagram  showing  the  interior  of 
this  heart;  AO.,  aorta  or  truncus  arteriosus;  SEPT. 
V.,  septum  of  the  ventricles;  OAV.,  aurieuloventric- 
ular  orifice;  CA.,  canalis  auricularis,  or  auricular- 
ventricular  channel ;  AUR.,  auricles;  S.R.,  sinus 
reuniens,  or  common  chamber  into  which  the  two 
vena;  cavse  empty,  which  corresponds  to  the  sinus 
venosus  of  the  lower  vertebrates. 


Fig.  240. — Schema  to  show  the  development  of  the  arterial  system  from  out  of  the  primitive  aortic 
arches.  A.  Schema  of  the  circulatory  system  at  about  the  same  stage  as  Fig.  237.  I— VI,  aortic  or  bran- 
chial arches  (the  fifth  branchial  arch  described  by  Tandler  arises  from  and  anastomoses  with  the  fourth, 
which  is  the  largest  of  the  branchial  arches).  AO,  AO,  primitive  aortae;  PA,  PA,  rudimentary  pulmonary 
arteries;  V,  primitive  common  ventricle;  RA,  LA,  auricular  pouches.  B.  Schema  of  the  adult  arterial 
system  derived  from  the  aortic  arches.  EXT  CAR,  external  carotid  artery  (3d  arch);  INT  CAR,  in- 
ternal carotid  artery  (connecting  bars  of  first  three  arches);  COM  CAR,  common  carotid  artery  connect- 
ing bar  between  third  and  fourth  arches.  A.  The  aorta  is  seen  to  be  derived  from  the  fourth  branchial  arch, 
the  pulmonary  arteries  arise  along  the  course  of  the  sixth.  The  ductus  arteriosus  (Botalli)  represents  the 
distal  end  of  the  sixth  branchial  arch.  The  dotted  lines  indicate  the  outline  of  embryonic  arteries  which 
have  atrophied. 


and  at  the  junction  of  the  two  halves  of  the  S  a  small  crescentic  infolding 
of  the  muscular  and  endothelial  wall  has  begun  to  protrude  into  the  cavity 
of  the  ventricle  (interventricular  septum,  Sept.  V.),  while  the  ascending 
limb  of  the  lower  half  of  the  S  represents  a  stenosis  in  the  lumen,  the  canalis 
auricularis  (CA.),  whose  , narrowest  part  forms  a  small  slit,  the  ostium 
auriculoventriculare  (atrioventriculare)   (OAV.). 


528 


DISEASES   OF   THE   HEART    AND    AORTA. 


The  development  of  the  interventricular  septum  continues  rapidly 
(Fig.  241),  and  also  a  similar  ridge  appears  running  longitudinally  along 
the  truncus  arteriosus,  changing  the  lumen  from  circular  to  U-shaped, 
each  arm  of  the  U  being  a  channel  leading  to  the  corresponding  half 
of  the  ventricle. 

The  auricular  (or  atrial)  cavity  is  now  also  widened  into  two  symmet- 
rical pouches,  the  right  and  left  auricles,  the  cavity  of  which  is  continuous 
with  the  junction  of  the  veins. 


OAV 


SeptV. 


Fig.  241. — A.  Heart  of  slightly  older  embryo  viewed  from  the  dorsal  aspect,  showing  the  separation 
of  the  aortic  and  the  pulmonary  channels  in  the  truncus  arteriosus.  (Drawn  from  a  His  model.)  B. 
Diagram  of  the  auricular  portion  of  the  same  heart.  Lettering  as  in  Fig.  239.  VE,  Eustachian  valve, 
separating  the  sinus  from  the  auricular  portion  of  the  heart.  The  arrows  indicate  the  course  of  the 
blood-currents.  C.  Diagram  of  the  ventricular  portion  of  the  same  heart,  showing  the  course  of  the  cur- 
rents through  the  separate  channels  of  the  truncus  arteriosus. 


The  trunks  of  the  veins  have  already  undergone  considerable  changes, 
such  that  the  left  duct  of  Cuvier  is  now  atrophied,  and  most  of  the  blood 
from  the  head  and  upper  limb  returns  to  the  heart  through  the  right  duct 
of  Cuvier,  foreshadowing  the  superior  vena  cava,  while  the  blood  from  the 
placenta  returns  through  the  two  omphalomesaraic  (or  omphalomesen- 
teric) veins,  which  along  with  anastomoses  from  the  body  wall,  intestinal 
tract,  and  liver  will  form  the  inferior  vena  cava.  The  junction  of  the 
two  vense  cavse  forms  the  sinus  reuniens  which  opens  into  the  auricular 
cavity.  In  the  wall  of  the  sinus  reuniens  at  this  stage  there  is  a  longi- 
tudinal valve-like  fold  of  endothelium  (VE,  Fig.  241,  B),  so  arranged  that 
blood  from  the  superior  vena  cava  flows  over  it  into  the  right  auricle 
(atrium),  while  the  blood  arriving  from  the  placenta  is  directed  under  it 
into  the  left  auricle. 


CONGENITAL   HEART    DISEASE. 


529 


Fig.  242. — Still  later  stage,  showing  com- 
plete division  of  the  truncus  arteriosus  into 
pulmonary  artery  and  aorta.  (Drawn  from  a 
Born  model  of  a  rabbit's  embryo  10  mm. 
long.)  The  arrows  show  the  course  of  the 
blood-stream.     DA,  ductus  arteriosus. 


Very  shortly  after  this  stage  the  most  important  changes  take  place 

in  the  heart  (Fig.  242).     The  two  channels  of  the  truncus  arteriosus  are 

now  completely  separated  off  from  one 

another,   and  exist   as  distinct  vessels, 

the  aorta  (AO)  and  the  pulmonary  ar- 
tery (PA),  connected  with  each  other 

at   only  one   point  through  the  ductus 

arteriosus  (DA).     The  interventricular 

septum  (septum  ventriculorum,  Sept  V., 

Fig.  241,  C)  is  now  found  to  be  almost 

completely    closed,    and    the    originally 

single     auriculoventricular    opening     is 

now  divided  into  two  portions  (mitral 

and  tricuspid,  Mit.  and  Trie.)  separated 

by  the  ingrowth  of  the  septal  ridge.     In 

the    auricles    also    great    changes   have 

occurred.     The   greater  portion  of  the 

sinus  reuniens  has  been  drawn  into  the 

cavity  of  the  auricle,  and  exists  there  as 

a  separate  chamber,  whose  right  margin 

opening  into  the  right  auricle  is  formed  by 

the  longitudinal  valve  (VE)   (described 

in  connection  with  the  previous  stage  of 

development,  now  known  as  the  valvula  venosa  dextra,  or  Eustachian 

valve) .     The  left  wall  of  the  right  auricle  is  formed  by  the  septum  auricu- 

lorum,  which  has  grown  considerably, 
partly  through  the  gradual  ingrowth 
of  the  septal  ridge  and  partly  by  the 
pushing  in  of  a  mass  of  connective 
tissue  arising  from  the  latter  and  from 
the  left  wall  of  the  sinus  reuniens 
and  known  as  the  septum  inter- 
posit  um.  The  left  wall  formed  in 
part  by  the  wall  of  the  vein  is  imper- 
fect, and  on  the  left  the  cavity  extends 
over  to  the  auricular  septum  (sep- 
tum atriorum).  This  septum  has 
also  not  completely  closed,  and  the 
reconstruction  (Fig.  243)  from  a 
model  by  Born  at  this  stage  shows  a 
double  opening  between  the  two  auri- 
cles. At  a  later  stage  (Fig.  245,  B) 
these  openings  have  broken  down 
into  one,  the  foramen  ovale,  and 
it  is  the  opinion  of  Born,  in  opposi- 
tion to  His,  Sr.,  that  the  latter  struc- 
ture   is    of   secondary  formation   and   does  not   arise   directly  from  the 

primitive  interauricular  openings,  although  it  performs  the  same  function, 

— namely,  of  allowing  the  blood  to  pass  from  the  right  into  the  left  auricle. 

34 


Fig.  243. — Auricular  end  of  the  same  heart. 
The  blood  enters  through  the  superior  and  inferior 
vena  cava  (SUP.V.C,  INF.V.C.)  into  the  sinus 
reuniens  (SR),  which  is  separated  from  the  right 
auricle  (R.AUR.)  by  the  Eustachian  valve  (VE), 
which  at  this  stage  forms  a  large  partition  between 
the  two  cavities.  The  foramen  ovale  (FOR.OV.) 
connects  the  sinus  reuniens  with  the  right  ventri- 
cle; it  is  divided  into  two  parts  by  a  thin  lamina 
formed  from  the  interauricular  septum.  TRIC, 
tricuspid  orifice;  P.V.,  pulmonary  veins. 


530 


DISEASES    OF   THE   HEART   AND    AORTA. 


In  the  later  stages  a  valve-like  flap  of  connective  tissue  projects  over  the 
foramen,  allowing  the  blood  to  flow  only  from  right  to  left. 

DEVELOPMENT    OF    THE    PERICARDIUM. 

The  pericardial  cavity  develops  as  a  part  of  the  original  body  cavity 
or  ccelom,  from  which  it  is  separated  at  a  later  stage.  In  the  earliest  em- 
bryos (Fig.  236)  the  pericardial  cavity  arises  as  a  small  space  lined  with 
endothelium,  surrounding  the  blood-vessels  on  each  side  of  the  embryo 
(Fig.  244,  A).  These  two  spaces  or  cavities  unite  at  the  head  end  of 
the  embryo  to  form  a  single  pericardial  cavity  which  surrounds  the 
primitive  heart.     At  a  slightly  later  stage  the  heart  and  the  pericardial 


Fig.  244. — Development  of  the  pericardial  cavity.  A.  Earliest  stage  in  the  development  of  the 
pericardial  cavity.  (After  Robinson.)  Embryo  corresponding  roughly  to  the  stage  shown  in  Fig.  23G.  E, 
ectoderm;  C,  coslom;  En,  entoderm;  PB,  primitive  blood-vessel.  The  pericardial  cavity  is  represented  by 
the  part  of  the  ccelom  present  at  this  level.  B.  Later  stage  showing  the  division  of  coelom  into  pleural 
and  pericardial  cavity.  (Schematic.)  The  arrow  points  to  the  channel  connecting  the  two  cavities.  C. 
Relations  of  the  pericardium  in  the  adult.     (Schematic).     ANTER.  MEDIAST.,  anterior  mediastinum. 


cavity  lie  upon  the  ventral  aspect  of  the  pharynx  and  the  pericardial 
and  pleural  cavities  together  form  the  anterior  or  cephalic  portion  of 
the  ccelom. 

At  a  later  stage  (Fig.  244,  B)  the  heart  has  grown  to  fill  almost  all  the 
ventral  portion  of  the  ccelom  in  its  vicinity,  and  about  its  contour  the 
connective  tissue  of  the  body  wall  is  closing  in,  as  shown  by  the  arrow, 
beginning  to  divide  the  original  ccelomic  cavity  into  a  pleural  and  a 
pericardial  portion. 


CONGENITAL   HEART   DISEASE.  531 

In  Fig.  244,  C  this  closure  has  become  complete,  and  we  have, 
represented  in  rough  diagram,  the  conditions  present  in  the  adult  chest. 
The  pericardial  cavity  is  completely  separated  from  the  pleural  cavity, 
and  is  lined  throughout  by  a  single  layer  of  flat  endothelial  cells, — 
the  portion  growing  directly  upon  the  heart  called  the  epicardium, 
and  the  portion  forming  the  opposite  wall  of  the  pericardial  cavity,  the 
pericardium  proper. 

The  pleural  cavity  has  now  grown  more  extensive  than  before,  owing 
to  the  growth  of  the  lungs,  which  have  pushed  forward  along  the  sides  to 
well  in  front  of  the  heart  and  almost  to  the  midline,  leaving  a  narrow  pleural 
cavity  between  them  and  the  chest  wall.  Like  the  pericardial  cavity  the 
pleural  cavity  is  lined  with  endothelium  which  extends  partly  over  the 
lung  (visceral  pleura)  and  partly  along  the  thoracic  wall  (parietal  pleura). 
The  anterior  portion  of  the  visceral  pleura  passes  over  the  pericardium, 
from  which  it  is  separated  only  by  a  very  thin  mass  of  connective  tissue, 
occasionally  containing  fat-cells.  The  three  layers — pleural  endothelium, 
connective  tissue,  and  pericardial  endothelium — are  so  closely  fused  that 
together  they  are  generally  designated  as  the  pericardium,  of  which  one 
speaks  of  the  pleural  and  pericardial  surface.  The  pericardium  does  not 
extend  quite  to  the  chest  wall,  while  the  pleura  does  so,  and  ventral  to 
the  heart  we  find  a  small  space  filled  by  connective  tissue  and  known  as 
the    anterior   mediastinum. 


PHYSIOLOGY  OF  THE  FETAL  CIRCULATION. 

The  blood  of  the  foetus  is  aerated  in  the  placenta  and  passes  back 
through  the  umbilical  veins  and  through  the  ductus  venosus  (D.V.)  to 
the  inferior  vena  (V.C.I.) ,  without  passing  through  the  liver.  The  sinus 
reuniens  has  now  become  part  of  the  main  cavity  of  the  auricle,  and  the 
inferior  vena  cava  (V.C.I.)  empties  into  the  latter  near  the  septum  ventric- 
ulorum.  Over  its  mouth  pass  the  remains  of  the  Eustachian  valve  (val- 
vula  venosa  dextra)  which  directs  the  blood  not  into  the  right  auricle  but 
away  from  it  across  the  right  auricle  to  the  limbus  fossae  ovalis.  According 
to  the  views  of  Galen  and  Harvey,  the  blood  from  the  superior  vena  cava 
and  that  from  the  inferior  are  mixed  in  the  right  auricle  before  any  of 
the  stream  passes  to  the  left  auricle.  Haller  and  Sabatier,  however,  believed 
that  no  such  mixing  took  place,  but  that  all  the  blood  from  the  inferior  vena 
cava  (aerated  blood)  passed  across  to  the  left  auricle,  while  the  blood  from 
the  superior  vena  cava  passed  down  into  the  right  ventricle.  Pohlman 
has  recently  given  an  excellent  review  of  the  subject.  He  has  investigated 
it  experimentally  on  the  fetal  pig's  heart  by  injecting  starch  granules  into 
the  superior  vena  cava  in  some  living  fetal  pigs  and  into  the  inferior  vena 
cava  in  others.  The  hearts  were  then  removed,  and  the  bloods  in  the  two 
ventricles  and  auricles  were  shown  to  contain  the  starch  granules  in  equal 
amounts,  confirming  the  theory  of  Galen  and  Harvey.  Pohlman  introduced 
capillary  glass  tubes  into  the  two  ventricles  and  demonstrated  that  the 
pressures  within  them  were  equal.  The  blood  from  the  left  ventricle  passes 
at  first  to  the  innominate  and  carotid  and  subclavian  arteries,  below  which 
the  aorta  is  joined  by  the  ductus  arteriosus  Botalli.     The  blood  from  the 


532 


DISEASES   OF   THE.  HEART    AND    AORTA. 


right  ventricle  passes  into  the  main  trunk  of  the  pulmonary  artery,  from 
which  about  one-fifth  enters  the  rami  passing  to  the  lungs  and  about  four- 
fifths  passes  onward  through  the  ductus  arteriosus  and  enters  the  descend- 
ing aorta.  As  the  ductus  arteriosus  carries  a  little  more  blood  than  the 
descending  aorta,  the  volume  of  blood  in  the  aorta  is  more  than  doubled 
and  the  lumen  considerably  widened  below  its  entry.  The  blood  below  this 
point  goes  to  the  kidneys,  the  alimentary  tract,  the  bladder,  and  the  lower 
limbs,  and  the  rest  goes  on  through  the  umbilical  arteries  (Umb.  A.),  to  be 
aerated  in  the  placenta  and  returned  as  described  above. 


FORAMEN  OVALE 
EUSTACHIAN  VALVE 


Fig.  245. — A.  The  circulation  in  the  fcetus  just  before  birth.  Course  of  the  blood  to  and  from 
the  placenta.  (Semi-schematic.)  UMB  A,  UMB  V,  umbilical  artery  and  umbilical  vein;  DV,  ductus 
venosus.  B.  The  heart  just  before  birth.  The  course  of  the  blood-stream  is  indicated  by  the  arrows. 
VCS,  VCI,  superior  and  inferior  vena  cava. 


These  are  the  conditions  present  up  to  the  time  of  birth.  After  the 
first  respiration  the  expansion  of  the  lungs  greatly  reduces  the  resistance 
in  the  pulmonary  circuit,  so  that  it  becomes  less  than  that  in  the  aorta, 
and  most  of  the  blood  is  diverted  from  the  ductus  arteriosus  into 
this  new  channel  of  low  resistance.  Hence  it  persists  only  a  year 
or  so  after  birth  and  soon  becomes  changed  into  a  simple  strand  of 
connective  tissue. 

On  the  other  hand,  the  pressure  in  the  left  auricle  becomes  greater 
than  that  in  the  right,  and  the  valve  of  the  foramen  ovale  is  therefore 
kept  closed  against  the  septum,  and  soon  becomes  organized  as  a  part 
of  the  latter. 

With  the  cessation  of  placental  circulation,  the  ductus  venosus  loses 
its  physiological  importance  and  soon  undergoes  atrophy  and  closure. 


CONGENITAL   HEART   DISEASE.  533 

CLASSIFICATION  OF  CONGENITAL  HEART  LESIONS. 

Classifications  of  congenital  heart  lesions  are  difficult,  and  from  a 
clinical  stand-point  not  always  satisfactory.  From  the  anatomical  stand- 
point they  may  be  classified  as  follows: 

I.  Malformations  about  the  heart. 

1.  Malformations  of  the  chest  wall  (ectopia  cordis). 

2.  Malformations  of  the  pericardium. 

II.  Abnormalities  in  the  position  of  the  heart. 

1.  Heart  on  the  right  side  (dextrocardia  or  dexiocardia) . 

2.  Position  of  all  the  organs  inverted  (situs  transversus). 

3.  Heart  situated  in  the  neck  (cervical  heart). 

4.  Heart  situated  within  the  peritoneal  cavity  (abdominal  heart). 

III.  Abnormalities  of  the  valvular  orifices. 

1.  Pulmonary  stenosis  or  atresia. 

2.  Supernumerary  or  defective  cusps  of  pulmonary  valves. 

3.  Tricuspid  stenosis  or  insufficiency;  malformation  of  the  valve. 

4.  Aortic  stenosis;  atresia  of  the  aorta;  malformations  of  the  aortic  valve. 

5.  Mitral  stenosis;  malformation  of  the  mitral  valve. 

IV.  Defects  in  the  septa. 

1.  Interventricular  septum. 

a.  In  the  septum  membranaceum. 

b.  In  the  muscular  part  of  septum  (below). 

2.  Interauricular  septum. 

a.  Defect  or  absence  of  valve  of  the  foramen  ovale. 

b.  Valve  normal  but  not  closed. 

c.  Defect  between  the  muscle  strands  in  the  lower  portion  of  interauricular 

septum. 
V.  Abnormalities  in  the  cavities. 

1.  Supernumerary  septa. 

2.  Cor  biatriatum  triloculare. 

3.  Cor  biloculare. 

4.  Cor  biventriculatum  triloculare. 

5.  Bifid  apex. 

6.  Double  heart. 

VI.  Deviations  of  the  septum  cordis  with  transposition  of  vessels. 
VII.  Persistence  of  ductus  Botalli. 
VIII.  Abnormalities  of  the  aorta. 

1.  Coarctation  of  the  aorta. 

a.  Above  the  ductus  arteriosus. 

b.  Below  the  ductus  arteriosus. 

2.  Hypoplasia  of  the  aorta. 

3.  Malformations  of  the  aortic  arch. 

IX.  Abnormalities  in  the  arrangement  and  formation  of  the  veins. 

GENERAL    CHARACTERISTICS. 

Such  a  purely  anatomical  classification,  though  sufficiently  complete, 
does  not  furnish  a  good  basis  for  the  study  of  the  cardiac  malforma- 
tions, because  it  does  not  take  into  account  the  relation  of  the  indi- 
vidual lesions  to  one  another.  For,  since  these  lesions  are 
usually  produced  in  groups  rather  than  singly,  it 
is  quite  as  important  from  a  clinical  stand-point  to  recognize  these 
groups  and  understand  their  effect  upon  the  circulation  as  to  recognize 
the  individual  lesions. 

Moreover,  as  will  be  seen,  the  mere  clinical  manifestations  show  great 
similarity  in  the  various  lesions,  and  may  be  summed  up  in  what  may  be 


534  DISEASES    OF   THE   HEART   AND    AORTA. 

termed  the  "syndrome  of  congenital  heart  lesions;"  or, 
in  the  words  of  Peacock  (1866),  ''the  characteristic  symptoms 
of  malformations  of  the  heart  —  cyanosis  (especially 
from  birth),  palpitation,  dyspnoea,  faintings,  occa- 
sional convulsive  attacks  and  lividity.''  Moreover,  the 
most  common  physical  sign  of  many  congenital  lesions  is  a  loud  superficial 
murmur,  most  intense  in  the  second  and  third  left  interspaces  at  the  sternal 
margin  in  both  systole  and  diastole  and  often  heard  over  the  entire  pre- 
cordium  and  the  arteries  as  well. 

ETIOLOGY. 

As  Lancereaux  has  well  said,  "cardiac  teratology  repre- 
sents the  pathology  of  intra-uterine  life."  The  chief 
pathological  conditions  which  affect  the  development  of  the  foetus  may 
be  classed  as — 

1.  Inflammation  (fetal  endocarditis  or  myocarditis,  the  formation  of 
adhesions  about  the  heart  or  vessels,  etc.). 

2.  Abnormal  torsions  of  the  cardiac  tube. 

3.  Underdevelopment  of  heart  or  branchial  arches. 

These  processes  lead  directly  to  the  production  of  malformations 
which  may  be  designated  as  primary  congenital  lesions,  such  as  stenosis 
and  atresia  of  the  pulmonary  artery,  transposition  of  the  great  vessels, 
stenosis  at  the  isthmus  of  the  aorta,  etc.  The  presence  of  these  lesions  in 
the  fcetus  in  turn  exercises  its  effect  upon  the  circulation,  which  alters  the 
course  of  development  and  brings  about  secondary  congenital  lesions. 
The  developmental  mechanics  which  results  in  the  formation  of  such 
groups  of  lesions  is  well  illustrated  in  pulmonary  stenosis  and  atresia,  the 
commonest  of  congenital  heart  lesions  which  may  be  considered  as  the 
prototype. 

PULMONARY  STENOSIS   AND   ATRESIA.1 

The  commonest  of  all  the  primary  congenital  lesions  is  pulmonary 
stenosis,  occurring  in  254  (68  per  cent.)  of  the  366  cases  of  congenital  heart 
disease  reported  by  Peacock  and  by  Keith.  Two  causes  have  been  ad- 
vanced to  explain  its  occurrence:  (1)  endocarditis  in  fetal  life;  (2)  defec- 
tive development  of  the  pulmonary  artery. 

1.  Bouillaud  (1835)  ascribed  it  to  endocarditis  in  fetal  life. 
This  theory  seems  certainly  to  be  applicable  to  those  cases  in  which  the  semi- 
lunar valves  have  already  formed,  but  just  as  in  the  adult  have  fused  along 
the  lines  of  closure.  This  is  well  shown  in  Fig.  246  and  in  a  case  figured  by 
Peacock.  Moreover,  a  number  of  cases  have  been  reported  in  which  rheu- 
matism or  infectious  disease  in  the  pregnant  mother  has  led  to  the  occur- 
rence of  endocarditis  in  the  fcetus.  On  the  other  hand,  it  must  be  borne  in 
mind  that  in  329  (82.5  per  cent.)  of  399  cases  of  pulmonary  stenosis  col- 
lected from  the  reports  of  Rauchfuss,  Vierordt,  and  Abbott  the  interven- 

1  Atresia — (Greek  arp^roc  (atretos),  not  perforated),  from  a  =  not,  and  rp^aig  =  a  bor- 
ing =  absence  or  extreme  constriction  of  any  natural  passage  or  opening  of  the  body. 


CONGENITAL   HEART    DISEASE. 


55 


tricular  septum  remained  incomplete,  indicating  that  the  primary  lesion 
had  taken  place  before  the  time  at  which  the  septum  had  closed  (eighth 
week  of  embryonic  life).  As  Osier  has  pointed  out,  "It  is  not  easy  to 
imagine  a  fetal  endocarditis  localized  to  so  small  an  area  as  the  pulmonary 
valves  must  be  before  the  eighth  week  of  fetal  life."    To  this  very  objec- 


Fig.  246. — Pulmonary  stenosis  due  to  fusion  of 
the  cusps.  (Drawn  from  a  specimen  in  the  Army 
Medical  Museum,  Washington,  D.  C.)  There  is 
also  a  patent  interventricular  septum. 


INF. 


Fig.  247. — Pulmonary  stenosis  due  to  a  lesion 
of  the  infundibulum.  (Drawn  from  a  specimen  in 
the  Army  Medical  Museum,  Washington,  D.  0.) 
INF,  infundibular  portion  of  the  right  ventricle. 


tion,  however,  the  advocates  of  this  theory  might  reply  that  in  very  many 
cases  the  lesion  is  by  no  means  confined  to  the  cusps  of  the  valves,  but  in- 
volves the  entire  infundibulum,  over  which  the  endocardium  may  be  thick- 
ened and  shrivelled  (Fig.  247).  Nor  does  it  necessarily  follow  that  even 
though  the  interventricular  septum  has  once  closed  it  must  remain  so, 


PATENT 

INTERVENTRICULAR 

SEPTUM 


PULMONARY  ARTERY 
PULMONARY  ORIFICE 


Fig.  248.— Complete  pulmonary  atresia.  (Drawn  from  a  specimen  in  the  Army  Medical  Museum, 
Washington,  D.  C.)  The  pulmonary  artery  ends  as  a  blind  sac  (shown  by  broken  lines)  just  above  the 
dot  which  marks  the  closed  pulmonary  orifice. 

since  it  may  rupture  under  increased  pressure  or  ulceration  may  result 
from  the  fetal  endocarditis.  Such  phenomena  have  occasionally  been 
observed    (Abbott) . 

2.  The  malformation  may  also  arise  by  "irregular  evolution 
of  the  branchial  arches."  Panum  has  shown  that  malformations 
can  be  produced  experimentally  in  birds  by  raising  the  temperature  of 
incubation  (fever  in  the  mother) ;  and  His  believes  that  at  least  a  consider- 


536 


DISEASES   OF   THE   HEART    AND    AORTA. 


able  portion  of  malformations  result  from  "disturbances  of  developmental 
conditions  caused  by  insufficient  nourishment,  insufficient  aeration  of  the 
blood,  and  mechanical  causes  resulting  from  malpositions  of  the  uterus,  dis- 
turbed placental  circulation,  etc." 

It  must  be  recalled  that,  as  shown  by  Rathke  in  1843,  the  pulmonary 
artery  separates  from  the  rest  of  the  truncus  arteriosus  about  the  eighth  week 
of  embryonic  life,  along  with  the  remains  of  the  sixth1  left  branchial  arch 
which  forms  the  ductus  arteriosus  and  the  left  pulmonary  artery  which 
springs  directly  from  this  arch  (Figs.  240  and  249) .  The  right  pulmonary 
artery,  according  to  Bremer,  has  sprung  in  a  similar  manner  from  the  right 
fifth  branchial  arch,  but  the  latter  has  atrophied  and  is  now  represented 

only  by  the  small  segment  con- 
necting the  right  pulmonary 
artery  with  the  truncus  pul- 
monalis.  In  the  twisting  of  the 
cardiac  tube  and  separation  of 
the  ventricles  the  part  of  the 
truncus  arteriosus  corresponding 
to  the  pulmonary  artery  pro- 
trudes ventrally  while  the  aortic 
portion  protrudes  dorsally.  The 
truncus  pulmonalis  thus  repre- 
sents the  ventral  half  of  the 
truncus  or  bulbus  arteriosus  and 
springs  directly  from  the  in- 
fundibulum  of  the  right  ventricle 
(Fig.  249).  Stenosis  or  atresia 
may  therefore  take  place  from 
arrest  of  development  in  three 
places:  1.  In  the  trunk  of  the 
pulmonary  artery  between  the 
semilunar  valve  and  the  point 
of  branching, — i.e.,  where  the 
pulmonary  artery  is  in  close 
contact  with  (and  perhaps 
pressed  upon  by)  the  main  trunk  of  the  aorta.  (This  condition  is  represented 
in  a  case  of  Peacock's  series.)  2.  At  the  orifice  itself  (as  in  Fig.  246), 
from  fusion  or  stenosis  of  the  valves.  3.  Below  the  valves  and  within  the 
infundibulum  of  the  right  ventricle,  as  in  Fig.  247.  In  some  cases  a 
supernumerary  septum  may  separate  the  infundibulum  from  the  main 
cavity  of  the  right  ventricle,  thus  producing  the  so-called  third  ventricle. 
Peacock  regarded  this  structure  as  representing  the  condition  present 
in   the   turtle,    but   states  that    "such    separation"    (into    two   cavities) 


Fig.  249. — Schema  illustrating  the  genesis  of  pul- 
monary stenosis.  A.  Fusion  of  the  -cusps.  B.  Fetal 
endocarditis  affecting  the  infundibulum.  C.  Normal 
mode  of  development  of  the  aortic  branchial  arches. 
D.  Maldevelopment  of  the  sixth  branchial  arch,  leading 
to  pulmonary  atresia. 


1  Rathke,  His,  and  the  older  writers  speak  of  the  last  branchial  arch  from  which  the 
pulmonary  artery  arises  as  the  fifth  branchial  arch;  but  Tandler  (Zur  Entwicklungsges- 
chichte  der  Kopfarterien  bei  den  Mammalia,  Morphol.  Jahrb.,  Leipz.,  1902,  xxx,  275)  has 
recently  shown  that  a  small  rudimentary  arch  is  present  upon  the  same  stem  with  the 
fourth.  He  terms  this  small  arch  (which  plays  no  important  role  in  development)  the 
fifth,  and  the  pulmonary  arch  accordingly  becomes  the  sixth. 


CONGENITAL   HEART    DISEASE.  537 

"may  be  produced  in  different  ways.  It  may  depend  simply  on  undue 
development  of  the  ordinary  muscular  bands,  or  on  this  in  conjunction 
with  thickening  of  the  endocardium  or  subjacent  fibrous  tissue."  Re- 
cently Arthur  Keith,  of  London,  has  revived  Peacock's  idea  that  this  is 
the  portion  of  the  heart  which  is  homologous  with  the  bulbus  cordis  of 
the  lower  animals,  and  which,  as  Greil  has  shown,  becomes  incorporated 
into  the  substance  of  the  ventricle  (infundibulum)  just  as  the  sinus  is 
swallowed  up  by  the  auricle.  Keith  believes  that  the  period  during 
which  this  is  taking  place  represents  the  crucial  epoch  in  the  production 
of  malformations.1 

Certain  it  is  that  most  fetal  lesions  arise  about  the  time  when  the 
pulmonary  artery  and  the  aorta  and  the  remnants  of  the  branchial  arches 
are  taking  their  final  form,  the  interventricular  septum  is  becoming  com- 
plete, and  the  original  portions  of  the  branchial  arches  are  disappearing, — 
i.e.,  between  the  fourth  and  the  eighth  week  of  fetal  life. 


SECONDARY    MALFORMATIONS. 

As  has  been  stated  above,  stenosis  of  the  pulmonary  orifice  results 
in  stasis  within  the  right  ventricle,  and  the  blood  is  forced  to  take  a 
new  channel. 

Patent  Interventricular  Septum  with  Pulmonary  Stenosis. — In  8  0  per 

cent,  of  the  cases  of  pulmonary  stenosis  the  interven- 
tricular septum  is  still  open,  and  the  blood  is  forced  through 
the  open  septum  and  passes  up  through  the  aorta.  As  the  condition  is  a 
permanent  one,  the  current  through  the  septum  continues  and  its  closure  is 
prevented  (stasis  theory  of  William  Hunter  and  Kussmaul) .  In  rare  cases, 
and  especially  those  in  which  the-  stasis  appears  at  a  very  early  stage,  the 
blood  current  eddies  through  and  keeps  open  a  passage  between  the  muscle 
strands  at  the  base,  in  contrast  to  the  usual  defect  at  the  septum  mem- 
branaceum.  This  opening  at  the  base  of  the  septum  is  often  accompanied 
by  defects  in  the  mitral  or  tricuspid  valves. 

Dextroversion  (Rechtslage)  of  the  Aorta.  —  Moreover,  the  pressure 
upon  the  septum  tends  to  deflect  it  toward  the  left  and  still  further  enlarge 
the  septal  opening  (Figs.  248  and  250). 

In  most  cases  the  deflection  of  the  septum  to  the  left  is  so  great  that 
the  aorta  comes  to  lie  in  the  axis  of  the  right  ventricle.  The  cavities  thus 
come  to  form  an  inverted  Y  whose  arms  are  formed  by  the  ventricles  and 
whose  shaft  is  the  aorta.  Since  the  shaft  is  inclined  to  the  right,  this  gives 
the  appearance  as  though  the  aorta  arose  directly  from  the  right  ventricle 
(Rechtslage — dextroversion  of  the  aorta).  This  condition  is  present  in 
the  majority  of  the  cases  reported  by  Abbott,  especially  in  those  in  which 
there  is  complete  atresia  of  the  pulmonary  artery  (Fig.  248) . 

1  It  is  possible  that  in  some  cases,  like  those  figured  by  Keith,  the  rudimentary  septa 
represent  endocardial  pockets  upon  the  wall  of  the  ventricle.  Schminke  (Endokardiale 
Taschenbildung  bei  Aorteninsuffizienz,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1908,  cxcii,  50) 
has  shown  that  similar  pockets  may  be  formed  in  the  left  ventricle  by  the  impact  of  a  re- 
gurgitant blood  stream. 


53S 


DISEASES   OF   THE   HEART    AND    AORTA. 


Open  Ductus  Botalli. — When  the  stenosis  reaches  a  considerable  grade, 
much  of  the  blood  that  reaches  the  lungs  must  pass  to  them  from  the  aorta 
back  through  the  ductus  arteriosus  (Botalli)  (Fig.  256),  which  is  therefore 

forced  to  remain  open  after  birth. 

Open  Foramen  Ovale.  —  If  the 
intraventricular  septum  has  closed 
before  the  pulmonary  stenosis  has 
occurred,  the  resulting  stasis  causes 
a  rise  of  pressure  in  the  right  auricle, 
and  the  path  of  least  resistance  to 
blood  flow  is  through  the  foramen 
ovale  to  the  left  auricle.  The  stream 
in  this  direction  is  therefore  larger 
than  usual  and  prevents  the  initial 
sclerosis  about  the  foramen,  or  even 
preserves  a  channel  in  the  lower  part 
of  the  septum,  so  that  sometimes  (as  in 
Fig.  250)  the  valve  of  the  foramen  may 
close  and  a  breach  through  this  por- 
tion of  the  septum  still  remain  patent. 

Three=chambered  Heart  (Cor  bia= 
triatum  triloculare). — When  the 
atresia  is  complete  and  the  intraven- 
tricular septum  is  closed,  the  right 
ventricle  becomes  converted  into  a 
blind  sac  into  which  no  more  blood 
can  enter.  The  tricuspid  orifice  thus 
falls  into  disuse,  and  the  valve  under- 
goes stenosis  and  atresia  until  it  is 
completely  closed.  The  cavity  of  the 
right  ventricle  remains  only  as  a  small 
blind  sac  in  the  wall  of  the  left,  from 
which  the  aorta  arises,  cor  biatriatum 
triloculare  (Fig.  251). 

Lesions  of  the  Peripheral  Vessels. 
— The  abnormalities  in  structure  sec- 
ondary to  congenital  heart  diseases  are 
by  no  means  confined  to  the  heart,  but 
especially  involve  the  finer  ramifica- 
tions of  the  vessels.  Recent  experimen- 
tal investigations  throw  much  light 
upon  the  distribution  and  formation 
of  these  abnormalities  in  a  manner 
which  is  of  great  practical  importance. 

J.  Loeb  in  1893  was  the  first  to  demonstrate  experimentally  the  effect  of  injury  to 
the  heart  upon  development.  He  poisoned  the  hearts  of  fish  (Fundulus)  embryos  by  tem- 
porary immersion  in  1.5  per  cent.  KC1  solution,  and  found  that,  though  the  hearts  of  such 
embryos  did  not  beat  at  all,  nevertheless  these  embryos  reached  adult  stage,  and  differed 
from  normal  fish  chiefly  in  the  irregular  structure  of  their  blood-vessels.  Knower,  working 
with  frog  tadpoles,  has  recently  confirmed  Loeb's  observations,  but  studied  the  changes 


Fig.  250. — Currents  and  lines  of  force  in  the 
embryonic  heart  which  result  from  pulmonary 
stenosis  and  tend  to  produce  patency  of  the  septa 
and  of  the  ductus  arteriosus.  A.  Ventricular 
end  of  the  fetal  heart  (before  the  eighth  week  of 
embryonic  life).  B.  Auricular  end  of  the  fetal 
heart  at  the  same  stage.  P  A,  pulmonary  artery; 
'  D  A,  ductus  arteriosus  (Botalli);  R  A,  right  auri- 
cle; R  V,  right  ventricle;  L  A,  left  auricle;  L  V, 
left  ventricle;  F  O,  foramen  ovale.  The  large 
arrows  indicate  blood  currents,  the  black  within 
the  ventricles,  the  white  those  within  the  auricles. 
The  small  arrows  indicate  the  forces  tending  to 
dilate  the  heart  and  to  deflect  the  septa.  In 
cases  of  extreme  grades  of  pulmonary  atresia 
the  current  in  the  ductus  arteriosus  flows  from 
aorta  to  pulmonary  artery,  instead  of  in  the 
reverse   direction. 


CONGENITAL    HEART    DISEASE. 


539 


in  more  detail,  and  has  found  that  after  mechanical  or  chemical  (acetone-chloroform) 
injury  to  the  heart  the  embryos  usually  become  very  cedematous  and  are  less  advanced 
than  the  controls.  These  embryos,  according  to  Mall,  are  very  similar  to  the  cedematous 
moles  frequently  met  with  in  gynaecological  practice.  Knower  also  found  that  the  devel- 
opment of  the  brain,  intestines,  liver,  and  pancreas  is  retarded,  ''both  arteries  and  veins 
are  very  much  distended,  and  follow  very  irregular  courses.  ...  Inmost  cases 
the  first  precapillary  loops  are  represented  by  large  sinuses, 
.  .  .  .  but  there  is  a  notable  absence  of  capillaries  in  the  fin.  The 
smaller  vessels  do  not  push  out  nor  form" characteristic  plexuses.  Their  development  is 
inhibited.  The  weaker  the  heart -beat  in  fact  the  less  does  the  blood  flow  outward  from 
the  larger  vessels  and  precapillary  loops."  Similar  changes  had  already  been  described 
by  Panum  and  Dareste  in  chick  embryos,  by  Stockard  upon  fish  embryos  poisoned  with 
lithium,  and  by  Bardeen  upon  toads  which  had  been  fertilized  with  sperm  previously 
exposed  to  the  action  of  X-rays.  Knower  also  notes  that  similar  malformations  are  com- 
mon in  frogs  at  the  end  of  the  breeding  season  (when  the  sperm  may  well  be  weakened). 

The  secondary  changes  in  man,  outside 
of  the  heart,  are  quite  homologous  with  those 
in  animals.  These  are  especially  underdevel- 
opment in  stature  and  in  intelligence  and  the 
occurrence  of  malformations  of  the  arterioles 
and  venules.  Just  as  in  Knower' s  frogs,  there 
is  a  dilatation  and  irregularity  of  venules  often 
in  the  skin,  viscera,  and  retina  (Fig.  253) ,  from 
which  hemorrhages  frequently  take  place. 
Thickening  and  clubbing  of  the  ends  of  the 
fingers  (clubbed  fingers,  Fig.  254)  also  take 
place,  from  proliferation  of  the  connective 
tissue  as  a  result  of  the  venous  stasis. 


RUD 


PATHOLOGICAL    PHYSIOLOGY 


Fig.  251. — Three-chambered  heart 
(cor  biatriatum  triloculare)  produced 
by  complete  atresia  of  the  pulmonary 
and  tricuspid  orifices.  (From  a  speci- 
men in  the  Army  Medical  Museum, 
Washington,  D.  C.)  RUD,  rudimen- 
tary cavity  corresponding  to  the  right 
ventricle;  F  O,  foramen  ovale.  The 
arrows  indicate  the  course  of  the 
blood  stream. 


The  effect  of  pulmonary  stenosis  upon  the 
mechanics  of  the  circulation  in  the  adult  is 
very  marked.  In  the  first  place  it  brings 
about  a  fall  in  blood-pressure  (both  arterial 
and   venous)  in   the    pulmonary    artery   and 

in    the    lungs    (Fig.   252),    and    consequently   a    corresponding   secondary 
lowering   of   pressure    in    the    aorta. 

The  extent  to  which  other  areas  of  the  circulatory  system  are  affected 
depends  as  much  upon  the  correlated  defects  as  upon  the  stenosis  itself. 
If  the  stenosis  is  the  only  lesion,  it  produces  a  fall  of  pressure  in  the 
pulmonary  artery,  a  rise  of  pressure  (from  stasis)  in  the  pulmonary  veins, 
and  a  marked  increase  in  pressure  within  the  right  ventricle,  like  that 
which  Liideritz  found  in  the  left  in  aortic  stenosis  (Fig.  252,  light  broken 
line).  This  always  leads  to  hypertrophy  of  the  right  ventricle  and  right 
auricle,  and  usually  to  the  signs  of  congenital  venous  congestion  to  be 
described  later. 

Between  these  two  grades  of  severity  there  exist  all  stages  of  cardiac 
insufficiency,  the  most  important  being  the  overloading  or  weakening  of 
the  right  ventricle,  which  leads  to  transitory  venous  stasis,  tricuspid  insuf- 
ficiency, and  cyanosis.    The  pressure  in  the  pulmonary  vein  and  left  auricle 


540 


DISEASES   OF  THE   HEART   AND   AORTA. 


is  by  virtue  of  the  pulmonary  stenosis  lower  than  usual,  while  that  in  the 
right  auricle  is  for  the  same  reason  higher.  Accordingly  the  tendency  is 
for  venous  blood  to  pass  into  the  left  auricle  and  ventricle  in  diastole  to  a 
much  greater  degree  than  when  the  pulmonary  orifice  is  normal,  and  hence 
to  cause  a  greater  tendency  to  cyanosis  and  dyspnoea  than  in  the  uncompli- 
cated patent  foramen  ovale. 

When  the  foramen  ovale  is  patent  but  the  septum  ventriculorum  closed 
(12  per  cent,  of  Abbott's  cases),  the  effect  upon  the  circulation  varies. 
Owing  to  the  pulmonary  stenosis,  the  path  of  least  resistance  is  through 
the  open  foramen  ovale  into  the  left  auricle  without  passing  through  the 
lungs,  and  much  blood  may  circulate  in  this  way.  Whether  or  not  this 
gives  rise  to  cyanosis  depends  upon  the  actual  amount  entering  the  lungs 
through  the  pulmonary  artery.     Under  ordinary  circumstances  this  may 


NORMAL 


PULMONARY 

STENOSIS 


PULMONARY 

STENOSIS 
AND  ATRESIA 


Fig.  252. — Diagram  of  the  circulation  in  pulmonary  stenosis  and  atresia.  Simple  pulmonary  stenosis. 
The  arrows  show  the  fall  of  pressure  in  the  aorta  and  pulmonary  artery  and  the  rise  of  pressure  in  the  vena 
cava  and  right  auricle.  The  broken  line  indicates  the  high  intraventricular  pressure  in  the  right  ventricle. 
Pulmonary  atresia,  with  patent  interventricular  septum  (SV),  patent  ductus  arteriosus  (DA),  and  patent 
foramen  ovale  (FO).  The  blood  current  passing  through  the  patent  interventricular  septum  is  indicated 
by  the  heavy  broken  line;  the  light  broken  lines  indicate  intraventricular  pressure.  The  shaded  curves 
indicate  mixed  blood.  BR,  bronchial  arteries.  The  relation  of  the  new  channels  to  the  other  arteries 
is  shown  in  the  diagram  below.  (Compare  Fig.  26.) 

keep  enough  blood  aerated  to  avoid  cyanosis,  but  in  exercise  or  exertion 
when  more  C02  is  produced,  this  excess  may  show  in  the  patient's  color. 
Moreover,  the  venous  pressure  may  rise  until  the  pressure  in  the  right 
auricle  still  further  exceeds  that  in  the  left,  and  thus  a  larger  proportion 
of  this  non-aeratecl  blood  enters  the  left  side  of  the  heart,  giving  rise  to  the 
vicious  circle  of  the  open  foramen  ovale  (Fig.  250,  B). 

/     Increased  work  of  heart    \ 
Cyanosis,  High  pressure  in 

Asphyxia  .  vena  cava 

\  Passage  of  unaerated  blood     s 
into  left  auricle 


SYMPTOMS. 


The  classical  picture  of  pulmonary  stenosis  and  especially  of  pulmonary 
atresia  is  the  "morbus  cceruleus"  or  "blue  sickness,"  as  which  it  has  been 
known  since  the  time  of  Senac  (1749).    The  patient  is  usually  a  small  child 


CONGENITAL   HEART   DISEASE.  541 

or  youth  below  the  normal  size  and  intelligence.  He  is  said  to  have  been 
blue  at  bi  r  t  h  (as  in  74  of  Peacock's  101  cases),  or  to  have  become  so 
during  the  first  year  or  two  of  life  (as  in  almost  all  of  Peacock's  other  cases) . 
He  has  suffered  from  cough  most  of  his  life,  as  well  as  shortness  of  breath. 
The  latter  becomes  extreme  or  may  come  on  in  severe  paroxysms  after 
exertion.  During  these  attacks  of  dyspnoea,  the  patient  may 
become  extremely  blue  or  even  black  in  the  face,  and  they  may  end  in  a 
fainting  spell  or  an  epileptiform  convulsion  (due  to  venous  stasis 
and  cerebral  ischsemia) .  He  may  also  have  frequent  headaches.  His 
hands  and  feet  are  usually  cold  (venous  stasis).  He  is  subject  to  frequent 
bleedings  from  the  nose,  mouth,  intestines,  or  other  mucous  membranes 
(due  to  congestion  in  dilated  venules),  which  may  even  suggest  the  diagnosis 
of  haemophilia. 

On  the  other  hand,  persons  with  a  considerable  grade  of  congenital 
pulmonary  stenosis  may  remain  free  from  symptoms  and  even  perform 
heavy  work,  as  in  the  case  quoted  by  Peacock  of  a  man  of  forty-four  who 
worked  as  a  navigator  until  six  weeks  before  his  death.  Such  cases,  however, 
constitute  only  a  small  percentage  of  every  series. 

Pulmonary  Stenosis  with  Patent  Interventricular  Septum. — However, 
when  the  interventricular  septum  is  defective  the  condition  is  entirely 
different.  The  lowered  pressure  in  the  pulmonary  artery  usually  continues 
unless  fully  compensated  by  the  anastomotic  circulation.  The  right  ven- 
tricle hypertrophies  until  -it  equals  or  even  exceeds  the  left  in  thickness, 
and,  owing  to  the  dextroversion  of  the  aorta,  sends  its  large  quota  of  blood 
into  the  aorta.  The  pressure  in  the  systemic  veins,  therefore,  depends  not 
upon  the  pressure  within  the  right  ventricle  but  upon  the  ability  of  the 
right  ventricle  to  force  the  blood  onward  and  prevent  it  from  accumulating 
in  the  veins.  The  presence,  extent,  or  absence  of  symptoms,  on  the  other 
hand,  depends  upon  the  aeration  of  blood  in  the  lungs.  Peacock  well  says 
that  "in  cases  of  this  description  the  open  state  of  the  foramen  ovale  and 
the  imperfection  in  the  ventricular  septum,  so  far  from  adding  to  the  danger, 
really  afford  the  means  of  relief  to  the  overcharged  right  auricle  and  ven- 
tricle without  which  life  could  not  be  prolonged  for  any  considerable  period." 
That  the  outlook  in  cases  where  defective  septa  accompany  the  pulmonary 
stenosis  is  graver  than  in  cases  where  the  stenosis  occurs  alone  is  due  merely 
to  the  fact  that  in  the  latter  case  the  lesion  is  usually  formed  late  in  fetal 
life,  and  hence  is  comparatively  mild;  or,  if  formed  early,  it  is  too  slight  to 
give  rise  to  the  stasis  which  keeps  the  septa  open. 

PHYSICAL    SIGNS. 

The  patients,  usually  children,  are  of  stunted  growth,  with  eyes 
watery,  veins  of  forehead,  face,  and  arms  large,  very  numerous,  and 
anastomosing  frequently. 

Cyanosis. — So  striking  and  so  frequent  is  the  occurrence  of  intense  cya- 
nosis in  congenital  heart  disease  that  this  term  has  become  almost  synony- 
mous with  the  "morbus  cceruleus"  (blue  sickness)  described  by  Senac. 

The  patients  may  be  persistently  livid  or  the  cyanosis  may  be  present 
only  at  times  of  exertion  or  ill  health.    It  may  then  come  in  attacks  asso- 


542  DISEASES   OF   THE   HEART    AND    AORTA. 

ciated  with  dyspnoea  and  sometimes  convulsions.     The  patients  may  be- 
come quite  black  in  the  face  and  may  remain  so  for  some  time. 

The  mode  of  origin  of  the  cyanosis  in  congenital  heart  disease  is  a 
matter  not  only  of  scientific  interest  but  of  the  greatest  practical  importance  in  diagnosis 
and  prognosis.  Theories:  1.  Mixture  of  venous  with  arterial  blood.  Senac  (1749),  William 
Hunter,  Forget,  Meckel,  Corvisart,  Gintrac,  Favre,  Paget,  and  others  supposed  that  the 
cyanosis  was  due  to  the  passage  of  venous  blood  directly  into  the  left  auricle  or  ventricle 
through  the  open  foramen  ovale  or  interventricular  septum.  While  this  may  play  a  role 
in  some  or  indeed  in  most  cases,  Moreton  Stille  (1844)  has  shown   "that    complete 

admixture    of     the     blood    may    take     place    without    cyanosis 

This  is  conclusively  demonstrated  by  the  two  following  cases. 

"First. — Foramen  ovale  open;  pulmonary  artery  arose  from  both  ventricles,  gave 
off  pulmonary  branches,  and  formed  the  aorta  descendens.  The  aorta  gave  off  the  branches 
to  the  head  and  upper  extremities  and  joined  the  pulmonary  artery  by  the  ductus  arterio- 
sus.    No   cyanosis.     Age  eight  months. 

"Second. — Heart  with  two  cavities;  aorta  and  pulmonary  arising  from  the  ventricle. 
No   cyanosis.     Age  eleven  days." 

Numerous  other  observations  in  the  literature  have  confirmed  Stille's  contention. 
On  the  other  hand,  when  there  is  mixing  of  venous  and  arterial  blood,  a  relatively  slight 
stasis  or  cardiac  weakness  from  overstrain  or  disease  may  bring  about  intense  cyanosis, 
which  would  not  occur  in  persons  with  healthy  hearts. 

2.  The  second  theory,  proposed  by  Morgagni  (1761)  and  subsequently  advocated  by 
Louis.  Bduillaud,  Valleix,  Hasse,  Stille,  and  Rokitansky,  was  that  owing  to  the  pulmonary 
stenosis  there  was  stasis  in  the  systemic  veins,  and  that  the  cyanosis  resulted  from  that 
factor  only.  To  this  theory  Grancher  adds  the  fact  that  the  capillaries  and  precapillaries 
are  already  markedly  dilated  (for  reasons  given  above  on  page  526)  and  that  in  these  dilated 
capillaries  slight  stasis  brings  about  marked  cyanosis. 

Another  factor,  to  which  attention  has  been  called  by  Vaquez,  Osier,  and  others,  is 
that  in  such  cases  cyanosis  is  usually  accompanied  by  intense  polycythemia,  and  the  in- 
crease in  the  amount  of  the  C02  haemoglobin  intensifies  the  cyanosis  which  might  other- 
wise be  present  in  moderate  degree. 

None  of  these  theories,  however,  explains  the  absence  of  cyanosis  in  cases  where  all 
the  venous  blood  passes  into  the  aorta.  In  these  cases  the  ventricles  are  strongly  exerting 
both  their  suction-pump  and  force-pump  action,  so  that  blood  does  not  accumulate  in 
the  veins.  On  the  other  hand,  the  pressure  in  the  aorta  (ranging  from  90  to  120  mm.  Hg) 
is  about  three  times  as  high  as  the  pressure  normally  present  in  the  pulmonary  artery, 
and  hence  is  capable  of  forcing  a  very  large  amount  of  blood  through  the  wide  bronchial 
arteries  or  open  ductus  arteriosus  (Botalli)  to  the  lungs. 

Whether  admixture  of  venous  blood  will  or  will  not  produce  cyanosis  depends  largely 
upon  the  amount  of  CO,  which  the  abnormal  pulmonary  circulation  can  take  care  of,  and 
which  in  most  cases  is  more  limited  than  in  the  normal  individual.  When  excessive  exer- 
cise, strain,  or  cardiac  weakening  causes  an  abnormal  increase  of  C02,  cyanosis  makes  its 
appearance,  and  owing  to  the  congenital  dilatation  of  the  capillaries  the  cyanotic  effect 
is  magnified. 

The  cases  in  which  cyanosis  occurs  in  spells  are  probably  examples  of  transitory 
venous  stasis  (in  congenitally  enlarged  capillaries  and  capillary  plexus).  In  cases  with 
open  foramen  ovale  stasis  in  the  systemic  veins  and  right  heart  will  divert  an  abnormally 
large  amount  of  venous  blood  through  the  foramen  ovale  (Fig.  250). 

The  head  occasionally  shows  signs  of  other  abnormalities  in  form.  There  may  be 
deficient  formation  of  bones  of  skull,  abnormalities  in  the  form  of  the  ears,  hare-lip,  cleft 
palate,  etc. 

Vascular  Changes  in  the  Retina. — Marked  changes  in  the  vessels  of 
the  retina,  seen  upon  examination  with  the  ophthalmoscope,  were  first 
reported  by  Knapp  in  1861.  In  cases  with  marked  cyanosis  elsewhere 
there  are  often  irregularities  in  the  lumina  of  arteries  and  veins,  which  are 
tortuous  ("resembling  large  angle-worms,"  Posey)  and  in  some  places 
very  wide  (twice  as  wide  as  normal) ,  in  others  very  narrow.     "  Both  veins 


CONGENITAL   HEART   DISEASE. 


543 


/CT1 


*'r% 


C^» 


m 


^MJJP 


'<# 


Fig.  253. — Dilatation  and  irregularity  of  the  reti- 
nal vessels.   V,  vein;  A,  artery.    (After  Posey.) 


and  arteries  become  much  darker  than  normal,  the  former  assuming  a  deep 
violet  color,  while  the  arteries  resemble  normal  veins.  The  peripheral 
twigs  of  the  retinal  vessels  are  distended,  and  vessels  which  are  usually 
invisible  may  be  seen  over  the  entire  fundus Small  hemor- 
rhages are  of  frequent  occurrence"  (Posey)  (Fig.  253).  In  doubtful  cases 
this  feature  may  be  of  great  diag- 
nostic value,  but  it  can  be  expected 
to  occur  only  in  those  cases  in  which 
there  is  a  considerable  degree  of  cy- 
anosis and  in  which  the  prenatal 
slowing  of  circulation  has  probably 
been  marked. 

Clubbed  Fingers  (Hippocratic  Fin= 
gers). — The  ends  of  the  fingers  under- 
go peculiar  changes  (clubbed  fingers, 
Hippocratic  fingers)  (Fig.  254),  which 
also  occur  in  chronic  pulmonary  dis- 
eases, tuberculosis,  chronic  cardiac 
disease,  especially  in  children  and  in 
conditions  producing  long-continued 
local  or  general  venous  stasis  (Eb- 
stein).     The  change  is  confined  to  the 

pulp  of  the  finger,  which  is  thicker  than  normal  and  broadest  near  the  tip, 
and  tapers  in  a  proximal  instead  of  a  distal  direction.  The  nails  are  very 
convex  in  both  longitudinal  and  transverse  diameters.  They  are  usually 
cyanotic.  The  form  of  the  bones  is  practically  unchanged.  E.  Ebstein 
has  collected  a  large  number  of  observations 
which  prove  that  clubbing  of  the  fingers  and  toes 
results  from  chronic  passive  congestion  either  gen- 
eral or  local  (from  pressure  on  veins).  The  earlier 
in  intra-uterine  or  in  extra-uterine  life  that  the 
congestion  occurs  and  the  longer  is  its  duration 
the  more  marked  is  the  clubbing. 

The  occurrence  of  clubbed  fingers  is  dependent 
on  almost  the  same  factors  as  cyanosis,  and  the  two 
features  usually  occur  together  or  are  both  absent. 
Cardiac  Signs. — The  precordium  almost  always 
bulges,  and  the  wavy  systolic  impulse  over  the 
precordium  due  to  systole  of  the  right  ventricle  is 
usually  seen.  A  systolic  impulse  at  the  apex  may 
or  may  not  be  present.  The  area  of  cardiac  dulness 
is  usually  enlarged  to  both  right  and  left.  On 
palpation  a  rough  systolic  thrill  is  felt  over  the  pulmonary  area, 
from  which  it  is  transmitted  diagonally  upward  toward  the  left  clavicle 
and  downward  over  the  precordium  (Fig.  255).  In  cases  in  which  there 
is  a  defect  in  the  septum  ventriculorum,  this  thrill  is  also  intensified  over 
the  third  and  fourth  left  interspaces  near  the  sternal  margin. 

The  characteristic  sign  of  pulmonary  stenosis  on  auscultation  is  a  sys- 
tolic   murmur   accompanying  the  above-mentioned  thrill  and  following 


Fig.  254. — Clubbed  fingers. 


544 


DISEASES   OF   THE   HEART   AND    AORTA. 


Fig.  255. 


-Distribution  of  the  pulmonary  systolic  mur- 
mur of  pulmonary  stenosis. 


the  first  sound,  loudest  over  the  pulmonary  area  or  just  beyond  it  in  the  sec- 
ond left  interspace.    In  sharp  contrast  to  the  murmur  of  aortic  stenosis,  it  is 

transmitted  upward  and  to 
the  left.  It  is  also  heard 
over  the  precordium,  but,  un- 
less the  interventricular  septum 
or  ductus  arteriosus  (Botalli)  is 
open,  it  is  not  usually  trans- 
mitted to  the  systemic  arteries. 
The  second  pulmonic  sound  is 
either  absent  or  suppressed  in 
spite  of  the  respiratory  distress. 
However,  it  is  noteworthy  that 
in  those  cases  in  which  there  is 
uniform  pulmonary  atresia  ex- 
tending over  one  or  two  cm. 
and  where  the  lesion  is  actually 
most  severe,  the  murmur  may 
be  entirely  lacking.  The  same 
applies,  of  course,  to  complete 
obliteration  of  the  pulmonary  artery.  Needless  to  say,  the  imperfectly 
formed  valves  may  be  insufficient  and  a  diastolic  murmur  due  to  regurgi- 
tation may  also  be  present.  However,  a  murmur 
of  this  type  is  most  frequently  due  to  the  defect 
in  the  interventricular  septum  (see  page  547). 
Open  foramen  ovale,  when  present,  rarely 
gives  characteristic  signs,  but  occasionally  may  be 
revealed  by  a  presystolic  murmur  heard  at  the 
base.  The  signs  due  to  an  open  ductus  arteri- 
osus Botalli  are  so  similar  to  those  of  pulmo- 
nary stenosis  that  even  in  typical  cases  it  is 
almost  impossible  to  diagnose  in  the  presence 
of  the  latter.  The  murmur  from  the  former 
is  more  frequently  heard  at  the  back  to  the 
left  of  the  third  and  fourth  dorsal  vertebrae 
with  a  very  marked  inspiratory  accentuation 
and  expiratory  diminution  (Francois-Franck) . 
The  chest  is  usually  poorly  expanded,  often 
pigeon-breasted.1  Harrison's  grooves  are  often 
prominent.  Signs  of  phthisis  (areas  of  dul- 
ness,  tubular  breathing,  increased  vocal  fremitus 
and  rales)  are  very  common,  especially  at  the 
apices  (80  per  cent,  of  Abbott's  cases),  in  cases 
which  have  passed  the  age  of  infancy,  and  tuber- 
cle bacilli  are  frequently  found  in  the  sputum. 


Fig.  256. — Direction  of  blood- 
streams and  propagation  of  mur- 
murs accompanying  defect  in  the 
interventricular  septum,  pulmon- 
ary stenosis,  and  open  ductus  arte- 
riosus (Botalli).  DEF.  SEPT., 
defect  in  the  interventricular  sep- 
tum; P.  ST.,  pulmonary  stenosis; 
PAT  DA,  patent  ductus  arterio- 
sus (Botalli);  1,  2,  3,  4,  5  represent 
the  corresponding  ribs. 


1  This  flatness  of  the  chest  may  perhaps  be  of  reflex  origin,  since  F.  Kauders  (Ueber 
einige  Experimente  zur  Lehre  von  der  cardialen  Dyspnoe,  Wien  klin.  Wchnschr.,  1891), 
under  v.  Basch's  direction,  has  shown  that  the  diaphragm  rises  when  the  blood  flow  through 
the  lungs  is  diminished. 


CONGENITAL   HEART   DISEASE. 


545 


Condition  of  Other  Organs. — The  abdomen  is  often  very  full,  the 
liver  and  spleen  enlarged,  especially  in  cases  with  cyanosis  and 
venous  stasis.     The  genitalia  are  usually  underdeveloped. 

The  blood  count  usually  ranges  between  6,000,000  and  9,000,000,  the 
haemoglobin  between  110  and  130  per  cent. 

There  are  often  albumin  and  casts  in  the  urine,  which  is  frequently 
scanty.    Occasionally  there  is  blood  from  the  dilated  capillaries. 

DIAGNOSIS. 

As  stated  by  Rauchfuss  in  1878,  the  diagnosis  of  congenital  pulmonary 
stenosis  can  usually  be  made  from  the  following  symptom  complex :  "  Cyan- 
osis, from  birth  or  following  signs  of  cardiac  affection  which  were  then  pres- 
ent; signs  of  dilatation  and  hypertrophy  of  the  right  auricle  and  ventricle; 
systolic  murmur  and  thrill  over  the  conus  arteriosus  and  pulmonary  artery, 
not  transmitted  to  the  carotid  arteries."  He  admits,  however,  as  do  all 
subsequent  authors,  that  the  exact  diagnosis  of  the  secondary  lesions  intra 
vitam  is  almost  impossible,  owing  to  the  multiplicity  of  the  lesions  which 
may  occur  and  the  fact  that  so  many  of  the  signs  overlap  one  another. 

TREATMENT  AND  PROGNOSIS. 

As  regards  prognosis  statistics  vary  considerably.  Of  Stoelker's  53 
cases  32  died  at  birth,  12  during  the  first  year,  and  11  during  the  first  decade. 
Only  4  reached  the  fourth  decade. 

The  age  of  death  in  Abbott's  series  was  as  follows: 


Pulmonary  Stenosis. 

Pulmonary  Atresia. 

Age  at  death. 

V.  S.  closed. 

F.  0.  closed, 
detect  V.S. 

F.  O.  patent, 
defect  V.  S. 

V.  S.  closed. 

F.  O.  closed, 
defect  V.  S. 

F.O.  patent, 
defect  V.  S. 

Before  1  year 

1-7 

0 
2 
4 
3 
6 
1 

4 
16 
5 
8 
3 
0 

3* 

8 

4 

5 

0 

0 

6 
0 
0 
0 
0 
0 

2 
3 
0 
0 
0 
0 

lot 

0 

7-14 

0 

14-20 

0 

20-28 

0 

28-45 

0 

61 

36 

20 

6 

5 

10 

*  9.7  per  cent. 


t  78  per  cent. 


One  can  hardly  fail  to  be  struck  by  the  contrast  between  the  cases  of 
pulmonary  atresia  and  pulmonary  stenosis,  since  78  per  cent,  of  the  former 
die  in  the  first  year,  while  this  is  the  case  in  only  9.7  per  cent,  of  the  latter. 
Even  of  these  only  36  per  cent,  survived  the  age  of  puberty  and  only  one 
reached  middle  age. 

In  the  individual  case  the  physician  may  be  guided  by  the  intensity 
of  the  sj^mptoms  even  more  than  by  the  physical-  signs,  severe  symptoms, 
as  a  rule,  portending  an  early  death.  When  the  symptoms  in  early  youth 
35 


546  DISEASES   OF   THE   HEART    AND    AORTA. 

are  comparatively  mild,  the  prognosis  is  a  little  better,  but  an  early  death 
from  phthisis  or  acute  endocarditis  is  always  to  be  feared,  even  when  the 
heart  failure  is  less  intense.  It  is,  therefore,  most  important,  as  Peacock 
suggested:  (1)  to  keep  the  patient  warm  by  both  warm  clothing  and 
sojourn  in  a  balmy  climate;  (2)  to  keep  him  leading  a  quiet  life  on  a  diet 
of  nourishing  but  easily  digested  food.  For  paroxysms  of  dyspnoea  and 
distress  free  purgation  should  be  resorted  to.  Venesection,  which  was  recom- 
mends "~  Peacock,  though  indicated  by  both  the  venous  stasis  and  the 
high  viscosity  of  the  blood,  is  a  dangerous  procedure  and  should  be  used 
only  as  a  last  resort,  for  the  coagulation  of  the  blood  in  these  cases  is 
often  retarded.  Before  performing  it  the  coagulability  should  always  be 
determined. 

The  general  cardiac  stimulants,  such  as  digitalis  and  strychnine,  are 
rarely  of  much  value,  since  in  most  cases  the  heart  has  already  reached  the 
maximum  of  its  power  and  cannot  be  stimulated  much  further.  Vasodila- 
tion from  amyl  nitrite  and  nitroglycerin  may  sometimes  help,  and  Peacock 
recommends  the  use  of  warm  baths  or  mustard  baths,  especially  for  the 
convulsions  of  children. 


DEFECTS   IN   THE   INTERVENTRICULAR   SEPTUM. 

OCCURRENCE    AND    PATHOGENESIS. 

As  has  been  stated  above,  defects  in  the  interventricular  septum  are 
usually  with  and  secondary  to  other  malformations,  this  being  the  case  in 
117  (78  per  cent.)  of  149  cases  studied  by  Abbott.  Pulmonary  stenosis  or 
atresia  was  present  in  75  cases  (58  per  cent.).  In  only  24  cases  (16.1  per 
cent.)  were  there  no  other  abnormalities. 

The  circulatory  mechanism  which  keeps  the  septum  from  closing  in 
the  presence  of  pulmonary  stenosis  has  been  discussed  above  under  the 
latter  condition.  In  the  other  cases,  in  which  Abbott  classes  it  as  a  "  second- 
ary lesion,"  the  mechanism  is  similar. 

In  the  uncomplicated  cases,  however,  the  causation  is  more  obscure. 
In  a  few  cases  it  is  accounted  for  by  fetal  endocarditis  affecting  the  septum 
interpositum  before  the  septum  membranaceum  has  formed.  In  other 
cases  the  septum  membranaceum  does  not  form  completely.  After  birth, 
when  the  pressure  in  the  left  ventricle  rises  high  above  that  in  the  right, 
the  rush  of  blood  from  the  left  ventricle  into  the  right  may  push  the  septum 
along  with  it  and  may  cause  it  to  protrude  as  a  funnel  into  the  right  ven- 
tricle (Tate,  Hebb) .  In  still  other  cases  the  septum  forms  and  protrudes  as 
an  aneurism  of  the  septum.  This  aneurism  may  rupture  later  and  give 
rise  to  the  defect. 

Some  cases  of  apparent  defect  in  the  septum  are  due  to  ulcerative 
septal  endocarditis,  but  these  are  probably  few.  Trauma  may  produce  a 
similar  effect  in  adult  life.  McOscar  and  Voelcker  report  the  case  of  a  man 
who  was  run  over  by  a  wagon.  Rupture  of  the  interventricular  septum 
resulted  and  the  patient  died  eight  days  afterwards.  Reiss  states  that 
pulmonary  tuberculosis  has  been  found  in  every  adult  in  his  series,  but  this 
is  by  no  means  always  the  case. 


CONGENITAL   HEART    DISEASE.  547 


PATHOLOGICAL    PHYSIOLOGY. 

When  the  defect  in  the  septum  is  secondary  to  a  severe  pulmonary 
stenosis  or  atresia,  as  has  been  seen,  its  effect  is  to  allow  blood  to  pass  from 
the  right  ventricle  into  the  left,  and  under  any  circumstances  this  is  the 
case  during  fetal  life. 

When  there  is  no  such  stenosis,  however,  and  the  strength  of  the  left 
ventricle  increases  after  birth,  the  current  passes  in  the  reverse  direction 
and  aerated  blood  passes  from  the  left  ventricle  into  the  right.  The  effect 
upon  the  work  of  the  former  is  consequently  about  the  same  as  that  of  a 
leak  at  the  mitral  valve;  intraventricular  pressure  is  lowered,  and  the 
systolic  output  must  be  increased  in  order  to  maintain  the  circulation. 
The  left  ventricle  consequentlyhypertrophies  as  a  result  of  the  strain;  the 
right  ventricle  hypertrophies  also  as  a  result  of  the  increase  in  the  blood 
forced  into  it.  The  extent  of  hypertrophy  of  the  latter  chamber  depends 
largely  upon  the  size  of  the  opening.  As  the  right  ventricle  hypertrophies 
and  pressure  in  the  right  ventricle  increases,  the  leakage  diminishes,  so 
that  the  effect  of  the  lesion  tends  to  correct  itself;  on  the  other  hand,  the 
pressure  in  the  pulmonary  artery  increases.  But  since  the  ordinary  resist- 
ance in  the  pulmonary  circulation  is  much  less  than  that  in  the  systemic, 
when  the  forces  of  both  ventricles  approximate  one  another,  the  effect  on 
the  pulmonary  circulation  is  the  same  as  though  the  left  ventricle  became 
weaker  and  the  right  remained  unchanged.  Pulmonary  engorgements 
may,  therefore,  result,  with  consequent  dyspnoea.  In  most  cases,  however, 
the  hypertrophy  does  not  reach  this  point,  and  it  is  only  when  the  heart  is 
stimulated  by  effort  or  exercise  that  pulmonary  engorgement  sets  in. 

SYMPTOMS. 

In  considering  the  symptoms  and  signs *of  defects  of  the  interventricular 
septum,  one  must  differentiate  sharply  between  those  cases  in  which  the 
condition  exists  alone  and  those  in  which  it  is  secondary  to  other  lesions. 
In  the  latter  case  the  manifestations  of  the  primary  condition  may  predomi- 
nate; and  these  are  discussed  in  the  corresponding  sections. 

The  symptoms  from  simple  defect  in  the  interventricular  septum  are 
few,  and,  as  a  rule,  are  confined  to  more  or  less  weakness,  dyspnoea,  and 
palpitation,  rather  than  the  extensive  symptom  complex  met  with  in 
pulmonary  stenosis. 

PHYSICAL    SIGNS. 

In  marked  contrast  to  pulmonary  stenosis,  marked  cyanosis  is  not 
one  of  the  signs  of  uncomplicated  defect  in  the  interventricular 
septum,  since  there  is,  as  a  rule,  no  stasis  in  the  veins  and  the  abnormal 
blood  stream  flows  from  left  ventricle  into  the  right.  Cyanosis  may  occur, 
however,  as  the  result  of  a  cardiac  overstrain,  just  as  in  any  other  condi- 
tion of  cardiac  weakness,  but  is  not  abnormally  intense.  The  fingers  are, 
as  a  rule,  not  clubbed.  Over  the  precordium  and  epigastrium  there  is 
usually  violent  systolic  retraction,  produced  by  the  hypertrophied  right 
ventricle.  There  may  be  violent  systolic  pulsation  of  the  conus  arteriosus 
in  the  second  left  interspace.    The  area  of  dulness  may  be  enlarged  to  both 


548 


DISEASES   OF   THE   HEART    AND    AORTA. 


right  and  left,  or  there  may  be  no  change  from  the  normal.  There  is 
almost  always  a  well-marked  systolic  thrill  over  the  third  left  interspace 
near  the  sternal  margin. 

Auscultation  reveals  the  presence  of  a  murmur  which  was  first  described 
by  Roger  in  1879  in  the  following  words: 

" It  is   in  general   remarkably   intense;   its   maximum  is   not   at   the   apex 
(as  in  alterations  of  the  auriculoventricular  orifices),  nor  at  the  right  base  (as  in  aortic 

stenosis),  nor  at  the  left  base  (as  in 
pulmonary  stenosis) .  This  maximum 
is  at  the  upper  third  of  the  precor- 
dial region  and  is  median  like  the  ven- 
tricular septum  itself.  It  is  single 
and  very  prolonged,  commencing  with 
systole  and  replacing  the  two  normal 
sounds.  It  is  fixed  without  propa- 
gation in  the  large  vessels,  as  is  the 
case  with  aortic  or  pulmonary  stenosis, 
and  decreases  in  intensity  equally  in 
all  directions  as  one  passes  away  from 
this  central  point.  .""...  The  mur- 
mur corresponds  with  a  very  extensive 
thrill  which  exactly  coincides  with  it. 
....  The  murmur  does  not  change 
in  the  course  of  years." 

However,  all  writers  do  not 
agree  with  Roger.  Cadet  de 
Gassicourt,  Potain,  and  Reiss 
claim  that  it  occurs  during  systole  only;  while  in  some  cases,  especially  where 
the  septal  defect  is  a  large  one,  it  is  totally  absent  (Bennetz) .  The  murmur 
is  sometimes  transmitted  to  the  carotid  arteries,  though  it  is  always  loud- 
est over  the  precordium.  The  second  pulmonary  sound  is  accentuated. 
The  pulse  may  be  small  and  weak,  or,  as  in  the  case  of  McOscar  and 
Voelcker,  collapsing.    The  blood-pressure  is  usually  low. 


Fig.  257. — Distribution  and  character  of  the  murmur  due 
to  a  patent  interventricular  septum  (Roger's  murmur). 


Case  of  Patent  Septum  Ventriculorum. 

The  following  notes  were  obtained  from  a  case  admitted  to  Prof.  Barker's  service 
in  the  private  wards  of  the  Johns  Hopkins  Hospital: 

The  patient  was  a  married  man,  a  scientist  of  some  note,  aged  59.  As  a  child  he  had 
been  subject  to  bad  dreams  and  disturbed  sleep  and  became  short  of  breath  on 
slight  exertion.  This  shortness  of  breath  on  exertion  followed  through  life,  but 
in  spite  of  the  ordinary  diseases  of  childhood,  three  mild  attacks  of  typhoid  fever,  and 
continued  use  of  tobacco,  alcohol,  and  strong  coffee,  he  was  able  to  lead  an  active  life  until 
past  middle  age. 

For  six  weeks  before  admission  to  the  hospital  he  has  been  very  weak  and  has  been 
troubled  with  nocturnal  dyspnoea,  though  these  symptoms  are  probably  refer- 
able to  his  renal  rather  than  to  his  cardiac  changes.  Swelling  of  the  feet  set  in  a  few  days 
before  admission. 

On  Feb.  15,  1908,  Dr.  Barker  made  the  following  note  on  his  cardiac  condition: 
The  radials  are  thickened,  the  blood-pressure  is  high;  there  is  a  blowing  systolic  murmur 
at  the  apex,  the  aortic  second  sound  is  fairly  loud,  the  pulmonic  second  very  loud.  The 
rough  systolic  murmur  is  also  heard  in  the  pulmonary  area, 
but  is  loudest  and  roughest  a  little  lateral  from  the  tricuspid 
area.  No  aortic  diastolic  murmur  is  heard.  There  is  no  marked  throbbing  of  the  neck; 
veins  in  the  neck  are  a  little  overfilled.  There  is  some  oedema  of  the  ankles  and  overfilling 
of  the  veins  of  the  lower  extremities. 


CONGENITAL   HEART    DISEASE.  549 

He  passed  over  2500  c.c.  of  urine  daily,  of  specific  gravity  1012-1014,  containing  a 
trace  of  albumen  and  some  hyaline  casts.  The  blood-pressure  varied  from  220  to  285 
mm.  Hg,  pulse-rate  80-90. 

During  his  stay  in  the  hospital  he  had  occasional  smothering  spells  which  were  relieved 
by  venesection.    He  spat  up  considerable  amounts  of  red  tenacious  sputum. 

The  patient  died  during  the  course  of  the  next  few  months.  Autopsy  revealed 
a  funnel-shaped  bulging  of  the  membranous  septum  into  the 
right  ventricle  with  a  perforation  3-4  mm.  in  diameter  at  the 
apex  of  the  funnel.  (This  condition  is  exactly  similar  to  the  lesion  described 
by  Hebb  and  by  Tate.) 

There  was  also  a  chronic  nephritis. 

Case  of  Probable  Patent  Septum  Ventriculorum. 

B.  J.,  an  unmarried  colored  woman  aged  26,  entered  the  Johns  Hopkins  Hospital 
complaining  of  pain  in  the  chest.  Except  for  shortness  of  breath  on  exertion  during  the 
last  ten  years,  the  history  is  negative. 

Her  heart  was  very  slightly  enlarged  to  the  right.  The  sounds  were  clear  at  the  apex, 
but  over  the  body  of  the  heart  a  peculiar  intense  high-pitched  murmur  was  heard,  loudest 
during  systole  but  lasting  through  the  whole  cardiac  cycle  (Roger's  murmur?).  This 
murmur  is  loudest  and  most  intense  over  the  third  left  interspace 
between  the  parasternal  line  and  the  sternum,  but  it  is  heard  also  in 
the  second  and  fourth  interspaces,  where  it  is  much  less  intense. 

Maximal  blood-pressure  varied  from  110  to  125  mm.  Hg;  venous  tracings  were  normal; 
retinal  vessels  normal.    The  urine  contained  a  trace  of  albumen  but  no  casts  nor  blood-cells. 

The  subsequent  history  was  uneventful. 

DIAGNOSIS. 

The  diagnosis  of  defect  in  the  interventricular  septum  can  be  made 
only  when,  in  the  absence  of  cyanosis  or  other  signs  of  congenital  heart 
disease,  the  vigorous  pulsation  of  the  right  ventricle  is  seen  in  the  second 
left  interspace,  and  both  the  peculiar  murmur  of  Roger  and  the  accentu- 
ated second  pulmonic  sound  can  be  heard.  In  the  presence  of  pulmonary 
stenosis  or  other  congenital  or  acquired  lesions,  signs  may  merge  into  one 
another  in  such  a  way  that  an  absolute  diagnosis  may  be  impossible. 
Simple  acquired  endocarditis  often  occurs,  as  in  Tebb's  case,  and  its  signs 
may  serve  further  to  confuse  the  clinical  picture. 

TREATMENT. 

Needless  to  say,  there  is  no  treatment  that  can  be  directed  against 
the  defect  itself.  However,  the  symptoms  in  many  cases  arise  only  during 
over-exertion,  and  the  most  important  factor  in  the  management  of  the 
case  is,  therefore,  directed  along  the  usual  lines  for  the  avoidance  of  over- 
strain,— rest,  graduated  exercise,  moderation  in  diet,  avoidance  of  dyspnoea, 
regulation  of  the  bowels,  and  if  necessary  digitalis  and  strychnine.  The 
most  important  point  is  the  avoidance  of  pulmonary  congestion. 

The  prognosis  in  simple  septal  defect  depends  less  upon  the  extent 
of  the  lesion  than  upon  the  apparent  impairment  of  the  function.  Simple 
defects  in  the  septum  are  compatible  with  quite  long  life,  and  many  cases 
are  reported  in  which  the  patients  have  reached  the  fourth  and  fifth  decades. 

When  other  lesions  are  present,  such  as  pulmonary  stenosis,  abnormali- 
ties of  the  blood-vessels,  etc.,  it  is  they,  rather  than  the  septal  defect,  which 
determines  the  prognosis. 


550 


DISEASES   OF   THE   HEART   AND   AORTA. 


PATENT   FORAMEN   OVALE. 


OCCURRENCE  AND  PATHOGENESIS. 


Mere  patency  of  the  foramen  ovale  to  the  passage  of  a  probe  is  by  no 
means  pathological.  In  statistics  of  1166  heterogeneous  autopsies  collected 
by  Vierordt,  it  was  present  313  times  (28  per  cent.),  and  also  in  80  (22.3  per 
cent.)  of  Zahn's  357  miscellaneous  autopsies  upon  persons  past  the  age  of 
40.  This  non-closure  is  probably  due  to  the  fact  that  both  the  auricular 
septum  and  the  valve  closing  the  foramen  are  lined  by  endothelium,  and 
no  fibrosis  takes  place  between  the  two  surfaces  until  the  endothelial  cells 
slough  off  or  are  injured.    The  valve  itself  remains  closed  against  the  septum 

during  life  and  no  symptoms  are 
produced.  Perhaps,  when  heart 
failure  from  any  cause  occurs  in 
such  cases  and  the  pressure  in  the 
right  auricle  exceeds  that  in  the 
left,  a  certain  amount  of  blood  may 
actually  pass  through  this  embryonic 
channel,  but  in  too  small  amounts 

VC 


RA      R?  LA 


Fig.  258. — Open  foramen  ovale.  (From  a  spec- 
imen in  the  Army  Medical  Museum,  Washington,  D. 
C.)  The  patient  was  a  soldier  who  had  never  shown 
any  cardiac  signs  or  symptoms  and  no  cyanosis. 


Fig.  259.  —  Diagram  showing  a  cross-section 
of  the  same.  VC,  vena  cava;  RA,  right  auricle; 
FO,  foramen  ovale;  LA,  left  auricle. 


to  give  signs  or  symptoms.  On  the  other  hand,  in  462  autopsies  by  Hinze 
and  by  Ogle  the  foramen  was  permeable  to  the  little  finger  (permanently 
patent)  in  only  9  cases  (1.9  per  cent.). 

The  mechanism  of  secondary  septal  defects  (auricular  stasis  of  Mor- 
gagni  and  William  Hunter)  by  which  more  than  the  usual  proportion  of 
blood  passes  through  the  foramen  ovale  has  been  discussed  under  pulmo- 
nary stenosis,  and  it  may  occur  with  other  congenital  lesions. 

The  truly  pathological  lesions  of  the  interauricular  septum  are  shrink- 
age or  total  absence  of  the  valve  and  perforation  of  the  septum  between, 
the  muscle  strands  (Fig.  260).  Occasionally  the  valve  has  closed,  but  is 
somewhat  weak  and  forms  an  aneurismal  bulging.  Peacock  reports  one 
and  Abbott  two  of  these  cases,  in  all  of  which  the  protrusion  was  from  right 
to  left,  indicating  that  the  pressure  in  the  right  ventricle  exceeded  that  in 
the  left. 


CONGENITAL   HEART    DISEASE. 


551 


Valv.F.O. 


PATHOLOGICAL    PHYSIOLOGY. 

A  defect  in  the  interauricular  septum  has  comparatively  little  effect 
upon  the  circulation  as  long  as  the  pressures  in  the  two  auricles  are  equal 
or  nearly  so.  When  the  left  ventricle  begins  to  fail  or  the  pressure  in  the 
left  auricle  rises  from  any  cause  whatever  (mitral  stenosis,  mitral  insuffi- 
ciency, etc.),  the  patent  foramen  ovale  exercises  a  sort  of  safety-valve  action 
and  relieves  the  pulmonary  congestion  by  allowing  the  excess  of  blood  to 
pass  back  into  the  right  auricle.  Ritter  (1856)  and  Rusch  (1862)  have 
shown  that  when  the  foramen  ovale  is  open  in  cases  of  mitral  insuf- 
ficiency, the  pulsation  in  the  jugular  vein  assumes  the  positive  ven- 
tricular type,  owing  to  the  crossing  of  the  regurgitant  stream.  How- 
ever, this  is  of  little  value  in  diagnosis,  since  the  positive  ventricular 
pulse  is  common  with  heart  weakness 
and  auricular  paralysis. 

On  the  other  hand,  when  the  right 
heart  begins  to  fail  and  pressure  in  the 
right  auricle  increases,  the  blood  follows 
the  same  course  as  it  does  in  the  foetus 
and  passes  from  the  right  into  the  left  foramina 
auricle.  Under  ordinary  circumstances 
this  would  exert  no  influence  whatever, 
and  would  not  even  produce  cyanosis. 
But  when  the  heart  is  already  weak,  the 
circulation  slow,  and  the  blood  heavily 
charged  with  C02,  this  sudden  admixture 
of  venous  blood  carries  the  C02  content 
past  the  physiological  limit,  and  gives 
rise  to  cyanosis  and  symptoms.  More- 
over, the  blood  entering  the  coronary 
arteries  is  also  less  aerated,  the  cardiac 
tonicity  and  cardiac  strength  are  im- 
paired, and  the  vicious  circle  of  the  open 
foramen  ovale  sets  in,  subsiding  again  with  inordinate  rapidity  as  soon 
as  the  pressure  in  the  systemic  veins  falls  below  that  in  the  pulmonary. 


Fig.  260. — Openings  between  strands  ot 
muscle  in  the  interauricular  septum.  (From 
a  specimen  in  the  Army  Medical  Museum, 
Washington,  D.  C.)  The  valvula  foraminis 
ovalis  (VALV.  F.O.)  is  closed  and  has  fused 
with  the  rest  of  the  septum.  FORAMINA, 
abnormal  openings  between  strands  of  mus- 
cle in  the  lower  part  of  the  septum. 


SYMPTOMS. 

In  most  cases  patency  of  the  foramen  ovale  alone  does  not  give  rise 
to  any  symptoms.  For  example,  the  patient  whose  heart  is  shown  in  Fig. 
258  was  able  to  perform  his  duties  as  a  soldier  in  heavy  campaigns  and 
died  from  dysentery  without  any  symptoms  referable  to  his  heart.  Pea- 
cock mentions  the  case,  reported  by  Spry  in  1805,  of  a  girl  of  seven  years 
who  had  no  cyanosis  during  life  and  whose  foramen  was  patent  and  two 
inches  in  circumference  (f  inch  in  diameter).  On  the  other  hand,  he  cites 
another,  case,  a  woman  of  twenty-one  whose  foramen  ovale  was  one  inch 
in  diameter,  who  from  the  age  of  three  months  "presented  characteristic 
symptoms  of  malformation  of  the  heart, — cyanosis,  palpitation,  dyspnoea, 
faintings,  occasional  convulsive  attacks,  and  lividity." 


552  DISEASES   OF  THE   HEART    AND    AORTA. 


PHYSICAL    SIGNS. 

Apart  from  the  paroxysmal  cyanosis  the  physical  signs  of  open  fora- 
men ovale  are  extremely  variable.  Cyanosis  and  abnormalities  in  the  retina 
may  be  present.  On  the  other  hand,  all  physical  signs  may  be  absent.  In 
some  cases  systolic,  in  others  diastolic,  murmurs  are  present  in  the  third 
left  interspace  at  the  sternal  margin.  Occasionally  there  is  heard  a  well- 
defined  presystolic  murmur  which  is  maximal  at  this  point,  and  which 
when  present  is  the  most  characteristic  sign  of  the  open  foramen  ovale. 

DIAGNOSIS. 

The  diagnosis  rests  upon  the  presence  of  paroxysmal  cyanosis 
and  of  murmurs  in  the  third  left  interspace  without  signs 
of  aortic  insufficiency  or  of  hypertrophy  of  the  right  ventricle  (well-marked 
systolic  retraction  over  the  right  ventricle  with  or  without  systolic  impulse 
in  the  second  left  interspace)  or  of  other  congenital  heart  lesions.  This  is 
especially  corroborated  if  the  child  was  a  blue  baby  at  birth  or  within  a 
few  months  afterwards,  even  if  only  during  intervals  of  a  few  hours  or  days. 
The  retinal  changes  are  valuable  signs  when  present. 

In  rare  cases  incidental  phenomena  may  help  in  the  diagnosis.  Cohnheim  cites  a 
case  in  which  the  diagnosis  was  made  from  the  occurrence  of  embolism  of  the  brain  when 
the  primary  thrombus  was  in  the  veins  of  the  leg  (crossed  embolism);  but  such  cases  are 
necessarily  extremely  rare,  and  before  such  inferences  are  made  all  commoner  factors  must 
be  carefully  excluded. 

TREATMENT. 

Treatment  between  attacks  of  cyanosis  and  dyspnoea  is  confined  to 
general  hygiene  and  regulation  of  the  patient's  life,  as  described  above  for 
pulmonary  stenosis,  though,  as  a  rule,  more  latitude  may  be  allowed. 

During  the  attacks  hot  baths  and  vasodilators  (such  as 
amyl  nitrite  and  nitroglycerin)  may  be  resorted  to,  and,  when  there  is  no 
diminished  coagulability  and  the  attack  is  severe,  venesection  may  be 
performed. 

PATENT   DUCTUS   ARTERIOSUS    (BOTALLI). 
PATHOGENESIS. 

In  many  cases  in  which  the  arterial  circulation  is  markedly  disturbed 
in  the  foetus,  the  ductus  arteriosus  (Botalli)  may  be  found  to  remain  patent 
after  birth.  This  is  a  common  concomitant  of  pulmonary  stenosis  and 
especially  pulmonary  atresia,  of  the  corresponding  conditions  at  the  aortic 
orifice,  and  of  congenital  lesions  at  either  of  the  auriculoventricular  valves. 

When  viewed  in  the  light  of  its  closure,  the  mechanism  of  this  secondary 
non-closure  of  the  ductus  is  tolerably  clear.  The  ductus  arteriosus  Botalli 
represents  the  remains  of  the  sixth  branchial  arch  (Fig.  240).  It  "is  in 
a  direct  line  with  the  pulmonary  trunk,  i«  the  direct  continuation  of  the 
same,  and  is  of  almost  equal  size,  while  it  is  of  greater  diameter  than  the 
descending  arch  of  the  aorta.  A  distinct  narrowing  of  the  aortic  arch  is 
to  be  observed  just  above  the  entrance  of  the  ductus  into  it."    (Klotz.) 


CONGENITAL   HEART   DISEASE.  553 

Closure  of  the  Ductus  Arteriosus. — Several  theories  have  been  advanced 
to  explain  the  closure  of  the  ductus  arteriosus  at  birth : 

Haller  thought  that  it  results  from  coagulation  of  the  blood  within  its  lumen.  Kiliani 
(1826)  was  the  first  to  show  that  with  the  expansion  of  the  lungs  at  birth  the  resistance 
in  the  pulmonary  circulation  was  diminished  and  a  large  amount  of  blood  thus  diverted 
from  the  channel  through  the  ductus.  A  number  of  theories  have  been  proposed  to  explain 
the  exact  manner  in  which  this  diversion  of  blood  through  the  pulmonary  channels  brings 
about  the  closure  of  the  ductus  arteriosus. 

Strassman  (1894)  attempted  to  explain  the  closure  on  purely  mechanical  grounds. 
He  called  attention  to  the  fact  that  the  ductus  arteriosus  penetrates  the  wall  of  the  aorta 
at  an  acute  angle,  so  that  the  tissue  included  in  this  angle  forms  a  sort  of  valve.  He 
believed  that  when  the  pressure  within  the  aorta  became  greater  than  that  in  the  pulmonary 
artery  (after  birth),  this  flap  of  vessel  wall  closed  down  over  the  mouth  of  the  ductus  and 
prevented  blood  from  entering  it.  Strassman  found,  moreover,  that  if  he  injected  fluid 
into  the  aorta  of  a  new-born  child  at  a  pressure  under  100  mm.  no  blood  entered  the  pul- 
monary artery.  These  experiments  have  been  very  carefully  repeated  in  a  large  number 
of  infants  by  Klotz,  who  found  that  "at  all  times  when  the  ductus  arteriosus  was  unob- 
literated  by  new-formed  or  forming  fibrous  tissue  the  colored  fluid  found  its  way  into  it 
for  some  distance  sufficient  to  stain  it."  However,  the  fact  that  the  communication  was 
not  a  free  one  demonstrates  that  this  valvular  action  is  probably  a  contributing  cause  in 
cutting  off  the  blood  flow  or  in  lessening  the  pressure  in  the  ductus. 

On  the  other  hand,  Schulze  in  1871  showed  that  the  walls  of  the  ductus  arteriosus, 
though  poor  in  or  lacking  elastic  fibres,  were  particularly  rich  in  muscle  fibres.  He  believed 
that  when  the  blood-pressure  in  the  pulmonary  artery  fell,  and  the  blood  was  diverted 
away  from  the  ductus  arteriosus,  the  muscle  fibres  in  the  wall  contracted  down  further 
until  the  lumen  was  finally  obliterated.  This  occurs  without  any  such  intravascular  co- 
agulation as  Haller  had  supposed;  but  Langer  (1857)  has  found  that  it  is  accompanied 
by  a  very  active  proliferation  of  the  cells  in  the  intima,  with  sloughing  off  of  the  endothelial 
lining  (Klotz).  The  proliferation  goes  on  till  the  wall  of  the  vessel  becomes  thicker  than 
that  of  either  the  pulmonary  artery  or  the  aorta,  and  it  is  finally  occluded  by  fibrosis. 

Factors  Causing  Persistence  of  Ductus. — Under  pathological  conditions 
it  is  clear  that  anything  which  causes  obstruction  to  the  flow  of  blood 
through  the  arch  of  the  aorta  during  fetal  life  (aortic  stenosis  or  atresia, 
congenital  mitral  stenosis,  coarctation  of  the  arch  of  the  aorta,  etc.)  will 
cause  the  right  ventricle  to  carry  on  the  greater  part  of  the  circulation  and 
to  force  more  blood  than  usual  through  the  ductus  arteriosus.  This  condi- 
tion, of  course,  persists  after  birth;  the  ductus,  which  now  represents  a 
main  blood  channel,  remains  open.  The  flow  continues  in  the  usual  direc- 
tion backward  from  the  pulmonary  artery  into  the  aorta. 

On  the  other  hand,  when  there  is  atresia  of  the  pulmonary  artery  the 
pressure  in  the  ductus  is  low  and  blood  enters  it  from  the  aorta,  passing 
forward  (ventrally)  into  the  rami  pulmonales.  These  facts  explain  the 
persistence  of  the  ductus  arteriosus  in  its  usual  occurrence  as  a  secondary 
congenital  lesion. 

The  occurrence  as  a  primary  lesion  is  rare,  only  26  cases  having  been 
collected  by  Vierordt  in  1898,  12  more  by  Abbott.  Klotz  believes  that 
these  may  be  "the  result  of  imperfect  expansion  of  the  lungs.  In  these 
cases  the  blood-pressure  has  never  been  lowered  in  the  pulmonary  system 
to'  the  point  which  allowed  the  walls  of  the  ductus  to  overcome  it."  It 
may  also  result  from  congenital  weakness  of  the  left"  ventricle  causing  a 
low  blood-pressure  in  the  aorta  at  the  time  of  birth. 

The  size  and  structure  of  the  patent  ductus  may  vary  greatly,  from  a 
short  and  narrow  passage  to  an  almost  aneurismal  dilatation.     Acute  or 


554  DISEASES   OF   THE   HEART   AND    AORTA. 

malignant  vegetations  are  not  uncommon  within  the  lumen,  and  the  pres- 
ence of  an  open  ductus  tends  to  predispose  to  endocarditis.  Arterioscle- 
rosis of  both  the  ductus  and  the  pulmonary  artery  also  occurs,  perhaps  as 
a  result  of  the  high  pulmonary  pressure. 

SYMPTOMS. 

The  symptoms  of  uncomplicated  patent  ductus  arteriosus  are  usually 
obscure  and  slight,  and  the  condition  is  often  found  incidentally.  Cyano- 
sis is  slight  and  transitory.  Slight  weakness  and  shortness  of  breath  on 
exertion  may  occur,  but  many  of  the  cases  are  devoid  of  symptoms. 

PHYSICAL    SIGNS. 

Several  diagnostic  features  of  open  ductus  arteriosus  have  been  pub- 
lished at  various  times.  Gerhardt  in  1867  described  a  small  quadrilateral 
extension  of  the  area  of  dulness  in  the  second  (and  first) 
left  interspace.  In  this  region  the  pulsation  of  the  pulmonary  artery  may 
be  seen,  and  the  well-marked  systolic  retraction  is  often  seen  over  the  inter- 
spaces corresponding  to  the  hypertrophied  right  ventricle.  Zinn,  de  la 
Camp,  and  others  have  found,  on  examination  with  the  fluoroscope,  that 
Gerhardt's  area  of  dulness  corresponds  to  a  round  shadow  of  a 
small  mass  along  the  left  upper  margin  of  the  cardiac  shadow,  where 
the  pulmonary  artery  and  left  auricle  are  usually  seen  (Fig.  261) .  This 
mass  shows  systolic  pulsation  and  corresponds  to  the  dilated  ductus  arterio- 
sus. This  dilatation  is  frequently  aneurismal.  The  picture  with  the  X-ray 
is  thus  of  great  diagnostic  value,  but  one  must  carefully  exclude  an  aneu- 
rism of  the  aorta  behind  the  sinus  of  Valsalva.  In  contrast  to  the  shadow 
of  the  left  auricle,  this  shadow  is  magnified  when  the  tube  is  placed  in  front 
of  the  body  as  compared  with  the  illumination  from  behind. 

On  auscultation  the  characteristic  sign  is  a  rough  or  blowing  murmur 
in  the  second  left  interspace,  which  follows  the  first  sound  and  may  continue 
into  diastole  (G.  A.  Gibson,  Med.  Press  and  Circ,  1906,  lxxxi,  572).  It  is 
caused  by  the  rush  of  blood  through  the  narrow  mouth  of  the  ductus.  The 
second  pulmonic  sound  is  present  and  accentuated.  The  murmur  is  sometimes 
absent  in  diastole.  Francois-Franck  has  shown  that  this  murmur  is 
heard  loudly  at  the  left  back  over  the  area  at  which  the  aorta 
comes  in  contact  with  the  chest  wall  (level  of  the  third  and  fourth  spines), 
to  which  it  is  transmitted  in  a  direct  line  (Fig.  256).  He  showed  that 
the  loudness  of  this  murmur  bears  a  definite  relation  to  the  phases  of  respi- 
ration. It  is  loudest  during  expiration,  for  at  that  time  the  resistance  in 
the  pulmonary  circuit  is  greatest,  and  hence  the  blood  flows  through  the 
ductus  more  rapidly;  but  becomes  feebler  in  inspiration  when  more 
blood  passes  through  the  lungs  and  less  through  the  ductus.  Francois- 
Franck  also  found  that  this  variation  in  the  blood  flow  into  the  aorta 
found  equally  marked  expression  in  the  pulse,  causing  a  rise  of  pressure 
and  full  pulse  in  expiration,  fall  and  small  pulse  during  inspiration 
(pulsus  paradoxus). 

These  signs,  however,  occur  only  in  cases  in  which  there  is  an  efficient 
circulation  through  the  pulmonary  orifice.     In  the  cases  associated  with 


CONGENITAL   HEART    DISEASE. 


555 


pulmonary  atresia  where  the  flow  through  the  ductus  is  in  the  opposite 
direction,  the  murmur  may  be  absent  at  the  back  and  will  be  loudest  during 
inspiration,  for  then  the  inflow  into  the  lungs  is  greatest.  Never- 
theless, the  pulse  will  remain  a  pulsus  paradoxus,  for  the  flow 
through  the  aorta  during  inspiration  will  be  diminished  just  the  same. 
This  respiratory  variation  of  murmur  and  pulse  is,  however, 
often  absent  in  spite  of  the  open  ductus,  as  is  the  systolic  murmur  itself 
in  some  cases.  Neither  bears  an  absolute  relation  to  the  degree  of  patency 
of  the  ductus. 


AA 


DB 


Fig.  261. — Radiograph  of  a  thirteen-year-old  boy  with  patent  ductus  arteriosus  (Botalli)  and  aneu- 
rismal  dilatation  of  the  ductus  and  pulmonary  artery.  (After  Hochsinger,  in  Pfaundler  and  Schlossmann's 
''Diseases  of  Children.")  A  A,  arch  of  the  aorta;  DB,  ductus  Botalli  and  pulmonary  artery  dilated  like 
an  aneurism,  giving  a  cap-shaped  top  to  the  shadow  of  the  heart;  MI,  internal  mammary  artery,  consider- 
ably dilated,  denoting  an  internal  collateral  circulation. 


A  diastolic  murmur  is  often  heard  along  with  the  systolic,  sometimes 
replacing  the  second  sound  but  more  often  accompanying  or  following  an 
accentuated  pulmonic  sound.  The  inequality  in  pressure  between  aorta 
and  pulmonary  artery-  persists  during  diastole,  and  the  abnormal  blood 
flow  therefore  continues  and  produces  the  murmur  in  diastole.  When  the 
difference  of  pressure  is  slight,  especially  with  low  peripheral  resistance, 
the  diastolic  murmur  may  be  absent. 


556  DISEASES   OF  THE   HEART   AND   AORTA. 

DIAGNOSIS. 

From  the  above  discussion  the  points  upon  which  the  diagnosis  of  the 
open  ductus  arteriosus  may  rest  are  sufficiently  clear, — pulsation  over  the 
right  ventricle,  Gerhardt's  dulness,  a  systolic  or  double  murmur  loudest  at 
second  left  interspace  and  heard  at  the  left  upper  back,  expiratory  accent- 
uation and  pulsus  paradoxus,  and  the  pulsating  mass  in  Gerhardt's  area 
seen  on  X-ray  examination.  In  addition,  the  history  may  show  that  the 
patient  was  blue  at  birth  (before  the  pulmonary  channels  have  opened  up) 
but  that  cyanosis  soon  passed  off. 

J.  Plesch  in  Kraus's  clinic  (Berl.  klin.  Wchnschr.,  1909,  xlvi,  391)  has  attempted 
to  make  the  diagnosis  by  analyses  of  the  expired  air.  By  a  very  simple  device  he  deter- 
mines the  percentage  to  which  the  blood  flowing  through  the  pulmonary  artery  is  satu- 
rated with  oxygen.  Under  normal  conditions  the  saturation  is  38-70  per  cent,  of  its  oxygen 
capacity.  In  patent  ductus  arteriosus  the  blood  in  the  pulmonary  artery  is  mixed  blood 
and  hence  its  oxygen  content  is  higher  (80-90  per  cent.).  The  aerated  blood 
could  enter  only  through  a  patent  ductus  arteriosus. 

TREATMENT. 

Treatment  for  the  persistence  of  the  ductus  consists  mainly  in  those 
methods  which  improve  pulmonary  circulation, — breathing  exercises, 
careful  hygiene,  avoidance  of  exposure  to  pulmonary  infections,  and  avoid- 
ance of  fatigue,  general  muscular  and  cardiac  overstrain.  Since  the  per- 
sistence of  the  ductus  is  in  itself  a  compensatory  process,  it  calls  for  no 
special  remedy.  To  ligate  it,  as  might  readily  be  done  after  opening  up 
the  thorax  under  positive  pressure,  would  be  harmful  rather  than  bene- 
ficial. Otherwise  general  hygienic  measures  and  cardiac  stimulants,  are 
of  value,  as  in  other  diseases.  But  in  many  cases  open  ductus  Botalli  has 
no  effect  upon  the  duration  of  life  and  requires  no  treatment. 

STENOSIS   OF   THE   AORTA. 

Stenosis  of  the  lumen  of  the  aorta  may  occur  in  three  places: 
I.  At  the  aortic  valve. 
II.  Stenosis  of  the  arch  of  the  aorta. 

1.  Above  the  entrance  of  the  ductus  arteriosus  Botalli. 

2.  Just  below  the  entrance  of  the  ductus  arteriosus  Botalli. 

I.  Stenosis  at  the  aortic  orifice  is  one  of  the  rarer  con- 
genital lesions  (2  per  cent,  of  Abbott's  series),  though  probably  many  of 
the  milder  cases  escape  detection.  It  is  usually  due  to  endocarditis  late  in 
fetal  life. 

Those  which  develop  earlier  in  fetal  existence,  in  which  true  aortic 
atresia  occurs,  are  quite  analogous  to  the  cases  of  pulmonary  atresia, 
except  that  the  posterior  instead  of  the  anterior  channel  of  the  common 
truncus  arteriosus  fails  to  develop.  The  changes  in  the  fetal  circulation 
are  similar  to  those  in  pulmonary  atresia,  but  affect  the  opposite  sides  of 
the  heart.  The  septa  remain  open,  and  occasionally  one  ventricle  (the  left) 
fails  to  develop.  Practically  the  entire  systemic  circulation  is  carried  on 
by  the  pulmonary  artery  through  the  ductus  arteriosus. 

The  consequences  of  the  lesion  are  very  severe  and  few  cases  survive 
birth,  in  striking  contrast  to  pulmonary  stenosis  and  atresia.     No  doubt 


CONGENITAL   HEART   DISEASE.  557 

this  is  due  to  the  fact  that,  since  the  right  ventricle  is  the  stronger  in  fetal 
life,  it  succeeds  in  establishing  a  better  compensatory  circulation  after 
atresia  of  its  orifice  than  does  the  left.  Moreover,  when  the  first  breath  is 
taken  after  stenosis  of  the  aorta,  it  is  venous  instead  of  arterial  blood 
which  is  thrown  into  the  organs. 

II.  Stenosis  in  the  vicinity  of  the  ductus  Botalli 
is  one  of  the  most  common  congenital  heart  lesions,  occurring  in  198  of 
Abbott's  412  cases.  Like  most  abnormalities  it  arises  as  an  exaggeration 
of  a  condition  which  is  normally  present  in  the  fcetus.  As  stated  above, 
Klotz  finds  that  there  is  a  distinct  narrowing  of  the  aortic  arch  just  above 
the  entrance  of  the  ductus  into  it.  This  is  no  doubt  due  to  the  fall  of  pres- 
sure in  the  aorta  which  occurs  below  the  left  carotid  artery  and  the  rise 
further  on  when  the  blood  enters  from  the  ductus. 

Hamernik  in  1844  divided  the  cases  into:  (1)  stenosis  above  the 
ductus,  (2)  those  at  the  entrance  of  the  ductus,  and  (3)  those  below  the 
ductus.  Bonnet,  who  made  an  exhaustive  study  of  the  subject  in  1903, 
discards  Hamernik's  second  group,  and  distinguishes  two  types: 

1.  The  type  in  the  new-born,  in  which  the  stenosis  occurs  above  the 

ductus  and  the  latter  remains  open. 

2.  The  type  found  in  adults,  in  which  the  stenosis  occurs  below  the 

ductus.    The  latter  is  closed  and  collateral  circulation  develops. 

Bonnet's  studies  were  based  upon  160  cases,  of  which  55  (34.3  per  cent.) 
were  of  the  new-born  type  and  105  (65.7  per  cent.)  were  of  the  adult  type. 

Type  of  the  New=born. — The  cases  of  the  new-born  type  represent  an 
exaggeration  of  the  slight  narrowing  in  the  aorta  which,  as  Klotz  states, 
is  present  above  the  left  subclavian  artery  and  the  ductus  Botalli.  Em- 
bryologically,  as  Longa  points  out,  this  represents  the  branch 
joining  the  fourth  and  sixth 
branchial  arteries  (Fig.  240) 
and  might  correspond  to  a  failure  of 
development  of  this  branch.  On  the 
other  hand,  the  amount  of  blood  in  the 
aorta  is  very  much  depleted  by  the 
flow  into  the  innominate,  left  carotid, 
and  subclavian,  so  that  its  lumen  is 
naturally  smaller  until  replenished  by 
the  inflow  from  the  ductus.  There  is 
consequently  a  region  of  functional 
stenosis  between  these  two  points 
which  may  be  exaggerated  by  con- 
traction of  the  muscle-fibres  in  the  FlG.  262.— stenosis  of  the  isthmus  of  the 
wall  of  the  aorta.      The  weaker  the     aorta  above  the  ductus  arteriosus  (Botalli),— 

...  type  of  the  new-born.      (From  a  specimen  in  the 

action   Of    the    left   Ventricle    the    more        Army  Medical  Museum,  Washington,  D.  C.) 

marked  will  be  this  functional  steno- 
sis. The  ductus  Botalli  therefore  takes  on  more  and  more  of  the  circu- 
lation in  the  lower  parts  of  the  body,  and  fetal  life  may  be  undisturbed  as 
long  as  the  right  ventricle  is  pumping  aerated  blood;  but  when  this  con- 
dition ceases  and  the  pulmonary  channels  widen  and  pressure  in  the  ductus 
falls,  the  aortic  circulation  may  become  insufficient  and  the  syndrome  of 


558 


DISEASES   OF   THE   HEART   AND    AORTA. 


congenital  heart  disease  may  result.  It  is  rare  for  these  children  to  live 
more  than  a  few  weeks,  or  at  most  a  few  months,  and  many  die  at  birth. 
Physical  s  i  g  n  s  are  indefinite,  confined  to  double  murmurs  over 
the  chest  and  back  and  in  most  cases  cyanosis.  There  are  very  often  asso- 
ciated malformations,  such  as  pulmonary  stenosis,  open  septum  ventric- 
ulorum,  etc.  • 

In  this  form  there  is  very  little  attempt  at  establishment  of  a  c  o  1 1  a  t- 
eral  circulation,  since  the  greater  part  of  the  systemic  circulation 
is  maintained  by  the  right  ventricle  through  the  open  ductus  arteriosus, 
just  as  it  is  before  birth.  Owing  to  the  completeness  of  this  compensation, 
there  may  be  little  difference  between  the  pulses  in  the  upper  and  in  the 
lower  extremities,  and  the  clinical  diagnosis  is  scarcely  ever  made. 

Adult  Type.  —  In  the  second  or  adult  type,  which  is  more 
common,  the  stenosis  occurs  just  below  the  entrance  of  the  ductus  Botalli, 
and  this  vessel  is  found  to  be  closed.     Indeed,  the  very  stasis  at  this  point 

assists  in  its  closure.  The  mode  of 
origin  of  the  stenosis  at  this  point  is 
not  clear.  Bonnet  calls  attention  to 
the  fact  that  the  lumen  of  the  aorta 
at  the  stenosis  (usually  2-4  mm.)  is 
about  that  of  the  normal  aorta  at  the 
time  of  birth,  and  thinks  that  the 
whole  anomaly  may  be  of  post- 
natal development.  It  is  possible, 
as  he  suggests,  that,  when  the  ductus 
Botalli  is  particularly  long,  the  fibro- 
sis of  the  latter  brings  about  a  kink- 
ing of  the  aorta  at  this  point,  and 
with  a  dilatation  above  and  stenosis 
at  the  point  of  kinking. 

Skoda,  on  the  other  hand,  has 
suggested  that  the  stenosis  may 
result  from  a  band  of  fibrosis  passing 
around  the  aorta  at  this  point;  but,  though  this  theory  is  alluring,  there 
is  no  definite  histological  evidence  in  its  support. 

The  stenosis  cuts  off  the  circulation  from  all  parts  of  the  body  below 
the  stenosis,  but  the  high  pressure  due  to  the  stagnation  above  it  causes  a 
progressive  dilatation  of  other  arterial  channels,  such  as  the  mammaries, 
thoracic  and  scapular  arteries,  which  are  always  found  to  be  much  dilated. 
Indeed,  the  collateral  circulation  may  be  so  good  that  the  lumen  of  the  aorta 
below  the  stenosis  may  be  as  great  as  above  it  (hour-glass  constriction), 
though  usually  it  is  somewhat  narrow  and  it  may  even  be  funnel-shaped. 
Clinically  the  presence  of  this  type  of  stenosis  does  not  necessarily 
shorten  life,  though  this  depends  largely  upon  the  completeness  of  the 
collateral  circulation.  The  symptoms  are  chiefly  those  of  cerebral  conges- 
tion,— headache,  vertigo,  buzzing  in  the  ears.  Occasionally  there  are  pains 
in  the  chest.  Bonnet  calls  attention  to  the  fact  that  in  his  105  cases  there 
was  never  intermittent  claudication,  showing  that  the  circulation  in  the 
lower  limbs  is  always  sufficient. 


Fig.  263. — Stenosis  below  the  ductus  arteri 
osus  (Botalli), — adult  type.  (After  Bonnet,  Rev 
de  Med.,  Par.,  1903,  xxiii.) 


CONGENITAL   HEART    DISEASE.  559 

PHYSICAL    SIGNS    AND    DIAGNOSIS. 

Cyanosis  is  not  common  and  not  a  sign  of  the  disease.  The  most 
definite  indication  is  the  difference  in  the  size  and  quality  of  the  pulse  in 
the  upper  and  lower  extremities,  the  carotid  and  radial  pulses  being  large 
and  throbbing,  the  femoral,  popliteal,  and  dorsalis  pedis  as  well  as  the 
abdominal  aorta  small  or  impalpable.  Though  the  diagnosis  intra  vitam 
is  rare,  Lepine  was  able  to  make  it  from  these  data  in  two  cases.  Dr.  W.  S. 
Morrow  calls  attention  to  the  possibility  of  diagnosis  from  marked  differ- 
ence in  the  brachial  and  tibial  bloocl-pressures,  but  just  as  in  aneurisms 
the  difference  in  size  and  quality  of  the  pulse  on  palpation  would  usually 
be  more  marked  than  that  of  the  blood-pressures.  Moreover,  Halsted 
has  found  little  difference  between  brachial  and  femoral  pressures  in  man 
after  the  abdominal  aorta  has  been  occluded  with  metal  bands  for  the  treat- 
ment of  aneurism.  The  presence  of  large  tortuous  mammary,  thoracic, 
and  scapular  arteries  aids  in  the  diagnosis.  There  are  usually  low  murmurs 
over  the  arteries,  especially  at  the  angle  of  the  left  scapula,  as  was  present 
in  a  case  diagnosed  by  Mercier  in  1839. 

Valvular  disease  of  the  heart  frequently  results  from  the  increased 
work  thrown  upon  the  heart  and  dilatation  of  aortic  and  mitral  orifices, 
and  their  signs  complicate  the  picture.  Before  making  the  diagnosis,  it  is 
always  necessary  to  exclude  aneurism  and  mediastinal  tumor  by  the  absence 
of  clulness  on  percussion  and  of  abnormal  shadows  on  X-ray  examination. 

TEEATMENT. 

Treatment  depends  purely  upon  symptoms,  occasional  venesection 
being  of  value  to  relieve  the  headaches.  It  is  most  important  for  the 
patient  who  suffers  from  these  symptoms  to  avoid  over-exertion  or  excite- 
ment, which  cause  too  vigorous  action  of  the  heart. 

DIFFUSE    NARROWING    OF    THE    AORTA. 

Virchow  has  also  called  attention  to  another  form  of  abnormality  in 
the  lumen  of  the  aorta,  a  diffuse  narrowing  of  its  entire  lumen  throughout 
its  whole  extent  (hypoplasia  of  the  aorta).  This  condition  is  associated 
with  under-development  of  the  elastic  and  muscular  elements  in  the  arterial 
walls.  As  Virchow  and  other  observers  have  found,  it  is  often  associated 
with  chlorosis  of  intense  grades  and  occasionally  accompanies  other  con- 
genital malformations  of  the  heart. 

About  the  objective  finding  there  is  little  dispute.  The  only  point  in 
question  is  whether  the  condition  is  to  be  regarded  as  a  true  congenital 
malformation  or  as  a  postnatal  development,  which,  like  the  changes  in 
rickets,  is  determined  by  conditions  of  growth  and  nutrition  during  child- 
hood and  may  be  corrected  by  cure  of  these  conditions.  It  is  possible  that 
it  may  be  secondary  to  the  conditions  which  bring  on  anaemia,  and  due  to 
the  fact  that  the  aortic  walls  have  never  been  subjected  to  the  stimulating 
influence  of  an  adequately  high  blood-pressure.  That  this  may  be  a  factor 
in  the  development  of  and  strengthening  of  blood-vessel  walls  has  been 
shown  especially  by  the  results  of  arteriovenous  anastomosis  and  trans- 


560 


DISEASES   OF   THE   HEART    AND    AORTA. 


plantation,  in  which  the  walls  of  the  transplanted  vein  become  thicker  and 
richer  in  elastic  and  muscular  elements  (Carrel).  It  is  of  course  extremely 
difficult  to  determine  what  would  have  occurred  if  such  cases  had  recovered 
from  their  anaemia  or  primary  debility  and  blood-pressure  had  reached  a 
normal  level.  It  is  equally  difficult  to  determine  that  any  such  cases  have 
recovered  under  these  conditions,  though  the  fact  that  the  lumen  of  the 
radial  artery  increases  (pulse  becomes  larger)  with  the  recovery  from 
chlorosis  is  of  course  definite. 

For  the  present,  therefore,  one  must  hesitate  somewhat  in  classing 
hypoplasia  of  the  aorta  among  the  definite  congenital  malformations. 


Fig.  264. — Transposition  of  the  viscera  in  embryo  and  adult.  (Schematic.)  A,B,  C,  position  of  organs 
in  the  embryo;  a,  b,  c,  position  of  organs  in  the  adult.  A,  a,  normal;  B,  b,  transposition  of  the  heart  and 
arteries  simple  dextrocardia;   C,  c,  complete  situs  transversus. 


COMPLETE   AND   PARTIAL   SITUS   TRANSVERSUS. 

It  is  not  extremely  rare  to  meet  with  a  case  of  complete  transposition 
of  the  viscera,  so  that  the  heart  and  stomach  are  found  to  lie  on  the  right 
side  (dextrocardia,  dexiocardia)  and  the  liver  upon  the  left. 
This  condition  is  probably  brought  about  by  a  change  in  position  of  the 
cardiac  tube  in  early  embryonic  development,  so  that  it  lies  in  the  position 
of  d  instead  of  the  normal  S  (Fig.  264).  Maude  Abbott  suggests  that 
in  these  cases  there  is  a  change,  the  embryo  lies  in  an  abnormal  position 
within  the  chorion  so  that  its  right  side  instead  of  its  left  is  closer  to  the 
blood  supply.    At  all  events  the  relation  of  the  organs  is  the  mirror  image 


CONGENITAL  HEART  DISEASE. 


561 


PLATE   XIX. 


T 


m#*nm<  m         -"    '    *M0£l( 


/««W<M^ 


Electrocardiogram  from  a  patient  with  complete  inversion  of  the  heart  dextrocardia  with  the  other 
organs  in  their  normal  positions,  showing  a  curve  of  normal  form. 


Electrocardiogram  from  a  case  of  complete  transposition  of  all  the  organs  (situs  inversus),  showing 

all  the  waves  inverted. 


at* 


562 


DISEASES  OF  THE  HEART  AND  AORTA. 


of  the  normal  condition.  In  complete  transposition,  however,  the  organs 
develop  normally,  and  the  condition,  though  unusual,  has  no  effect  upon 
the  function.  Persons  whose  hearts  lie  on  the  right  side  are  quite  as  free 
from  symptoms  as  those  whose  hearts  are  on  the  left,  provided  the  other 
viscera  are  normal;  and  the  condition  is  usually  discovered  accidentally 
during  routine  physical  examination.     In  such  cases  the  apex  impulse  and 


PULMONARY  ARTERY 


TRICUSPID  VALVE 


AORTA 

MITRAL  VALVE 
INTERVENTRICULAR  SEPTUM 

FORAMEN  OVALE 


Fig.  265. — Transposition  of  the  valves.  (From  a  specimen  in  the  Army  Medical  Museum,  Wash- 
ington, D.  C.)  The  course  of  the  interventricular  septum  is  indicated  upon  the  heart  wall.  The  course 
of  the  blood  stream  is  shown  by  the  arrows. 

heart  sounds  are  heard  in  the  fifth  right  interspace,  and  the  second  aortic 
is  heard  on  the  left  side  instead  of  on  the  right.  The  diagnosis  may  always 
be  made  with  the  X-ray.  The  electrocardiograph  shows  sometimes  inverted 
waves,  sometimes  a  curve  that  is  practically  normal. 

Dextrocardia  (dexiocardia)  without  transposition  of  other  viscera  is 
much  rarer.  Most  frequently  it  is  due  to  a  pushing  or  pulling  of  the  heart 
to  the  right  by  intrathoracic  growths  or  adhesions,  but  occasionally  (in  2 


PULMONARY  ARTERY 


AORTA 


Fig.  266. — Pulmonary   artery   with    four   cusps.      (From    a    specimen   in    the   Army   Medical    Museum, 

Washington,  D.  C.) 

of  Abbott's  412  cases)  it  is  due  to  alteration  in  development.  Under  these 
circumstances  the  pulmonary  artery  is  given  off  from  the  left  ventricle, 
the  aorta  from  the  right.  Great  variations  may  be  seen  in  the  arrangement 
of  vense  cavse,  which  sometimes  enter  the  left,  sometimes  the  right  auricle. 
The  results,  as  in  other  cases  in  which  the  blood  is  mixed,  vary  greatly. 
The  syndrome  of  congenital  heart  disease  may  be  present,  owing  to  the 
mixing  of  blood,  but  the  exact  transposition  of  vessels  can  rarely  be 
diagnosed  intra  vitam. 


CONGENITAL  HEART  DISEASE.  563 

ABNORMALITY   OF   THE  VALVES. 

The  number  and  formation  of  the  cardiac  valves  may  also  undergo 
alteration  in  fetal  life.  In  the  aortic  and  pulmonic  this  is  usually  due  to 
inflammatory  fusion  of  two  cusps  forming  a  bicuspid  valve  (Fig.  265), 
or  to  the  fact  that  one  of  the  leaflets  is  divided  into  two  parts  by  a  slit  and 
finally  under  the  influence  of  the  blood-pressure  grows  to  form  symmetrical 
cusps  (Fig.  266). 

In  the  mitral  and  tricuspid  valves,  especially  in  association  with  open 
septum  ventriculorum,  there  may  be  a  split  in  the  middle  of  one  leaflet, 
practically  converting  it  into  two  separate  cusps.  Except  for  the  forma- 
tion of  valvular  insufficiencies  which  result,  multiplicity  or  paucity  of  the 
cusps  has  no  pathological  effects. 

A  large  number  of  other  malformations,  such  as  partial  separation  of 
the  two  ventricles  to  form  a  "bifid  apex,"  defective  formation  of  the  chest 
wall  with  exposure  of  the  heart  (ectopia  cordis),  malposition  of  the  heart 
causing  it  to  lie  in  the  abdomen  or  the  neck,  transposition  and  malformation 
of  the  great  arteries  and  veins,  are  encountered.  Space  does  not  permit 
of  a  complete  discussion  of  these  conditions,  for  which  the  reader  is  referred 
to  the  magnificent  article  by  Dr.  Maude  Abbott  in  Volume  IV  of  Osier's 
Modern  Medicine. 

BIBLIOGRAPHY. 

Development  of  the  Normal  Heart. 

The  development  of  the  normal  heart  is  well  discussed  in  Piersol's,  Morris's,  and 
Quain's  anatomies  and  in  the  various  text-books  of  embryology. 

The  following  articles  may  be  consulted  also: 
Eternod:    Premiers  stades  de  la  circulacion  sanguine  dans  l'ouef  et  l'embryon  humains, 

Anat.  Anzeig,  1899,  xv,  181. 
His,  W.:    Anatomie  menschlicher  Embryonen,  Leipzig,  1880.     For  an  excellent  series  of 

figures  see  also  Kollman,  J. :    Handatlas  der  Entwicklungsgeschichte  des  Menschen, 

Jena,  1907. 
Born,  G.:    Beitrage  zur  Entwicklungsgeschichte  des  Saugethierherzens,  Arch.  f.  mik.  Anat., 

Bonn,  1889,  xxxiii,  p.  284. 
Robinson,  A.:    Early  Stages  of  Development  of  the  Pericardium,  J.  Anat.  and  Physiol., 

Lond.,  1903,  xxxvii,  1. 
Pohlman,  A.  G.:    The  Course  of  the  Blood  through  the  Heart  of  the  Fetal  Mammal,  etc., 

Anat.  Rec,  Phila.,  1909,  iii,  75. 

Congenital  Heart  Diseases. 

Lancereaux:  Das  anomalies  cardiaques,  Gaz.  d.  hop.,  Paris,  1880,  liii,  850,  875,  883,  890, 

906,  930,  981. 
Morgagni:  De  sedibus  et  causes  morborum,  Venet.,  1761. 
Peacock,  T.  B.:  Malformations  of  the  Human  Heart,  Lond.,  1866. 
Keith,  A.:  Malformations  of  the  Bulbus  Cordis,  Studies  in  Pathol.,  Quatercent.  Pub., 

Aberdeen  Univ.,  1906,  55. 
Bouillaud:  Traite  clinique  des  maladies  du  ceeur,  Paris,  1835. 
Rauchfuss:    Missbildungen  des   Herzen's,   Gerhardt's    Handb.   d.    Kinderkrankh.,    1878, 

iv,  1  part. 
Vierordt,  H.:  Die  angeborene  Herzkrankheiten,  Nothnagel's  Handb.  d.  spez.  Pathol,  u. 

Therap.,  Wien,  1901,  xv,  II  part  1. 
Abbott,  M.  E.:  Congenital  Cardiac  Disease,  Mod.  Med.,  ed.  by  Wm.  Osier  and  Thos.  Mc- 

Crae,  Phila.,  1908,  iv,  323. 


564  DISEASES  OF  THE  HEART  AND  AORTA. 

Osier,  Wm.     Quoted  from  Abbott. 

Panum,  P.  L.:  Ueber  die  Entstehung  von  Missbildungen,  Berl.,  1860. 

His,  Wm.,  Sr.:  Anatomie  menschlicher  Embryonen,  Leipz.,  1880. 

Rathke,  H.:  Die  Entwickelung  der  Arterien,  welche  beiin  Saugethier  von  den  Bogen  der 

Aorta  ausgehen,  Arch.  f.  Anat.,  Physiol,  u.  wissench.  Med.,  Berl.,  1843,  276. 
Bremer,  J.  L.:  On  the  Origin  of  the  Pulmonary  Arteries  in  Mammals,  Am.  J.  Anat.,  Balto., 

1901-1902,  i,  137. 
Greil,  A.:  Beitrag  zur  vergleichende  Anatomie  und  Entwickelungsgeschichte  des  Herzens 

und  des  Truncus  arteriosus  der  Wirbeltiere,  Morph.  Jahrb.,  Leipz.,  1903,  xxxi,  123. 
Hunter,  Wm.:  Medical  Observations  and  Enquiries,  1784,  vi,  300.    (Quoted  from  Peacock.) 
Kussmaul,  A.     Quoted  from  Vierordt. 
Loeb,  J.:  Ueber  die  Entwicklung  von  Fisch-embryonen  ohne  Kreislauf,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1893,  liv,  528. 
Knower,  H.  McE.:  Effects  of  Early  Removal  of  the  Heart  and  Arrest  of  the  Circulation 

on  the  Development  of  Frog  Embryos,  Anat.  Rec.  (Am.  J.  Anat.),  Balto.,  1907. 
Mall,  F.  P. :  A  Study  of  the  Causes  underlying  the  Origin  of  Human  Monsters,  J.  Morphol., 

Phila.,  1908,  xix,  3. 
Dareste:  Recherches  sur  les  monstrosites,  Paris,  1891.     Quoted  from  Mall. 
Stockard,  C.  R.:  The  Development  of  the  Fundulus  Heteroclitus  in  Solution  of  Litliium 

Chloride,  with  Appendix  on  its  Development  in  Fresh  Water,  J.  Exper.  Zool.,  Balto., 

1906,  hi,  99. 
Bardeen,  C.  R.:  Abnormal  Development  of  Toad  Ova  fertilized  by  Spermatozoa  exposed 

to  the  Rontgen  Rays,  ibid.,  1907,  iv,  1. 
Senac,  quoted  from  Bard,  L.,  and  Curtillet,  J.:  Contribution  a  l'etude  de  la  physiologie 

pathologique  de  la  maladie  blue.     Forme  tardier  de  cette  affection.     Rev.  de  med., 

Paris,  1889,  ix,  993,  from  whom  Grancher  et  al.  are  quoted. 
Stille,  Moreton:  On  Cyanosis  or  Morbus  Cceruleus,  Am.  J.  M.  Sci.,  Phila.,  1844,  N.  S.  viii,  25. 
Osier,  Wm.:  Chronic  Cyanosis,  with  Polycythemia  and  Enlarged  Spleen:  a  new  Clinical 

Entity,  Am.  J.  Med.  Sci.,  1903. 
Knapp,  quoted  from  Posey,  W.  O:  Cyanosis  Retinae,  Am.  J.  Med.  Sci.,  Phila.,  1905, 

cxxx,  415. 
Tate,  W.  W.  H. :  Case  of  Malformation  of  the  Heart,  Trans.  Path.  Soc,  Lond.,  1892,  xliii,  36. 
Hebb,  R.  G.:  Hearts  with  Congenital  Defects  and  Inflammatory  Disease,  ibid.,   1897, 

xlviii,  41. 
McOscar,  J.,  and  Voelcker,  A.:    On  a  Case  of    Traumatic  Rupture  of    the  Ventricular 

Septum,  ibid.,  1897,  xlviii,  47. 
Reiss,  P.:  Contribution  a  l'etude  des  malformations  congenitales  du  cceur,  Maladie  de 

Roger,  These,  Par.,  1893. 
Roger,  H.:    Recherches  cliniques  sur  la  communication  des  cceurs  par  inocclusion  du 

septum  interventriculaire,   Bull,   de  l'Acad.   de  Med.,   Paris,    1879,   ser.  viii,   t.   ii, 

1074  and  1189. 
Cadet  de  Gassicourt,  Potain.     Quoted  from  Reiss,  1.  c. 
Klotz,  O.:  The  Closure  of  the  Ductus  Arteriosus  and  its  Bearing  on  Arteriosclerosis,  Trans. 

Asso.  Am.  Phys.,  1907,  xxii,  213. 
Gerhardt,  C. :  Persistenz  des  Ductus  arteriosus  Botalli,  Jenaische  Ztschr.  f .  Med.  u.  Natur- 

wissench.,  1867,  hi,  105.     (Quoted  from  Vierordt.) 
Zinn,  W.:  Zur  Diagnose  der  Persistenz  des  Ductus  arteriosus  Botalli,  Berl.  klin.  Wchn- 

schr.,  1898,  xxxv,  433. 
De  la  Camp,  O.:  Familiares  Vorkommen  angeborener  Herzfehler;    zugleich  ein  Beitrag 

zur  Diagnose  der  Persistenz  des  Ductus  arteriosus  Botalli,  Berl.  klin.  Wchnschr., 

1903,  xl,  48. 
Frangois-Franck,  A.:  Sur  le  diagnostic  de  la  perseverance  du  canal  arteriel,  Cong,  de 

l'avancement  des  sciences,  Paris,  1878. 
Bonnet:  Sur  la  lesion  de  la  st£nose  de  l'isthmus  congenitale  de  l'aorte  dans  la  region,  Rev. 

de  Med.,  Paris,  1903,  xxiii,  108,  255,  335,  419,  481. 


XI. 
HEART-BLOCK  AND  THE  ADAMS-STOKES  SYNDROME. 

HISTORICAL. 

In  1827  Robert  Adams,  of  Dublin,  reported  the  case  of  a  revenue 
officer,  aged  68,  whose  pulse-rate  was  30  per  minute  and  who  suffered 
from  dyspncea,  cough,  and  attacks  of  fainting  (" apoplectic  attacks"), 
"during  which  his  pulse  would  become  even  slower  than  usual.  .  .  . 
He  recovered  from  them  without  paralysis."  In  the  same  year  an  exactly 
similar  case  was  reported  in  great  detail  by  Wm.  Burnett.  Burnett's 
observations  were  reported  even  more  carefully  and  in  greater  detail  than 
those  of  Adams  and  ill  deserve  to  have  fallen  into  oblivion.  Burnett 
further  called  attention  to  the  fact  that  Morgagni  had  described  two  casea 
of  "epilepsy  with  slow  pulse"  in  1761.  Holberton  described  another  case 
in  1841,  but  general  attention  was  not  attracted  to  the  condition  until 
Wm.  Stokes  published  four  cases  in  1846. 

Since  then  the  condition  of  persistent  extreme  brady- 
cardia with  syncopal  or  convulsive  seizureshias  been 
known  as  the  Adams-Stokes  syndrome,  though  it  may  more 
accurately  be  designated  by  the  names  of  Morgagni-Adams-Stokes,  as 
Pletnew  has  done,  or  by  that  of  Morgagni-Adams-Burnett  or  Adams-Bur- 
nett syndrome. 

As  but  little  can  be  added  to  the  clinical  descriptions  of  these  cases, 
one  of  Stokes's  histories  may  be  reported  in  some  detail: 

"Edmund  Butler,  aged  68,  stated  that  his  health  had  been  robust  until  three  years 
before  admission,  at  which  time  he  was  suddenly  seized  with  a  fainting  fit.  This  occurred 
several  times  during  the  day  and  always  left  him  without  any  unpleasant  effects.  Since 
that  time  he  has  never  been  free  from  attacks  for  any  considerable  length  of  time,  and  has 
had  at  least  fifty  such  seizures.  The  fits  are  very  uncertain  as  to  their  period  of  invasion 
and  very  irregular  as  to  their  intensity,  some  being  much  milder  and  of  shorter  duration 
than  others.  They  are  induced  by  any  circumstance  tending  to  impede  or  oppress  the 
heart's  action,  such  as  sudden  exertion,  distended  stomach,  or  constipated  bowels.  There 
is  little  warning  given  of  the  approaching  attack.  He  feels,  he  says,  a  lump  first  in  the 
stomach,  which  passes  up  through  the  right  side  of  the  neck,  where  it  seems  to  explode 
and  pass  away  with  a  noise  like  thunder  by  which  he  is  stupefied.    This  is  often  accompanied 

by  a  fluttering  sensation  about  the  heart At  first  he  found  that  spirits  were  the 

best  restorative  or  prophylactic,  but  latterly  he  has  not  used  them,  being  'afraid  to  die 
with  spirits  in  his  belly.' 

"On  admission  he  was  haggard  and  emaciated On  percussion  the  chest 

is  universally  resonant.  The  respiratory  murmur  is  louder  and  combined,  especially  pos- 
teriorly, with  large  mucous  rales.    The  impulse  of  the  heart  is  slow  and  of  a  dull  heaving 

character The  first  sound  is  accompanied  by  a  soft  bruit  de  soufflet.    The  second 

sound  is  also  imperfect We  remarked  to-day  that  on  listening  attentively  to  the 

heart's  action  we  perceived  that  there  were  occasional  semi-beats  between  the  regular  con- 
tractions,— very  weak,  unattended  with  impulse,  and  corresponding  to  a  similar  state  of  the 
pulse,  which  thus  amounts  to  about  28  in  the  minute,  the  evident  beats  being  only  28.  .  .  . 

565 


566 


DISEASES  OF  THE  HEART  AND  AORTA. 


"  (June.)  The  cardiac  phenomena  remain  as  before,  but  a  new  symptom  has  appeared, 
namely,  a  very  remarkable  pulsation  in  the  right  jugular  vein.  This  is  most  evident  when 
the  patient  is  lying  down.  The  number  of  reflex  pulsations  is  difficult  to  be  established, 
but  there  are  more  than  double  the  number  manifest  contractions.  About  every  third 
pulsation  is  very  strong  and  sudden  and  may  be  seen  at  a  distance;  the  remaining  waves 
are  much  less  distinct. 

"  He  has  scarcely  had  any  of  the  cardiac  attack  since  he  was  discharged." 


THE  CONCEPTION  OF  HEART-BLOCK. 

Stokes  did  not  appear  to  have  any  definite  understanding  of  the  nature 
of  these  "  semi-beats  "  nor  of  the  functional  disturbance  associated  with 
them.  A  similar,  more  accurate  observation  was  made  by  A.  Chauveau. 
Chauveau  in  1882  made  observations  upon  a  case  whose  usual  pulse-rate 
was  24  per  minute,  and  who  suffered  from  occasional  attacks  of  vertigo 
and  loss  of  consciousness.  Tracings  made  from  the  apex  showed  a  series 
of  large  beats  at  regular  intervals  corresponding  to  the  loud  heart  sounds 
and  to  the  radial  pulse,  and  also  a  second  series  of  very  small  notches  occur- 
ring at  equally  regular  inter- 
vals but  bearing  no  relation 
whatever  to  the  beats  of  the 
ventricle.  As  in  Stokes's  case, 
these  small  pulsations  were  ac- 
companied by  "  small  sounds 
which  may  give  the  illusion  of 
reduplication  of  either  heart 
sound."  The  usual  presystolic 
notch  due  to  the  auricular  beat 
was  absent,  and  Chauveau  cor- 
rectly concluded  that  these 
small  notches  were  due  to  the 
contractions  of  the  auricles,  which  were  beating  at  a  rate  of  66  per  minute 
while  the  rate  of  the  ventricles  was  24.  Chauveau  investigated  the  matter 
experimentally,  and  was  able  to  demonstrate  that  in  horses  upon  stimulation 
of  the  vagus  the  auricles  could  be  observed  to  beat  more  frequently  than 
the  ventricles.  He  therefore  naturally  considered  the  dissociation  of  auricular 
and  ventricular  rhythm  as  due  to  over-stimulation  of  the  vagus. 

Chauveau's  conclusions  that  heart-block  may  result  from  stimulation  of 
the  vagus  have  been  confirmed  recently  by  Rothbergerand  Winterberg,  Garrey, 
and  Robinson  and  Draper,  who  have  shown  that  it  is  chiefly  the  left  vagus 
which  acts  upon  the  auriculoventricular  bundle;  and  the  latter  have  even  been 
able  to  produce  partial  heart-block  in  man  by  pressure  upon  the  left  vagus. 

While  Chauveau  was  experimenting  in  France,  Wooldridge  under  Ludwig's  direc- 
tion was  investigating  the  course  of  the  nerves  in  the  cardiac  septum.  Wooldridge  found 
that  when  he  tightened  a  ligature  which  embraced  only  the  septum,  the  auricles  and  ven- 
tricles beat  independently  and  the  ventricles  no  longer  responded  to  vagus  inhibition. 
When  the  ligature  was  loosened  the  rhythm  returned  to  normal.  Tigerstedt  in  1884  also 
obtained  dissociation  of  auricles  and  ventricles  by  cutting  the  septum. 

These  observations  under  Ludwig's  direction  were  made  with  the  view 
only  of  cutting  the  intracardiac  nerves.  As  a  matter  of  fact,  the  muscular 
connections  were  severed  as  well,  but  the  importance  of  these  was  disregarded. 


RESP. 


RADIAL 


APEX 


SECONDS 


Fig.  267. — Tracing  of  the  apex  beat  in  a  case  of  Adams- 
Stokes  disease.      (After  Chauveau.) 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME. 


567 


The  myogenic  conduction  from  auricle  to  ventricle  was,  however,  at  this 
very  period  being  demonstrated  by  Gaskell  in  Cambridge  upon  the  heart 
of  the  tortoise  and  frog,  in  which  the  auriculoventricular  function  is  repre- 
sented by  a  wide  band  of  muscle  whose  properties  differ  somewhat  from 
those  of  either  the  auricle  or  the  ventricle.  Gaskell  demonstrated  that  "  if 
this  auriculoventricular  ring  were  clamped,  the  auricle  continued  to  beat 
at  unaltered  rhythm,  but  as  the  clamp  was  tightened  the  period  between 
auricular  and  ventricular  contractions  (As-Vs  interval,  on  conduction  time) 
was  gradually  lengthened;  then  the  ventricle  failed  to  respond  to  some  of 
the  impulses  from  the  s  auricle,  and,  according  to  the  tightness  of  the  clamp, 
the  ventricle  could  be  made  to  ...  .  respond  to  every  second  contraction 
of  the  auricles  (partial  heart-block),  to  respond  to  every  third,  fourth,  or 


A  SEC. 


JUGULAR 


APEX 


BRACH. 


>jjjjjjimjiiiLrto\MN\t\i\i^^ 


Fig.  268. — Partial  heart-block  (3  :  1  rhythm)  produced  by  pressure  upon  the  vagus  in  a  patient  with 
disturbed  conductivity  who  was  also  subject  to  attacks  of  the  Adams-Stokes  syndrome.  (Tracing  made  by 
Dr.F.  W.Peabodyand  the  writer.)  A,  A,  A,  A,  auricular  contractions  to  which  the  ventricles  do  not  respond. 


other  contraction,  or  to  remain  quiescent.  When  the  clamp  was  closed  very 
tightly  the  ventricle  remained  still  for  a  variable  time,  then,  in  accordance 
to  its  inherent  rhythmical  power,  developed  a  rhythm  of  its  own  (rhythm  of 
development),  the  rate  of  that  rhythm  when  fully  developed  and  the  length 
of  time  that  the  standstill  lasted  being  correlated  with  the  rhythmicity  of 
the  tissues."  The  condition  in  which  the  contractions  of  the  ventricle  no 
longer  follow  any  of  the  impulses  from  the  auricles  is  termed  complete  heart- 
block,  in  contrast  to  the  partial  heart-blocks  in  which  the  ventricle  is  respond- 
ing to  some,  but  not  all,  of  the  impulses  arising  in  the  auricles. 

Gaskell  showed  that  heart-block  also  set  in  when  the  bridge  of  tissue 
connecting  the  auricles  and  ventricles  was  cut  down  to  a  sufficiently  narrow 
strip.  He  was  able  to  produce  similar  blocks  between  portions  of  the  auricle 
or  ventricle  by  clamping  or  cutting,  just  as  Romanes  had  done  for  the  muscle 
in  the  bell  of  the  medusa.  Gaskell  demonstrated  also  that  the  block  between 
auricles  and  ventricles  remained  complete  when  the  only  connection  between 
the  auricles  and  the  ventricles  was  formed  by  the  coronary  nerve. 


568 


DISEASES  OF  THE  HEART  AND  AORTA. 


THE   AURICULO(ATRIO) VENTRICULAR   MUSCLE   BUNDLE. 

Anatomy. — The  existence  of  muscular  connections  between  the  auricles 
and  ventricles  in  man  and  mammals  was,  however,  denied  until  G.  Paladino 
(1876)  and  A.  F.  Stanley  Kent  (1893)  described  certain  fibres  in  the  septum 
membranaceum  which  they  thought  bridged  this  gap.  Paladino  was  some- 
what indefinite,  and  Kent's  figures  showing  connections  between  the  left 
auricle  and  left  ventricle  are  apparently  erroneous,  so  that  the  real  discovery 
dates  from  the  same  year,  when  Wm.  His,  Jr.,  described  the  presence  in  the 
mouse,  dog,  and  man  of  a  bundle  of  muscle-fibres  which  "  arises  from  the 

posterior  wall  of  the  right  auricle  near 
the  interauricular  septum,  in  the  atrio- 
ventricular groove,  lies  upon  the  upper 
edge  of  the  muscular  interventricular 
septum,  passes  forwards  and  to  the  vicin- 
ity of  the  aorta,  where  it  divides  into  a 
right  and  a  left  branch.  The  latter 
passes  down  to  the  base  of  the  anterior 
mitral  cusp." 

These  anatomical  findings  of  His 
have  been  confirmed  by  Braeunig,  Hum- 
blet,  Retzer,  and  Tawara.  The  latter 
found  that  the  fusiform  cells  described 
by  Kent  were  really  Purkinje  fibres,  and 
that  the  muscles  bundle  of  His  is  in 
reality  continuous  with  the  entire  net- 
work system  of  Purkinje  fibres  which 
permeates  both  ventricles.  Saigo  has 
found  that  these  fibres  are  much  richer 
in  glycogen  granules  than  are  the  ordi- 
nary cardiac  muscle  fibres.  Tawara  also 
demonstrated  the  presence  of  nerve- 
fibres  within  the  His  bundle,  and  Gordon 
Wilson  has  recently  demonstrated  ganglion  cells  as  well. 

Lhamon  (Amer.  Jour.  Anat.,  1912,  xiii,  55)  has  shown  that  the  bundle  has 
a  separate  connective  tissue  sheath  and  the  whole  conducting  system  can  be 
injected  with  india  ink  from  beneath  the  endocardium. 

Mall  (Am.  Jour.  Anat.,  1912,  xiii,  247)  has  shown  that  the  auriculoven- 
tricular  bundle  is  formed  from  the  wall  of  the  auricular  canal  in  the  embryo, 
and  that  it  arises  as  a  broad  band  connecting  auricle  with  ventricle  and  is 
later  constricted  down  and  separated  into  two  branches  by  the  upward  growth 
of  the  septal  musculature. 

The  idea  that  the  cardiac  impulse  must  pass  from  sinus  to  auricle  before 
reaching  the  auriculoventricular  bundle  is  borne  out  also  by  the  observation 
of  Dr.  G.  S.  Bond  that  in  the  frog  the  auriculoventricular  muscle  can  be  seen 
to  contract  considerably  later  than  the  auricle  but  before  the  ventricle. 

Experimental  Physiology  of  the  Aariculoventricular  Bundle. — The  first 
experiments  upon  the  physiology  of  heart-block  in  mammals  were  per- 
formed by  Stanley  Kent,  the  discoverer  of  the  auriculoventricular  bundle, 


Fig.  269. — The  right  branch  of  the  auriculo- 
ventricular bundle  in  the  dog's  heart.  (After 
Barker  and  Hirschfelder,  Arch.  Int.  Med.,  1909.) 


L= ^n^aa/wvvW\i\^  — ■ — 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.         569 

in  1893,  and  were  recorded  by  him  in  his  original  publication  in  the  following 
words:  "By  the  use  of  a  suitably  constructed  clamp.  .  .  I  have  been  able 
to  verify  for  the  mammal  (i.e.,  in  the  excised  heart  of  the  rat)  almost  all 
the  effects  described  by  Gaskell  as  obtained  in  the  frog."  Kent  thus  seems 
to  have  forestalled  all  the  later  experiments  upon  the  subject,  but  the  brevity 
of  his  physiological  note  left  much  to  be  investigated.  In  1895  His  repeated 
the  experiments  of  Wooldridge  and  Tigerstedt,  and  demonstrated  that  in 
order  to  bring  about  dissociation  of  the  auricles  and  ventricles  it  was  not 
necessary  to  injure  the  entire  septum  but  merely  this  auriculoventricular 
muscle  bundle. 

In  1899  he  applied  his  anatomical  and  physiological  studies  to  a  case 
of  Adams-Stokes  disease,  in  which  he  confirmed  Chauveau  by  finding  inde- 
pendent action  of  the  auricles  and  ventricles,  and  designated  this  by  Gas- 
kell's  term  "  heart-block."  His  also  gave  an  excellent  tracing,  taken  during 
a  syncopal  attack,  demonstrating  that  the  auricles  continued  at  their  usual 

1  2  3*456 


jug.  r 

BRACH 

RESP 

Fig.  270. — Tracings  from  the  carotid  artery  and  jugular  vein  of  a  patient  with  Adams-Stokes 
disease,  showing  stoppage  of  the  ventricles  and  continuance  of  the  auricular  contractions  during  the 
attack.  (After  His,  Deutsches  Arch.  f.  klin.  Med.,  1899,  lxiv.)  1,  2,  3,  4,  5,  6  represent  the  onset  of 
independent  ventricular  contractions. 

rate  while  the  ventricles  ceased  to  beat  for  several  seconds  and  then  resumed 
their  beat  at  a  gradually  increasing  rate  (corresponding  to  Gaskell's  "rhythm 
of  development"). 

The  experiments  of  Kent  and  His  and  their  predecessors  were  confirmed 
by  Humblet,  Hering,  and  Tawara,  and  led  to  the  conclusion : 

1.  That  the  slow  pulse  of  Adams-Stokes  disease  was  due  to  dissociation 
between  the  auricles  and  ventricles  (heart-block)  and  the  slow  independent 
rhythm  of  the  ventricles. 

2.  That  the  syncopal  attacks  (Adams-Stokes  syndrome)  were  due  to 
cessation  of  ventricular  beat  but  not  of  the  auricular  beat. 

Experimentally  they  had  produced  the  former  but  not  the  latter  in 
mammals,  while  Gaskell  had  produced  it  in  the  frog  and  tortoise. 

Factors  Affecting  Degree  of  Heart=block. — In  1904  E  r  1  a  n  g  e  r  began 
a  series  of  experimental  and  clinical  investigations  upon  this  condition. 
He  first  confirmed  all  of  His's  findings  in  man,  and  refuted  Chauveau's 
claim  that  the  heart-block  was  due  to  the  vagi,  by  showing  that  when  in 
his  cases  the  latter  were  paralyzed  with  atropine  the  heart-block  did  not 
pass  off.1  Then  he  devised  a  modification  of  Gaskell's  clamp,  an  L-shaped 
hook  of  steel  wire  whose  arm  could  be  pressed  against  a  brass  block  by  means 
of  a  bolt  and  screw. 

The  hook  was  introduced  into  the  right  wall  of  the  aorta  just  above  its  origin  (the 
pericardial  fat  having  been  dissected  off),  the  point  passed  backwards  and  downwards 
into  the  left  ventricle,  and  then  pushed  through  the  ventricular  septum  till  it  entered  the 

1  Edes  had  previously  shown  that  belladonna  had  no  effect  in  his  cases  of  Adams- 
Stokes  disease. 


570 


DISEASES  OF  THE  HEART  AND  AORTA. 


right  ventricle  (Fig.  271).  The  brass  block  was  then  pushed  down  over  the  long  arm  of 
the  L  and  the  nut  gradually  screwed  taut.  The  first  effect  observed  was  lengthening  of  the 
conduction  time  (As-Vs  or  A-V  interval);  then  alternate  ventricular  beats  disappeared 
(2  :  1  rhythm),  at  first  occasionally,  then  regularly.  With  further  tightening  of  the  clamp 
a  3  :  1  rhythm  occurred,  and  finally  complete  heart-block.  "After  the  ventricles  have 
emptied  themselves  it  may  be  seen  that  each  contraction  of  the  auricles  sends  into  the 
former  a  distinct  wave,  upon  the  subsidence  of  which  the  volume  of  the  ventricles  is  seen 
to  have  been  considerably  increased."  In  many  but  not  in  all  of  his  experiments  the  com- 
plete block  began  with  a  complete  stoppage  of  the  ventricles,  exactly  like  that  in  the 
Adams-Stokes  syndrome,  in  which  "the  ventricles  stop  beating  without  warning.     The 

auricles  continue  to  beat  with  an  apparently  unaltered  rate. 
....    The  ventricles  enlarge  with  each  contraction  until 

their  distention  becomes  really  huge Respiratory 

convulsions  may  begin.  Witnesses  are  almost  convinced 
that  the  experiment  has  come  to  a  close  when  it  may  be 
that  after  more  than  twenty  seconds  the  ventricles  suddenly 
empty  themselves  with  one  great  effort."  This  is  sooner  or 
later  followed  by  another  and  another  until  the  slow  ven- 
tricular rate  is  gradually  assumed. 


Factors  Affecting  Stoppage  of  the  Ventricles. — 

It  is  this  "  stoppage "  of  the  ventricles  which 
brings  on  the  cerebral  anaemia,  syncopes,  convul- 
sions, and  death  in  man;  but  as  long  as  the  pulse 
remains  regular,  though  slow,  the  circulation  is 
maintained  and  the  patients  may  remain  quite  free 
from  symptoms. 

Erlanger  and  Hirschfelder  found  that  stoppage 
of  the  ventricles  was  produced  most  frequently  when 
the  clamp  was  tightened  suddenly,  so  that  the  stimuli 
cut  off  at  once,  especially  when  a  certain  degree  of 
When  partial  block  had  once  set  in,  tightening  the 
clamp  further  usually  produced  complete  block  without  stoppage;  and  when 
complete  block  had  once  been  established  stoppage  of  the  ventricles  during 
complete  block  was  very  rare,  although  in  man  it  is  relatively  common. 


Fig.  271.— The  Erlanger 
heart-block  clamp  compressing 
the  auriculoventricular  bundle 
(AVB).  SM,  septum  mem- 
branaceum;  MV,  mitral  valve. 

from  the  auricles  were 
asphyxia  was  present. 


wmwwpnnrv~- 


....,tl..,.,.,.MTrr„„ntt,lMtMititMlmlim .■■■mmnn '""» mim.iiiiii tiiini 


1:1    OamfOBg 


2-J 


Stoppage 


Undamped 


Fig.  272. — Effect  of  gradually  tightening  the  clamp.  (After  Erlanger  and  Hirschfelder.)  Shows 
2  : 1  rhythm,  finally  stoppage  of  the  ventricles  with  complete  block.  After  this  the  ventricles  can  be  seen 
to  contract  at  an  independent  rhythm. 


The  duration  of  stoppage  of  the  ventricle  seemed  to  depend  largely 
upon  the  irritability  and  spontaneous  rhythmicity  of  the  ventricle,  and  varied 
greatly  in  different  hearts;  in  some  cases  it  was  entirely  absent  or  extremely 
short,  whereas  in  one  animal  it  lasted  55  seconds  and  death  would  then 
have  resulted  had  not  the  heart  been  revived  by  mechanical  stimulation.     In 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        571 

general,  the  tendency  to  stoppage  seems  to  depend  largely  upon  the  condi- 
tion of  the  heart,  and  especially  upon  the  degree  of  asphyxia. 

Whenever  the  rate  of  the  auricles  was  increased  from  any  cause  (stimu- 
lation of  the  right  accelerator,  application  of  heat,  or  rhythmic  induction 
shocks)  the  degree  of  block  was  also  increased,  a  normal  rhythm  passing  to 
a  2  : 1  rhythm,  a  2  : 1  to  a  4  : 1  or  even  complete  block;  conversely,  slowing 
the  auricles  by  application  of  cold,  etc.,  improved  conductivity  and  caused 
the  block  to  pass  off. 

In  this  respect  the  experimental  heart-block  differs  greatly  from  the 
clinical,  since  in  a  number  of  cases  (Gibson,  Thayer)  it  has  been  found  that 
stimulation  of  the  vagus  increases  the  degree  of  block  while  atropine  removes 
a  partial  but  not  a  complete  block.  In  other  cases  (Edes,  Erlanger,  Schmoll) 
it  has  no  such  effect. 

The  duration  of  the  period  of  "  stoppage  "  (during  which  the  ventricles 
remained  quiescent)  varied  greatly,  and  was  greatest  in  those  hearts  which 
could  be  inhibited  longest  by  stimulation  of  the  vagus.  As  in  Gaskell's 
tortoise,  it  seemed  to  be  definitely  "  correlated  to  the  rhythmicity  "  of  the 
ventricles,  which  is  greater  in  some  hearts  and  at  some  stages  of  the  experi- 
ment than  at  others.  In  general  it  has  appeared  to  the  writer  that  the  poorer 
the  condition  of  the  ventricular  muscle  the  longer  the  period  of  stoppage. 
Slight  asphyxia,  though  it  did  not  in  itself  bring  about  stoppage  of  the  ven- 
tricles, seemed  to  lengthen  the  period  of  stoppage  from  clamping. 

In  some  experiments  the  ventricle  remained  quiescent  for  so  long  (more 
than  55  seconds)  that  the  animal  would  have  died  at  once  had  not  the  heart 
been  revived  by  mechanical  stimulation. 

In  a  subsequent  paper  Erlanger  has  shown  that  the  condition  of  block 
on  clamping  or  injury  depends  upon  the  condition  of  the  cells  in  the  His 
bundle.  Each  cardiac  impulse  leaves  them  in  a  condition  of  lowered  irrita- 
bility from  which  they  recover  gradually.  When  the  injury  is  slight  they 
recover  just  too  late  for  the  next  impulse  from  the  auricle  and  are  only  ready 
to  receive  the  second  stimulus  (a  2  : 1  rhythm  resulting).  When  they  are 
injured  a  little  more  they  recover  in  time  for  every  third  or  every  fourth 
impulse,  and  finally  the  stimulus  always  remains  below  the  threshold  of 
irritability  and  complete  block  sets  in.  Similarly,  the  more  rapid  the  rhythm 
the  less  time  the  cells  have  had  to  recover  and  the  less  the  intensity  of  impulse 
from  the  auricles,  hence  the  greater  the  block. 

As  regards  the  ventricle,  the  greater  its  irritability  and  rhythmicity 
the  sooner  it  will  respond  to  its  own  internal  stimuli  with  a  contraction 
and  the  shorter  the  stoppage  and  the  more  rapid  the  rhythm.  A  low  ven- 
tricular rhythm  (under  25  per  minute)  is  therefore  often  a  sign  of  poor  con- 
dition of  the  ventricle  and  of  a  tendency  to  stoppage  during  the  period  of 
complete  block  in  spontaneous  attacks. 

The  experiments  of  Erlanger  and  Hirschfelder  have  been  confirmed 
by  v.  Tabora  under  Hering's  direction.  The  latter  has  found  that  stimula- 
tion of  the  vagus  may  under  certain  circumstances  increase  the  degree 
of  heart-block  and  facilitate  the  onset  of  stoppage,  especially  when  digi- 
talis has  been  administered.  The  apparent  discrepancy  between  their 
findings  is  probably  due  to  the  presence  of  the  different  nerve-fibres  in  the 
vagus,  so  that  sometimes  conductivity,  sometimes  irritability  is  most  affected. 


572  DISEASES  OF  THE  HEART  AND  AORTA. 

Other  Factors  Affecting  Heart=block. — Mere  cooling  of  the  heart-muscle, 
as  was  shown  by  v.  Kries  upon  the  hearts  of  cold-blooded  animals,  is  suffi- 
cient to  bring  on  the  various  grades  of  heart-block.  Florence  Buchanan  has 
found  an  example  of  this  (2  :  1  rhythm)  in  hibernating  dormice  whose  body 
temperature  is  much  reduced. 

Asphyxial  Heart=block. — Heart-block  very  frequently  comes  on  in  dying 
animals,  and  may  be  brought  on  by  the  action  of  many  poisons  (digitalis, 
strophanthus,  aconite,  etc.),  as  well  as  by  asphyxia  alone.  As  Lewis,  Oppen- 
heimer  and  Matthison  have  shown,  heart-block  from  asphyxia  is  as  inde- 
pendent of  the  central  nervous  system  as  is  the  block  produced  by  clamping 
the  bundle,  and  it  is  probable  that  this  may  be  a  factor  to  be  reckoned  with 
in  many  clinical  conditions. 

Heart=block  from  Diminished  Irritability  of  the  Ventricular  Muscle 
without  Injury  to  the  Auriculo ventricular  Bundle. — When  the  auriculo ven- 
tricular bundle  is  injured  or  its  activity  depressed  by  vagus  stimulation, 
the  conduction  of  the  impulse  from  auricle  to  ventricle  usually  becomes 
slower  and  the  conduction  time  (a — c  interval  in  the  venous  pulse,  P-R 
interval  upon  the  electrocardiogram)  is  prolonged.  Occasionally,  however, 
as  in  a  case  recently  reported  by  A.  M.  Gossage,  partial  heart-block  may  be 
present  without  prolongation  of  the  conduction  time,  and  in  such  cases  it  is 
assumed  that  the  auriculoventricular  bundle  is  uninjured  and  conducts  the 
impulse  in  the  usual  manner,  but  the  irritability  of  the  ventricular  muscle 
is  so  much  depressed  that  it  fails  to  respond  to  all  the  impulses  that  reach  it. 

Hirschfelder  has  shown  that  if  the  auricle  of  the  dog  is  stimulated  with 
weak  rhythmic  induction  shocks  at  increasing  rates  they  soon  fail  to  respond 
to  each  stimulus  and  then  respond  to  only  alternate  stimuli.  Increasing  the 
intensity  of  the  stimulus  or  increasing  the  irritability  of  the  heart  muscle 
by  pouring  on  warm  salt  solution,  without  changing  the  rate  of  stimulation, 
causes  the  auricles  to  respond  to  every  stimulus. 

This  condition  simulates  a  "  block  "  from  loss  of  irritability,  without 
loss  of  conductivity,  and  represents  the  condition  of  the  ventricular  muscle 
in  the  case  reported  by  Gossage. 

Interaction  of  the  Muscular  and  Nervous  Elements  in  Heart=block. — 
As  can  be  seen  from  the  studies  of  Chauveau  on  the  one  hand  and  His  and 
Erlanger  on  the  other,  heart-block  may  be  brought  about  either  by  over- 
action  of  the  vagi,  by  injury  to  the  muscle  of  the  auriculoventricular  bundle, 
or  most  probably  by  diminished  irritability  of  the  ventricular  muscle.  It  is 
therefore  not  surprising  to  find  that  in  most  cases  there  is  a  summation  of 
the  effects  of  all  three  actions,  though  in  very  many  of  them  the  effect  of  one 
of  them,  either  the  vagus,  the  lesion  of  the  bundle,  or  the  diminished  irri- 
tability of  the  ventricular  muscle,  predominates.  This  is  true  for  heart- 
block  which  results  from  the  action  of  drugs  or  bacterial  poisons,  as  well  as 
from  mechanical  lesions. 

Thus,  as  in  the  case  shown  in  Fig.  268,  and  in  those  reported  by  G.  A. 
Gibson,  Thayer  and  Peabody,  and  a  number  of  other  writers,  it  is  common 
to  find  patients  with  lesions  of  the  auriculoventricular  bundle  sufficient  to 
impair  its  function  a  little,  in  whom  direct  or  reflex  stimulation  of  the  vagus 
is  sufficient  to  bring  on  a  partial  heart-block  which  may  be  of  a  severe  grade 
(3  : 1  or  4  : 1)  but  which  is  entirely  removed  by  the  administration  of  atropine. 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        573 

Complete  heart-block,  as  in  the  cases  of  Edes  and  Erlanger,  is  usually- 
unaffected  by  the  administration  of  atropine,  because  it  is  usually  entirely 
organic  in  origin. 

Irregular  Rhythm  in  Complete  Block. — Occasionally,  as  in  two  of  the 
nineteen  animals  of  Erlanger  and  Hirschfelder,  the  ventricular  rate  is  irreg- 
ular, owing  to  the  occurrence  of  ventricular  extrasystoles  which  arise  spon- 
taneously during  the  long  diastoles.  They  are  of  no  special  significance, 
except  in  so  far  as  they  affect  the  rate  of  blood-flow. 

RELATION  OF  HEART-BLOCK  TO  ADAMS-STOKES  SYNDROME. 

It  cannot  be  too  strongly  emphasized  that:  (1)  heart-block  (complete) 
and  Adams-Stokes  syndrome  are  by  no  means  synonymous;  the  former 
represents  merely  the  dissociation  of  rhythms,  while  the  Adams-Stokes 
syndrome  brought  on  by  cerebral  anaemia  during  ventricular  stoppage  is 
a  totally  different  matter;  (2)  heart-block  may  persist  for  months  or  years 
without  the  occurrence  of  the  syndrome,  as  in  the  case  about  to  be  described. 


Fig.  273. — Tracing  from  jugular  vein  and  carotid  artery,   in  a  case   (J.  L.)  of  complete  heart-block 
after  the  syncopal  attacks  had  subsided. 

Attacks  of  the  Adams-Stokes  syndrome  may  occur  in  three  ways:  (1) 
at  the  transition  from  normal  rhythm  to  complete  block;  (2)  in  the  midst 
of  complete  block;  (3)  probably  also  from  stimulation  of  the  vagus  in  certain 
cases  where  conductivity  is  already  diminished. 

In  the  cases  where  the  Adams-Stokes  syndrome  (ventricular  stoppage) 
appears  at  the  transition  from  normal  rhythm  to  complete  block,  the  attacks 
are  usually  preceded  by  quickening  of  the  pulse;  and  the  block  passes  off 
and  reappears  suddenly.  When  the  complete  block  becomes  permanently 
established,  the  Adams-Stokes  syndrome  may  disappear,  as  is  well  shown 
by  the  following  case,1  seen  by  the  writer  in  consultation  with  Dr.  H.  G. 
Beck.  The  Adams-Stokes  syndrome  may  be  present  only  in  the  initial  and 
not  the  later  stages  of  the  heart-block. 

Case  of  Heart-block,  with  Adams-Stokes  Syndrome  only  at  Onset  of  Block. 

J.  L.,  aged  72,  had  been  perfectly  healthy  all  his  life  except  for  attacks  of  malaria 
when  between  14  and  40  years  of  age,  and  pneumonia  about  ten  years  ago.  Denies  syphilis 
and  gonorrhoea;  drinks  little,  but  smokes  considerably.  Had  been  a  blacksmith  until 
July,  1907.  At  this  time  he  was  struck  on  the  head  by  a  railroad  gate,  became  unconscious 
for  one  or  two  minutes,  after  which  he  recovered  at  once  except  for  a  slight  transitory 
weakness  of  the  right  arm  and  slight  transitory  aphasia.  He  remained  well  until  Novem- 
ber, 1907,    pulse    being    60    to    64.    In  the  latter  part  of  November  he  began  to 

1 A  study  of  this  case  has  been  reported  by  Drs.  H.  G.  Beck  and  W.  R.  Stokes,  Arch. 
Int.  Med.,  Chicago,  1908. 


574 


DISEASES  OF  THE  HEART  AND  AORTA. 


have  weak  spells  in  which  he  fell  but  did  not  lose  consciousness.  He  was  seen  by 
the  writer  on  January  12,  when  he  had  been  having  numerous  attacks  for  about  a  week. 
Patient  was  fairly  nourished  man  of  good  rosy  color,  pupils  reacting  normally;  no  signs 
of  intracranial  disturbance  or  of  lues.  Chest  clear.  Heart  not  enlarged;  action  regular; 
pulse-rate  33  per  minute.  Sounds  accompanying  the  beats  are  loud  and  the  first 
sound  is  accompanied  by  a  flowing  systolic  murmur  not  transmitted  to  axilla.  Second 
sound  clear.  Between  these  in  the  long  pause  there  can  be  heard  two  or  three  very 
soft  distant  sounds  like  the  ticking  of  a  watch,  accompanying  which  small 
undulations  may  be  seen  over  the  jugular  vein,  and  on  most  delicate  pal- 
pation of  the  radial  a  slight  impulse  can  be  felt  there  as  well, 
due  to  the  beating  of  the  auricles  against  the  root  of  the  aorta.  The  venous  tracing  (Fig. 
273)  showed  complete  heart-block.  At  this  time  he  had  no  attacks.  On  January  17, 
however,  he  was  again  seen.  His  attacks  had  been  very  numerous,  the  pulse-rate  rising 
and  falling  with  great  rapidity.  Tracings  from  the  jugular  vein  and  carotid  arteries,  taken 
as  an  attack  came  on,  show  the  following  sequence  events :  At  first  a  period  of  com- 
plete heart-block  lasting  a  few  minutes.  This  then  passed  off  and  was  succeeded 
by  a  few  moments  of  2:1  rhythm.    The  2  : 1  rhythm  passed  suddenly  into  a  1  : 1  rhythm 


Fig.  274.  —  Diagram  representing  the  conditions  found  in  the  tracing  Fig.  273.  A,  auricular 
contractions ;  V,  ventricular  contractions ;  1,  2,  first  and  second  heart  sounds  ;  a,  a,  sounds  due  to 
contractions  of  the  auricles. 

at  a  rate  of  about  90  per  minute  and  began  to  quicken.  It  was  then  prophesied 
that  an  attack  was  imminent,  and  in  an  instant  the  ventricles  suddenly 
ceased  to  beat.  The  patient  cried  out,  became  ashy  pale,  and  a  convulsion 
set  in,  during  which  the  auricles  continued  to  beat  at  the  old  rate.  In  about  11  seconds 
the  ventricles  began  to  beat,  and  soon  resumed  their  regular  independent  rate  of  2  8  to 
30  per  minute  in  complete  block.  After  a  few  more  seizures  an  hour  or  so  passed 
without  further  change  in  rate  or  further  symptoms.  When  seen  in  the  afternoon  and 
again  on  the  next  day  the  pulse-rate  had  not  varied.  It  was  then  prophesied  by  the  writer 
that  no  more  attacks  were  imminent,  but  the  patient  was  kept  in  bed 
for  several  weeks  afterwards.  A  few  weeks  later  he  had  a  sinking  spell  with  weakness  of 
the  pulse,  but  no  change  in  rate  and  regularity  and  no  unconsciousness  or  convulsions. 
This  he  also  recovered  from  and  remained  free  from  symptoms  and  attacks  until  his  death 
two  months  later.  He  died  rather  suddenly  but  was  conscious  to  the  last;  his  pulse- 
rate  had  not  changed,  and  he  died  not  from  the  Adams-Stokes  syndrome  but  from  his 
coronary  sclerosis.  The  lesion  found  in  the  His  bundle  will  be  discussed  below.  In  this 
patient  the  Adams-Stokes  syndrome  passed  off  as  the  complete 
block  became  established. 

Variations  in  Pulse=rate. — This  case  is  no  isolated  example  of  such  a 
condition.  Even  Burnett's  case  (1824)  furnishes  an  example,  for  he  says, 
"  The  pulse  beats  at  the  rate  of  74  in  the  minute  for  the  space  of  about  a 

minute,  then  intermits  for  7,  8,  or  10  seconds In  the  evening.  I  found 

that  he  had  been  attacked  many  times  but  was  then  much  better 

He  complained,  however,  of  more  pain  about  the  precordia  and  his  pulse 
beat  only  20  in  the  minute."  A  similar  tendency  to  improvement  after 
heart-block  set  in  has  been  noted  in  Stokes's  first  case  (1846),  in  that  of 
Alfred  Webster  (1900),  in  one  of  the  cases  reported  by  Edes  (1901),  and  in 
one  of  Erlanger's  cases  (1905). 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        575 


Fig.  275. — Heart  of  a  patient  (J.  L.)  showing  calcifications  which  produced  Adams-Stokes  disease. 
(Drawn  from  the  specimen.)  A,  B,  C,  D,  E.  Sections  through  the  interventricular  septum,  showing  the 
calcification  pressing  upon  the  auriculoventricular  bundle.  (After  Beck  and  Stokes.)  F.  Section  through 
a.     (Photomicrograph  by  Dr.  C.  S.  Bond.) 


576 


DISEASES  OF  THE  HEART  AND  AORTA. 


Stoppage  of  the  Ventricles  during  Complete  Heart=block. — Unfortu- 
nately, the  Adams-Stokes  syndrome  does  not  always  end  with  the  estab- 
lishment of  permanent  complete  block.  Just  as  in  the  two  experiments 
of  Erlanger  and  Hirschf elder  mentioned  above,  stoppage  of  the  ventricles 
sometimes  occurs  in  the  midst  of  a  complete  block  when  the  pulse-rate  is 


ii 


Fig.  276. — Diagram  showing  the  two  types  of  ventricular  stoppage  producing  the  Adams-Stokes 
syndrome.  1.  Ventricular  stoppage  only  at  the  moment  when  conduction  ceases.  2.  Stoppage  of  the 
ventricles  setting  in  during  the  periods  of  complete  block.  A,  auricular  contractions;  V,  ventricular 
contractions;    A— V,  conduction  of  impulses  from  auricles  to  ventricles. 

slow  and  without  preliminary  variations  in  rate.  This  took  place  in  the  case 
reported  by  His  and  in  Erlanger's  first  case.  The  influences  producing  this 
stoppage  act  directly  upon  the  ventricles,  the  auricular  rate  being  unchanged 
or  quickened,  but  the  nature  of  these  influences  is  not  well  understood. 
Erlanger  has  shown  that  the  plugging  of  a  coronary  artery  in  animals  does 

not  bring  stoppage  from  com- 
plete block.  On  the  other  hand, 
slight  asphyxia,  such  as  holding 
the  breath  after  slight  exercise, 
brought  them  on  regularly.  How- 
ever, it  cannot  be  said  that  the 
prognosis  is  much  if  any  more  un- 
favorable in  these  than  in  the  other 
group  of  cases,  since  Erlanger's 
case  at  least  lived  several  years 
after  observation,  and  this  point 
has  not  been  noted  in  most  of 
the  reported  cases.  Prof.  Thayer 
has  recently  reported  a  case  in 
which  the  block  has  passed  off. 

LESIONS    OF    THE    AURICULO  VEN- 
TRICULAR   BUNDLE. 


Fig.  277. — Section  of  a  luetic  infiltration  of  the 
auriculoventricular  bundle.  (After  Ashton  Norris  and 
Lavenson.)     INF.,  area  of  round-cell  infiltration. 


These  two  groups  represent 
cases  in  which  the  block  appears 
to  be  myogenic;  and  pathological  evidence  indicates  that  such  is  the  case. 
Although  Adams  (1872)  mentions  fatty  degeneration  of  the  ventricular  septum 
in  his  case,  and  many  other  autopsies  had  been  performed,  the  first  case  in 
which  a  lesion  of  the  auriculoventricular  (or  atrioventricular)  muscle  bundle 
was  demonstrated  was  that  of  Luce  in  1902  in  which  a  sarcoma  was  found  in- 
volving the  auriculoventricular  bundle.  Luce,  however,  did  not  regard  this  as 
a  causal  factor  for  the  Adams-Stokes  syndrome,  and  the  first  case  in  which  this 
connection  was  definitely  established  was  reported  by  Stengel,  of  Philadelphia, 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        577 


PLATE    XX. 


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Electrocardiogram  from  a  case  of  complete  heart-block.  The  P  waves,  which  correspond  to  the 
auricular  contractions,  bear  no  relation  to  the  R  waves  of  the  ventricular  systoles.  There  is  also  splitting  of 
the  P  waves  and  fine  tremor  of  the  galvanometer  string  due  to  extraneous  causes. 


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Electrocardiogram    from    a    case    of     auricular    fibrillation    with    complete     heart-block.      (Kindness    of 

Prof.  Thayer.) 


37 


578  DISEASES  OF  THE  HEART  AND  AORTA. 

in  1905,  -with  excellent  figures  showing  fibrosis  of  the  bundle.  Soon  after  this 
Schmoll  reported  a  case  in  which  no  lesion  could  be  discovered  macroscopi- 
cally,  but  fibrosis  of  the  His  bundle  was  demonstrated  with  the  microscope. 

In  the  case  of  J.  L.,  reported  above,  autopsy  showed  extensive  atheroma 
of  the  aorta;  the  coronary  arteries  were  converted  into  pipes  of  bony  hard- 
ness. Large  calcifications  were  present  upon  the  mitral  valve  and  in  the 
upper  part  of  the  interventricular  septum,  in  which  a  long  tongue  of  calci- 
fication can  be  seen  to  intercept  the  auriculo ventricular  bundle. 

In  the  past  two  years  a  considerable  number  of  cases  have  been  studied 
both  histologically  and  physiologically,  lesions  in  the  His  bundle  being  uni- 
formly found.     The  following  represent  some  of  the  lesions  reported: 

Gumma,  7:  Handford  (1904),  Keith  and  Miller  (1906),  Griinbaum  (1906),  Ashton, 
Norris,  and  Lavenson  (1907),  Heineke  (1907),  Fahr  (1907),  Rendu  (1895). 

Calcined  patches  involving  the  bundle,  4:  Stengel  (1905),  Hay  and  Moore  (1906), 
Beck  and  Stokes  (1908),  Heineke,  Miiller,  and  Hoesslin  (1908). 

Fibrosis  of  the  bundle,  6:  Schmoll  (1906),  Gibson,  G.  A.  (1906),  Fahr  (1907),  Gibson, 
A.  G.  (1908),  Dock,  G.,  Vaquez  and  Esmein. 

Tumors  in  the  septum:  Fibroma:  Sendler  (1892).     Round-celled  sarcoma:  Luce. 

Anasmic  infarction  of  the  auriculo  (atrio)  ventricular  bundle :  Jellinek,  Cooper,  Ophuls 
(1906),  MacCallum  (1908). 

Simple  round-celled  infiltration  of  the  auriculoventricular  bundle,  1 :  Heineke,  Miiller, 
and  Hoesslin  (1908). 

Mural  ulceration  involving  the  auriculoventricular  bundle  (ulcerative  endocarditis) : 

James  (1908). 

Fatty  degeneration :  Butler  (1907). 

Arteriosclerosis  of  artery  supplying  auriculoventricular  bundle :  D.  Gerhardt  (1908). 

Heart=block  in  Acute  Infections  and  Intoxications. — As  can  be  seen 
from  the  above  list,  a  considerable  number  of  cases  occur  during  the  course 
of  acute  febrile  diseases.  Dunn,  Fleming  and  Kennedy,  F.  W.  Peabody  and 
Tanaka  have  collected  these  cases  and  report  the  occurrence  of  heart-block 
and  the  Adams-Stokes  syndrome  in  rheumatic  fever,  ulcerative  endo- 
carditis, typhoid  fever,  pneumonia,  diphtheria,  as  well  as  in  the  gonorrheal 
infection  described  by  Jellinek,  Cooper,  and  Ophuls.  In  all  these  cases  the 
lesions  were  either  ulcerative  anaemic  necrosis  or  fibrous  degeneration  of  the 
His  bundle.  Tanaka  finds  that  the  lesions  of  the  conducting  system  do  not 
correspond  to  those  in  the  rest  of  the  heart  muscle.  In  a  few  cases  like  that 
reported  on  page  581,  heart-block  and  the  Adams-Stokes  syndrome  occur 
during  the  course  of  some  form  of  acute  gastro-intestinal  disturbance;  and 
may  then  be  transitory  (Taylor)  or  subject  to  recurrences  (case  on  page  581, 
also  reported  by  Thayer  and  Peabody). 

Heart=block  without  Demonstrable  Lesion  in  the  Auriculoventricular 
Bundle. — In  spite  of  the  anatomical  and  physiological  demonstrations  showing 
the  connection  between  lesions  of  the  auriculoventricular  bundle  and  heart- 
block  Heineke,  Miiller  and  Hoesslin,  and  Krumbhaar  and  B.  S.  Oppenheimer 
(Proc.  Soc.  Exper.  Biol,  and  Med.,  1913,  x,  86)  have  reported  cases  of  heart- 
block  during  life  with  no  demonstrable  lesions  of  the  bundle  at  autopsy.  The 
whole  literature  has  recently  been  compiled  by  W.  E.  Hume  (Heart,  1913,  iv, 
v,  149)  who  added  another  case. 

This  absence  of  even  microscopic  lesion,  however,  does  not  prove  that 
the  function  of  the  auriculoventricular  bundle  was  undisturbed:  In  Krumb- 
haar's  case  there  was  very  marked  atherosclerosis  of  the  coronary  arteries, 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        579 

and  it  seems  not  unlikely  that  there  may  have  been  some  ischsemia  of  the 
auriculoventricular  bundle  which  just  sufficed  to  diminish  conductivity. 
Experiments  showing  the  ready  production  of  heart=block  by  the  action  of 
various  drugs  and  poisons  and  by  asphyxia  without  the  production  of  demon- 
strable lesions  show  how  readily  heart-block  may  be  set  up.  And  since  it  is 
not  unusual  to  find  death  setting  in  from  failure  of  the  whole  heart  without 
the  presence  of  demonstrable  anatomical  lesions,  it  need  not  be  surprising 
if  such  lesions  are  sometimes  absent  during  functional  insufficiency  of  one 
part  of  the  heart,  the  auriculoventricular  bundle. 

CASES    OF    ADAMS-STOKES    SYNDROME    NOT    DUE    TO    LESION    OF    THE 
AURICULOVENTRICULAR   BUNDLE. 

Although  the  overwhelming  majority  of  cases  of  the  Adams-Stokes 
syndrome  (persistent  bradycardia,  complete  heart-block,  and  syncopal 
attacks)  have  been  proved  to  be  due  to  lesions  of  the  auriculoventricular 
bundle,  a  few  cases  in  the  literature  remain  which  must  be  regarded  as  due 
to  over-stimulation  of  the  vagus. 

The  most  typical  of  these  attacks  is  described  by  Thanhoffer  (1875).  A  colleague 
was  compressing  his  own  vagi  in  the  neck,  when  suddenly  he  "stared  at  me  with  glassy 
eyes,  without  releasing  his  grip  and  without  answering.  I  could  remove  his  fingers  from 
his  throat  only  with  the  greatest  force  and  they  still  remained  clenched.  Consciousness 
did  not  immediately  return  even  after  removing  his  fingers." 

Another  case  was  reported  by  Neuberger  and  Edinger  in  1898:  The  patient  was  a 
neurasthenic  man,  aged  46,  who  had  been  repeatedly  examined  by  various  physicians  but 
no  signs  of  organic  nervous  disease  discovered.  He  suffered  from  severe  constipation. 
From  Nov.,  1896,  to  January,  1897,  he  occasionally  fainted  when  at  stool.  His  pulse  dur- 
ing that  period  was  usually  60  between  attacks.  On  January  1,  1897,  he  fell  in  a  faint 
while  having  a  desire  to  go  to  stool;  his  head  and  eyes  were  drawn  to  the  left  and  the  eyes 
twitched.  During  that  day  he  had  several  similar  attacks,  before  each  of  which  the  pulse 
disappeared,  returning  during  the  attack  to  a  rate  of  16  to  18  per  minute.  By  evening  the 
rate  had  returned  to  60.  He  died  in  one  of  these  attacks  on  January  8.  Autopsy,  per- 
formed by  Carl  Weigert,  showed  almost  complete  atrophy  of  the  right  half  of  the  cere- 
bellum and  a  varicose  dilatation  of  the  ependymal  vessels  in  the  medulla.  It  is  probable 
that  at  stool  or  during  effort  the  pressure  in  these  varices  rose  and  caused  them  to  compress 
the  medulla  near  the  vagus  nucleus.  In  spite  of  a  very  careful  search  by  Weigert,  no  myo- 
cardial lesion  could  be  found.  It  is,  therefore,  fair  to  assume  that  in  this  case  the  attacks 
and  the  probably  existing  heart-block  were  vagal  in  origin. 

Dr.  Walter  James  also  reported  a  case  in  which  recurrent  groups  of  ineffectual  extra- 
systoles  caused  the  circulation  to  become  so  slow  at  times  as  to  produce  syncopal  attacks. 

A  somewhat  similar  case  was  that  of  Holberton  (1.  c.)  (1841),  in  which  the  attacks 
dated  from  a  fall  from  a  horse,  and  no  myocardial  lesion  was  found.  On  the  other  hand, 
our  case  (page  601)  illustrates  the  need  of  caution  in  reaching  this  conclusion,  since  there 
the  attacks  dated  from  a  blow  upon  the  head,  and  yet  autopsy  proved  the  presence  of  a 
most  typical  lesion  of  the  auriculoventricular  bundle.  Since  these  lesions  may  be  micro- 
scopic (Schmoll,  Gerhardt),  it  is  evident  that  a  neurogenic  origin  of  the  syndrome  can  be 
diagnosed  only  when  the  bundle  has  been  examined  by  serial  sections.  The  writer  has 
also  seen  in  consultation  a  case  of  complete  heart-block  associated  with  a  tumor  along  the 
course  of  the  vagus. 

Since  it  requires  a  very  considerable  lesion  to  produce  the  neurogenic 
syndrome,  and  since  death  occurs  from  the  latter  cause  as  well  as  from  the 
syndrome,  the  prognosis  is  no  better  in  these  cases  than  in  the  myogenic, 
except  in  cases  where  the  causal  factor  (tumor,  etc.)  may  be  removed  by 
operation  or  by  treatment.     However,  it  must  be  added  that  even  with 


580  DISEASES  OF  THE  HEART  AND  AORTA. 

the  most  liberal  interpretation  neurogenic  cases  are  relatively  rare,  and  the 
presence  of  the  Adams-Stokes  syndrome  may  in  most  cases  be  regarded  as 
'prima  facie  evidence  of  a  lesion  of  the  auriculoventricular  bundle. 

Atropine  Test. — The  origin  of  the  block  in  these  cases  can  be  readily 
demonstrated  by  paralyzing  the  vagi  by  the  administration  of  atropine, 
1  mg.  (¥V  gr-)>  which  causes  the  block  to  pass  off  in  the  neurogenic  cases  and 
the  pulse-rate  to  become  rapid,  but  does  not  affect  it  in  the  myogenic.  In 
most  cases  of  the  typical  Adams-Stokes  disease  (Edes,  Erlanger,  Schmoll), 
atropine  does  not  affect  the  rate,  and  the  organic  nature  is  further  proved. 
In  our  own  two  rather  exceptional  cases  the  atropine  test  was,,  unfortunately, 
not  permitted.  Gibson  and  Ritchie  have  reported  a  most  interesting  case  in 
which  both  neurogenic  and  myogenic  factors  seemed  to  be  at  work,  since  the 
complete  block  disappeared  promptly  upon  giving  atropine  and  reappeared  an 
hour  later  when  the  effect  had  worn  off.  However,  conductivity  was  always 
diminished  (conduction  time,  a-c  interval,  being  0.6  second  instead  of  0.2)  even 
when  the  vagi  were  paralyzed,  so  that  the  auriculo(atrio)  ventricular  bundle 
was  probably  injured  as  well.  Professor  Thayer  and  Dr.  F.  W.  Peabody  have 
found  that  atropine  caused  the  partial  block  (4  :  1  rhythm)  to  pass  off,  but 
had  no  effect  when  the  block  was  complete.  This  observation  harmonizes 
well  with  the  other  experimental  and  clinical  evidence  regarding  complete 
and  partial  blocks. 

CONTRIBUTING    FACTORS. 

The  Adams-Stokes  syndrome  is  more  common  in  men  (84  per  cent, 
of  Edes's  cases),  of  which  48  per  cent,  occurred  between  the  ages  of  50  and 
70.  This,  as  well  as  the  autopsy  series  mentioned  above,  establishes  the 
importance  of  coronary  sclerosis  as  an  etiological  factor.  It  is  quite  striking 
that  in  two  cases  of  this  small  series  (that  of  Cooper,  Jellinek,  and  Ophuls 
and  one  of  those  mentioned  by  Dietrich  Gerhardt)  gonorrhceal  infection  was 
the  etiological  factor.  Mackenzie  describes  cases  of  partial  heart-block 
(2  :  1  rhythm)  as  a  result  of  influenza  and  pneumonia,  and  the  writer  has 
seen  a  similar  depression  of  conductivity  during  the  course  of  the  latter. 
Powers  has  reported  a  case  with  partial  halving  of  the  rate  after  pneumonia. 
Saigo  has  found  extensive  vacuolization,  fatty  and  parenchymatous  degen- 
eration, and  cellular  infiltration  in  the  Purkinje  fibres  of  the  conduction 
system  following  acute  rheumatism  and  other  diseases. 

These  were  especially  marked  in  the  left  branch  of  the  auriculoventricular 
bundle.  The  importance  of  infectious  diseases  as  directly  causal  factors 
is  further  shown  by  the  case  of  Butler,  in  which  the  bradycardia  dated  from 
an  attack  of  typhoid  fever,  and  also  in  Dunn's  case,  in  which  a  radial  pulse 
(18  per  minute)  and  typical  Adams-Stokes  syndrome  occurred  in  a  boy 
of  11  on  the  ninth  day  of  diphtheria.  There  can  be  no  doubt  that  many 
of  the  sudden  deaths  from  pneumonia  and  diphtheria  are  due  to  heart-block. 

Cardiac  overstrain  may  also  be  a  factor,  as  in  the  case  of  a  boy  of  15 
reported  by  Strubing,  who  when  otherwise  healthy  ran  a  considerable  dis- 
tance, fainted,  then  walked  home,  and  had  several  other  syncopal  attacks 
with  convulsions.  His  heart  was  enlarged,  and  the  pulse  16  to  18  per  minute. 
Rest  and  proper  treatment  brought  some  improvement,  and  his  pulse  finally 
.rose  to  44,  but  he  died  soon  afterwards. 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.         581 

It  is  possible  that  ptomaine  poisoning  or  autointoxication  due  to  severe 
gastro-intestinal  upset  may  give  rise  to  the  syndrome. 

Case  of  Adams-Stokes  Disease  with  Subsidence  and  Recurrence  of  Symptoms, 
and  with  Attacks  during  Complete  Block. 

Recently  the  writer,  with  Professor  Thayer  and  Dr.  H.  M.  Thomas,  examined  a 
gentleman  who  had  lately  suffered  from  a  severe  acute  gastro-enteritis  with 
vomiting  and  severe  diarrhoea  lasting  several  days.  During  this  time  he  had  fainted  several 
times  while  at  stool,  and  his  physician  found  him  with  a  pulse-rate  of  20  per 
minute.  With  the  improvement  in  digestion  this  bradycardia  passed  off  within  a  few  days, 
and  he  had  no  further  syncopal  attacks.  When  examined  ten  days  later  his  pulse-rate 
was  60,  increasing  normally  upon  slight  exercise.  There  was  no  sign  of  heart-block,  and 
conduction  time  (a-c  interval)  was  normal  (0.2  second).  No  signs  of  nervous  disturb- 
ance were  present.  After  a  few  weeks  of  good  health  the  fainting  spells  and  bradycardia 
returned,  and  lasted  for  several  months.  Prof.  Thayer  informs  the  writer  that  during  this 
period  the  rhythm  varied  from  1:1  to  2:1,  and  4:1,  returning  to 
normal  rate  when  atropine  was  administered.  Syncopal 
attacks  also  occurred  frequently  in  the  midst  of  complete 
heart-block,  and  during  the  periods  of  complete  heart-block  the  rate  was  very  slow 
and  irregular.    In  complete  block  the  rate  was  unaffected  by  atropine. 

After  some  months  conductivity  gradually  returned,  and  at  the  time  of  writing  the 
patient  has  remained  quite  well  and  has  had  a  normal  pulse- 
rate   for  several  months. 

The  presence  of  a  hemorrhage  in  the  auriculoventricular 
bundle  or  its'  vicinity  (apoplexy  of  the  bundle)  would  ac- 
count for  the  occurrence  and  the  subsidence  of  these  symp- 
toms. An  infiltration  or  fatty  degeneration  of  the  bundle  might  account  for  the  occur- 
rence and  subsidence  of  the  first  attack,  but  scarcely  for  the  sudden  recurrence  during  a 
period  in  which  the  patient  had  been  in  excellent  health. 

Prentiss  also  mentions  a  case  brought  on  by  heavy  lifting,  in  which 
either  hemorrhage  or  myocardial  degeneration  may  have  been  the  cause. 

Partial  heart-block  is  very  common  after  overdoses 
of  digitalis  (Mackenzie,  Hewlett,  A.  G.  Gibson)  (page 249 and  Plate  XV), 
but  these  have  never  given  rise  to  complete  block  or  Adams-Stokes  syndrome. 

Heart=block  with  Auricular  Fibrillation  (Essential  Bradycardia). — A 
certain  number  of  cases  have  been  reported  in  which  the  ventricular  rate 
is  as  slow  as  in  the  ordinary  form  of  Adams-Stokes  disease.  The  venous 
pulse  is  of  the  "  single  "  ventricular  or  "  positive  "  type  and  no  regular  "A" 
wave  can  be  discerned  upon  it.  Mackenzie  formerly  believed  that  in  these 
cases  the  auricles  and  ventricles  were  beating  simultaneously,  but  studies 
with  the  electrocardiograph,  by  Thomas  Lewis  and  by  Thayer,  have  shown 
that,  on  the  contrary,  the  auricles  were  fibrillating,  but  their  impulses  were 
prevented  from  reaching  the  ventricles  by  an  auriculoventricular  block. 

As  very  many  of  the  impulses  from  the  fibrillating  auricle  are  smaller 
than  normal,  a  relatively  slight  injury  to  the  bundle  will  prevent  them  from 
passing,  especially  if  the  effect  of  this  is  enhanced  by  the  effect  of  digitalis. 

Indeed,  the  bradycardia  which  is  produced  intentionally  in  the  thera- 
peutic administration  of  digitalis  for  auricular  fibrillation  represents  a  partial 
blocking  of  the  impulses  between  the  auricles  and  the  ventricles.  This 
therapeutic  bradycardia  differs  from  the  essential  bradycardia  not  only  in 
the  fact  that  the  latter  is  spontaneous,  but  particularly  because  in  the  latter 
the  auriculoventricular  block  remains  complete,  and  the  ventricular  impulses 
arise  in  the  ventricle  or  the  Purkinje  fibres  below  the  auriculoventricular 


582  DISEASES  OF  THE  HEART  AND  AORTA. 

bundle.  In  these  cases,  as  in  the  ordinary  cases  of  heart-block,  the  important 
consideration  is  the  maintenance  of  a  sufficient  blood  flow  through  the  walls 
of  the  heart  and  brain;  this,  in  the  last  analysis,  depends  upon  keeping  up 
the  pulse-rate  and  the  blood-pressure. 

The  indications  for  treatment  in  this  condition  are  exactly  the  same  as 
in  the  ordinary  forms  of  Adams-Stokes  disease  and  will  be  discussed  as  such. 

Heart=block  with  a  Very  Rapid  Ventricular  Rate. — Hewlett  and  Bar- 
ringer  and  J.  D.  Windle  have  reported  cases  in  which,  in  spite  of  complete 
block,  the  rate  of  the  ventricle  was  beating  with  an  extremely  rapid  inde- 
pendent rhythm.  Hewlett  and  Barringer  have  shown  that  this  may  be 
brought  on  in  certain  cases  by  the  administration  of  digitalis,  although  in 
other  cases  it  probably  arises  spontaneously.  In  their  case  in  which  the 
ventricular  rate  reached  120  per  minute  in  spite  of  complete  block  the  rapid 
rate  may  have  represented  the  toxic  stage  of  digitalis  action ;  while  in  Windle's 
case  of  idiopathic  heart-block  the  ventricular  rate  ranged  between  50  and  60 
per  minute,  about  double  the  usual  ventricular  rate  in  complete  block. 

PHYSICAL   SIGNS   AND    DIAGNOSIS. 

As  the  Adams-Stokes  syndrome  may  occur  in  cases  having  valvular 
lesions,  the  physical  signs  over  the  heart  may  vary,  and  all  forms  of  mur- 
murs and  of  cardiac  insufficiency  may  occur.  Those  which  are  character- 
istic of  the  condition,  as  observed  by  Stokes  and  Chauveau,  are  the  very 
slow  pulse  disappearing  entirely  before  the  onset  of  the  attack;  the  presence 
of  small  visible  pulsations  in  the  jugulars,  of  more  than  double  the  number  of 
the  pulse  in  the  carotids,  with  the  small  jugular  pulsations  and  occurring  at  a 
regular  rhythm  which  is  more  rapid  than  that  of  the  ventricles;  a  faint  sound 
like  the  ticking  of  a  watch  may  often  be  heard  near  the  left  sternal  margin,  i.e., 
the  right  auricle;  and  a  slight  pulsation  or  shock  may  at  the  same  time  be 
seen  or  felt  over  the  apex.  On  barely  touching  the  radial  a  faint  shock  of  the 
same  rhythm  may  also  be  felt  in  the  radial  pulse.  This  corresponds  to  the 
small  auricular  wavelets  upon  the  pulse,  which,  as  Francois-Franck  has  shown, 
are  due  to  the  beating  of  the  auricles  against  the  root  of  the  aorta. 

If  the  number  of  diastolic  waves  over  the  vein  or  the  number  of  auricular 
sounds  varies  in  successive  diastoles,  the  heart-block  is  one  complete;  if  it  is 
constant  the  block  is  partial  (Hirschfelder,  Virginia  Med.  Semi-Monthly, 
1914,  xviii,  576). 

In  X-ray  examination  the  independent  contraction  of  the 
auricles  may  be  readily  seen  (Deneke),  and  this  of  course  settles  the  diagnosis. 
Similarly  G.  A.  Gibson  and  Einthoven,  as  well  as  Pick  and  Barker,  Bond, 
and  the  writer,  have  demonstrated  heart-block  by  the  electrocardiogram. 

The  usual  and  the  most  satisfactory  method  of  diagnosis  is  by  comparison 
of  the  venous  pulse  tracing  with  that  from  the  carotid  artery  or  the  apex, 
by  which  means  the  exact  relation  of  auricular  to  ventricular  contraction, 
the  degree  of  block,  and  the  variations  of  conductivity  are  readily  shown. 

Difficulties  in  diagnosis  may  occur  from  the  following  causes: 

1.  The  pulse-rate  may  be  so  slow  that  heart-block  may  be  suspected. 
This  occurs  especially  in  old  persons,  in  athletes  when  at  rest,  and  in  con- 
valescents from  infectious  diseases.  For  the  absolute  exclusion  of  heart- 
block  a  venous  tracing  may  be  necessary,  in  which  the  absence  of  a  wave 
midway  between  the  normal  a  waves  excludes  the  presence  of  a  heart-block. 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.         583 

The  writer  has  seen  a  number  of  cases  whose  pulse-rate  was  44  to  48  per 
minute  with  no  sign  of  heart-block  on  the  venous  tracing.    (Figs.  48  and  106.) 

2.  The  early  diastolic  wave  (h  wave  of  Hirschfelder,  b  wave  of  Gibson) 
may  sometimes  occur  midway  between  auricular  waves,  and  may  thus  simu- 
late a  2  : 1  rhythm.  Moreover,  the  "third  heart  sound"  is  usually  present  in 
these  cases,  and  may  easily  be  taken  for  the  sound  of  auricular  contraction. 
The  presence  of  the  h  wave  may  be  differentiated  from  that  of  partial  block  by 
increasing  the  heart-rate,  by  rapid  respiration,  mild  exercise,  etc.,  upon  which 
the  h  wave  is  no  longer  found  midway  between  a  waves,  but  maintains  its  old 
interval  from  the  v  wave  and  approaches  the  second  a,  whereas  in  partial 
heart-block  it  would  maintain  the  mid-position.  This  point  is  of  great  im- 
portance, since  the  presence  of  heart-block  is  a  grave  sign,  and  it  should  not 
be  diagnosed  without  due  care.  The  writer  has  seen  a  number  of  cases  in 
which  heart-block  might  have  been  diagnosed  had  this  precaution  not  been 
exercised,  as  for  example  the  patient  whose  phlebogram  is  shown  in  Fig.  106. 

Slow  pulse  of  vagal  origin  may  also  occur  in  brain  tumor,  fracture 
of  the  skull,  meningitis,  etc.,  and,  especially  in  the  first,  may  be  accompanied 
by  syncopal  attacks.  In  these  cases  there  is  rarely  any  degree  of  heart-block 
between  attacks,  and  the  site  of  the  cardiac  disturbance  can  readily  be  deter- 
mined by  its  disappearance  after  the  administration  of  atropine. 

A  slow  pulse  with  occasional  attacks  of  vertigo  may  also  occur  as  the  result 
of  extrasystoles  too  weak  to  open  the  aortic  valves,  and  thus  give 
rise  to  a  rhythm  which  is  too  slow  to  nourish  the  brain  (W.  James  and  Norris), 
and  a  true  Adams-Stokes  syndrome  arises  without  heart-block.  The  diag- 
nosis is,  however,  readily  made  on  auscultation,  from  the  fact  that  between 
effective  beats  a  single  loud  sound  is  heard  (whole  rhythm  being  lub  dub 

1  12  1 

lub,  pause, lub  dub  lub)  and  not  the  feeble  tickling  auricular  sound 

of  auricular  contractions.  The  venous  pulse  and  electrocardiogram  char- 
acteristic of  extrasystoles  (see  page  115)  establish  the  diagnosis. 

In  occasional  cases,  paroxysms  of  tachycardia  are  accompanied  by 
fainting  spells,  the  pulse  between  attacks  being  quite  normal  or  even  very  slow. 

Case  of  Paroxysmal  Tachycardia  Suggesting  Adams-Stokes  Disease. 

A  few  years  ago  the  writer  examined  such  a  case  in  consultation  with  Professor  Barker 
and  Dr.  I.  P.  Lyon  of  Buffalo.  The  patient  was  a  man  past  middle  age,  had  a  pulse-rate 
of  60,  and  had  been  subject  to  attacks  of  palpitation  with 'fainting  spells.  The  case  had 
been  seen  by  several  specialists  in  various  cities,  who  had  diagnosed  it  Adams-Stokes 
syndrome.  Physical  examination  was  negative  except  for  a  slight  grade  of  arteriosclerosis. 
Tracings  of  the  venous  pulse,  however,  showed  conductivity  to  be  normal  (a-c  interval 
0.2  second),  and  this  continued  to  be  the  case  even  when,  upon  exercise,  the  pulse-rate 
rose  to  120  per  minute  without  dropping  a  beat.  The  Adams-Stokes  syndrome  was  thus 
excluded.  From  the  sudden  onset  and  the  fainting  spells  during  the  attacks,  it  was  con- 
cluded that  the  condition  was  most  probably  paroxysmal  tachycardia.  The  patient  was 
subsequently  seen  in  a  typical  attack,  with  sudden  approximate  doubling  and  sudden 
halving  of  the  rate,  and  the  diagnosis  was  thus  verified.  Dr.  Lyon  informs  the  writer  that 
the  patient  is  much  improved  and  has  now  only  mild  attacks  of  tachycardia. 

Case  of  Heart-Block  of  Long  Duration. 

In  1910  the  writer,  in  consultation  with  Prof.  L.  F.  Barker,  examined  a  gentleman 
over  sixty  years  of  age,  whose  pulse-rate  was  from  30  to  35  per  minute,  in  whom  venous 
pulse  and  electrocardiogram  showed  a  complete  heart-block.     From  the  accounts  of  his 


584  DISEASES  OF  THE  HEART  AND  AORTA. 

family  his  pulse  had  maintained  this  rate  for  at  least  thirty-five  years,  during  which,  to 
the  great  alarm  of  his  physicians,  he  had  led  an  active  life  free  from  symptoms  of  cardiac 
weakness,  and  devoid  of  cardiac  symptoms  until  a  few  extrasystoles  with  palpitation  ap- 
peared a  few  years  ago.  These  extrasystoles  produced  no  ill  effects  on  the  circulation,  and 
at  last  accounts  he  was  maintaining  perfect  health. 

Extrasystoles  Simulating  Heart=BIock. — Walter  James  and  Norris  have 
reported  typical  syncopal  bradycardia  due  to  the  occurrence  of  ventricular 
extrasystoles  too  weak  to  open  the  aortic  valves  and  to  the  length  of  the  pauses 
between  effectual  pulse  waves.  Such  cases  should  be  easily  differentiated 
from  true  heart-block  by  simple  inspection,  for  no  extra  waves  occur  upon  the 
venous  pulse  in  diastole,  and,  moreover,  the  loud  sharp  heart  sounds  accom- 
panying the  ventricular  extrasystole  can  easily  be  differentiated  from  the 
feeble,  just  audible  sound  that  is  produced  by  the  auricle.  The  circulation 
of  the  blood  through  the  body  in  such  cases  is  accordingly  maintained  entirely 
by  the  regular  forcible  heart-beats,  although  the  venous  pulse  or  the  cardio- 
gram shows  that  the  ventricle  is  beating  during  the  whole  period. 

There  may  occasionally  be  difficulty  in  differentiating  the  Adams- 
Stokes  syndrome  from  epilepsy  and  brain  tumor.  Heart-block  is,  however, 
never  present  in  the  former,  very  rarely  in  the  latter;  so  that  the  diagnosis 
can  usually  be  made  from  simple  inspection  of  the  jugular  vein.  If  necessary, 
venous  tracings,  supplemented  by  the  atropine  test,  may  be  resorted  to. 

PROGNOSIS, 

The  course  of  cases  suffering  from  the  Adams=Stokes  syndrome  is  very 
variable.  It  is  probable  that  many  cases  die  in  the  first  attack,  but  the 
condition  remains  undiagnosed  or  is  ascribed  to  coronary  sclerosis.  It  is 
not  unlikely  that  histological  examinations  of  many  cases  of  sudden  death 
would  reveal  lesions  in  the  bundle  of  His  or  its  artery.  In  some  cases  death 
occurs  within  a  few  weeks  or  months  after  the  first  attack,  but  in  very  many 
the  heart-block  may  last  for  many  years,  with  or  without  disappearance 
of  the  syncopal  attacks.  Many  cases  of  Edes's  series  lived  seven  or  eight 
years  after  the  first  attack.  Osier's  case  lived  thirty,  our  patient  has  lived 
thirty-six  years  after  the  onset  of  bradycardia. 

It  is  stated  that  the  pulse-rate  of  Julius  Caesar  and  of  Napoleon  were 
abnormally  slow  (Napoleon's  being  sometimes  40,  but  at  Elba  50  to  55), 
and  that  the  epilepsy  of  the  latter  was  a  sign  of  the  Adams-Stokes  syndrome, 
but  this  is  not  proved.  However,  it  is  certain  that  the  presence  of  com- 
plete heart-block  is  compatible  with  ability  to  do  a  considerable  amount  of 
work.  Vigouroux  had  under  observation  a  laborer  with  complete  heart- 
block  who  during  five  years  did  hard  work,  driving  a  cart  with  six  oxen  in 
the  hottest  weather.  His  heart  always  beat  at  a  rate  of  20.  Dr.  Archibald 
Hewan  was  able  to  climb  a  mountain  several  thousand  feet  high  when  his 
pulse  ranged  from  32  to  40  and  never  rose  above  the  latter.  Most  of  the 
cases  die  in  the  attacks  (Edes),  but  death  from  coronary  sclerosis  without 
Adams-Stokes  syndrome,  as  in  our  case,  is  not  uncommon.  Gerhardt  has 
recently  reported  three  cases  in  which  not  only  the  syncopal  attacks  but 
also  the  heart-block  completely  disappeared,  owing  to  subsidence  of  the 
pathological  process  in  the  auriculoventricular  bundle  which  was  not  totally 
destroyed.    Prof.  Thayer's  case,  quoted  above,  probably  belongs  to  this  group. 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        585 

TREATMENT   OF   HEART-BLOCK   AND   THE   ADAMS-STOKES   DISEASE. 

The  problem  of  the  treatment  of  Adams-Stokes  disease  presents  several 
distinct  phases  and  aims.  1.  To  bring  about  retrogression  of  the  lesion  to 
the  bundle.  2.  To  remove  as  many  factors  as  possible  which  tend  to  increase 
the  block.  3.  To  increase  the  irritability  and  rhythmicity  of  the  ventricular 
muscle,  so  as  to  shorten  the  periods  of  stoppage  and  to  increase  the  rate 
of  the  ventricles. 

Retrogression  of  the  lesion  in  the  bundle  can  be  brought  about  by  medi- 
cation only  in  the  cases  of  syphilitic  origin,  in  which  the  gummata  and  luetic 
infiltrations  may  sometimes  be  made  to  subside  under  vigorous  treatment 
with  iodides  and  inunctions  of  mercury.  Sodium  or  potassium  iodide  should 
be  given  in  doses  gradually  increasing  up  to  4  Gm.  (3i)  or  more  three  times  a 
day,  and  these  along  with  mercury  should  be  kept  for  long  periods  and  re- 
sumed at  frequent  intervals.  In  a  considerable  number  of  cases,  as  in  those 
reported  by  Schmaltz  and  by  Erlanger,  subsidence  of  the  lesion  may  be 
accomplished  and  the  heart-rate  restored  to  normal.  In  these  cases  Ehrlich's 
salvarsan  ("  606  ")  would  be  very  desirable  if  it  could  be  administered,  but 
in  its  present  mode  of  administration  it  is  too  dangerous  to  use. 

In  non-luetic  lesions,  medication  is  of  little  use,  but  it  is  important  to 
put  the  patient  at  complete  rest  for  as  long  a  period  as  practicable,  in  the 
hope  that  by  reducing  the  strain  upon  the  heart  as  far  as  possible  cedema, 
infiltration,  and  hemorrhages  may  be  gradually  absorbed  or  at  least  may 
suffer  no  further  increase. 

In  the  cases  in  which  the  lesion  itself  cannot  be  caused  to  subside,  espe- 
cially in  cases  in  which  the  block  is  a  partial  one,  it  may  be  possible  to  bring 
about  an  improvement  which  is  sometimes  temporary  and  which  may  some- 
times last  for  several  weeks  or  even  months  by  the  administration  of 
atropine  (Gibson  and  Ritchie,  Thayer  and  Peabody).  This  removes  the 
effect  of  tonic  action  of  the  vagus. 

In  patients  in  whom  the  heart-block  is  due  to  a  combination  of  a  vagal 
and  a  muscular  element,  a  double  vicious  circle  is  operating: 

Vagal  block 

/ 

/    Muscular 

/        block 

/    /     \ 

Asphyxia  of      Slowing 

the  heart  ■< of  the 

muscle  circulation 

The  administration  of  atropine,  by  removing  the  vagal  block  and  increas- 
ing the  velocity  of  the  circulation,  also  improves  the  nutrition  of  the  auric- 
uloventricular  bundle  and  may  do  so  to  an  extent  that  permits  it  to  regain 
its  function.  In  patients  in  which  the  block  is  due  entirely  to  the  muscular 
lesion,  however,  as  Erlanger  and  Hirschfelder  have  shown,  the  degree  of 
block  is  entirely  unaffected  by  atropine  or  may  even  be  increased  somewhat 
by  the  increase  in  the  pulse-rate. 

In  the  cases  of  partial  heart-block  digitalis  is  usually  either  without 
effect  or  positively  harmful,  since,  as  v.  Tabora  has  shown,  it  diminishes  the 


586  DISEASES  OF  THE  HEART  AND  AORTA. 

conductivity  of  the  auriculoventricular  bundle,  although  this  effect  is  some- 
what lessened  by  the  administration  of  atropine. 

On  the  other  hand,  the  duration  of  ventricular  stoppage  brought  on  by 
clamping  the  bundle  with  an  Erlanger  clamp  is  greatly  diminished  by  digi- 
talis, as  v.  Tabora  has  shown.  Other  drugs  seem  to  have  little  effect  in  influ- 
encing the  duration  of  stoppage  and  the  onset  of  syncope.  August  Hoffmann 
reports  a  case  in  which  inhalations  of  oxygen  afforded  distinct  relief,  and  this 
measure  is  worthy  of  trial  in  every  case.  In  most  cases  little  benefit  need  be 
expected,  for  during  the  cessation  of  the  pulse  the  blood  does  not  circulate 
from  the  lungs  to  the  brain. 

Peculiar  postures  sometimes  help  in  warding  off  syncopal  attacks  by 
improving  the  blood  through  the  brain  until  the  ventricular  rhythm  has 
become  established.  Stokes  (1846)  writes  that  his  patient  "  had  two  threaten- 
ings  of  fits  since  his  admission,  and  warded  both  off  by  a  peculiar  manoeuvre : 
as  soon  as  he  perceives  symptoms  of  the  approaching  attack  he  directly  turns 
on  his  hands  and  knees,  keeping  his  head  low,  and  by  this  means  he  says  he 
often  averts  what  otherwise  would  end  in  an  attack."  This  was  the  patient's 
physiological  therapy  to  prevent  cerebral  anaemia.  Another  patient  has  been 
reported  who  made  use  of  a  similar  procedure  by  lying  on  the  floor  and  rais- 
ing his  legs  upon  the  arms  of  a  chair,  by  which  he  obtained  still  better  filling 
of  the  cerebral  vessels. 

After  the  complete  block  has  once  been  established,  the  patient  is  still 
beset  with  three  dangers: 

1.  The  circulation  under  the  regular  ventricular  rhythm  may  be  too 
slow  to  nourish  the  brain  and  the  tissues,  including  the  heart  itself,  and  the 
patient  may  thus  be  kept  a  bedridden  invalid  or  may  even  die  as  the  result. 

2.  The  ventricular  rate  may  become  irregular,  through  the  appearance 
of  ventricular  extrasystoles  and  even  of  periods  of  stoppage  during  complete 
heart-block,  exactly  similar  to  those  occurring  at  the  onset  of  the  block,  and 
syncope  or  death  may  occur,  as  in  the  latter. 

3.  The  block  may  pass  off  spontaneously,  the  rate  and  rhythm  become 
normal,  but  the  condition  become  so  unstable  that  the  patient's  life  becomes 
constantly  endangered  by  the  possible  onset  of  heart-block,  stoppage,  and 
the  Adams-Stokes  syndrome. 

Though  no  drug  is  specific  for  these  conditions,  v.  Tabora  and  also 
Erlanger  have  shown  that  digitalis  increases  the  ventricular  rate  in  experi- 
mental complete  block,  and  Bachmann  found  that  the  rate  of  a  ventricle 
of  a  patient  with  the  Adams-Stokes  syndrome  was  accelerated  during  com- 
plete heart-block  and  the  patient's  condition  somewhat  improved.  Hewlett 
and  Barringer  and  others  have  confirmed  these  observations,  and  it  appears 
certain  that  more  or  less  acceleration  of  the  independently  beating  ventricles 
may  be  obtained  with  drugs  of  the  digitalis  series. 

This  acceleration  of  rate,  as  long  as  it  is  not  accompanied  by  weakening 
of  the  heart-beat,  is  a  thing  to  be  desired,  but  it  must  not  be  forgotten  that 
acceleration  of  the  ventricles  may  appear  during  the  last  stages  of  digitalis 
poisoning,  and  therefore  the  mere  acceleration  of  the  ventricular  rate  does 
not  necessarily  indicate  an  improvement  in  the  circulation.  Similarly,  the 
maximal  blood-pressure  may  fall  either  from  better  nutrition  of  the  vaso- 
motor centre  in  the  medulla  or  fiom  the  fact  that  with  the  increasing  pulse- 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        587 

rate  the  pulse-pressure  for  each  beat  is  diminished.  The  best  index  is,  there- 
fore, the  general  condition  of  the  patient,  his  ease  of  respiration,  clearness 
of  mind,  and  bodily  activity. 

Drugs  of  the  digitalis  series,  therefore,  are  contraindicated  in  partial 
heart-block,  but  should  be  used. as  soon  as  the  block  has  become  complete. 

Other  drugs  seem  to  be  entirely  without  effect:  caffeine,  theobromine, 
strychnine,  and  amyl  nitrite  have  all  been  used  by  certain  writers,  but  with- 
out special  benefit  to  the  patient,  and  the  writer  has  been  unable  to  find  any 
effect  from  them  upon  the  ventricular  rate  in  complete  heart-block  in  dogs. 

Ammonium  carbonate  has  not  been  extensively  employed,  although 
Burnett  claimed  to  have  been  able  to  abort  attacks  in  his  patients  by  its  use. 

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Physiol.,  Bost.,  1906,  xv,  153. 

Erlanger,  J.,  Blackman,  J.  R.,  and  Cullen,  E.  K.:  Further  Studies  on  the  Physiology  of 
Heart-block  in  Mammals,  ibid.,  1908,  xxi,  p.  xviii. 

v.  Kries,  J.:  Ueber  eine  Art  polyrhythmischer  Herzthatigkeit,  Arch.  f.  Physiol.,  Leipz., 
1902,  477. 

Buchanan,  F.:  The  Frequency  of  the  Heart-beat  in  the  Sleeping  and  Waking  Dormouse, 
J.  Physiol.,  Camb.,  1910,  xl,  Proc.  Physiol.  Soc,  p.  xlii. 

Lewis,  T.,  and  Oppenheimer,  B.  S.:  The  Influence  of  Certain  Factors  upon  Asphyxial 
Heart-block,  Quart.  J.  M.,  Oxford,  1911,  iv,  145. 

Lewis,  T.,  and  Mathison,  G.  C. :  Auriculoventricular  Heart-block  as  a  Result  of  Asphyxia, 
Heart,  Lond.,  1911,  ii,  47. 

Gossage,  A.  M.:  Independent  Ventricular  Rhythm,  Heart-block  and  the  Adams-Stokes 
Syndrome  without  Affection  of  the  Conductivity,  Heart,  Lond.,  1909-1910,  i,  283. 

Gibson,  G.  A.:  Certain  Clinical  Features  of  Heart  Disease,  Johns  Hopkins  Hosp.  Bull., 
Bait.,  1908,  xix,  361. 

Dunn,  A.  L. :  Atrioventricular  Dissociation  following  Diphtheria,  J.  Am.  M.  Asso.,  Chicago, 
1908,  1,  1985. 

Luce,  H.:  Zur  Klinik  und  Pathologische  Anatomie  des  Adams-Stokes'schen  Symptomen- 
complexus,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1902,  lxxiv,  370. 

Stengel,  A.:  Fatal  Case  of  Stokes-Adams  Disease,  with  Autopsy,  Am.  J.  M.  Sc,  Phila., 

1905,  cxxx,  1083. 

Schmoll,  E.:  Adams-Stokes  Disease,  J.  Am.  M.  Asso.,  Chicago,  xlvi,  361.  Zwei  Falle 
von  Adams-Stokes'scher  Krankheit  mit  Dissoziation  von  Vorhof  und  Kammerrhyth- 
mus  und  Lasion  des  His'schen  Bundels,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1906, 
lxxxvii,  554. 

Handford:  Brit.  M.  J.,  Lond.,  1904,  ii,  1745. 

Keith,  A.,  and  Miller,  C:  Lancet,  Lond.,  1906,  ii,  1429. 

Griinbaum,  also  reported  by  Keith  and  Flack  (1.  c). 

Ashton,  T.  G.,  Norris,  G.  W.,  and  Lavenson,  R.  S.:  Adams-Stokes  Disease  (Heart-block) 
due  to  a  Gumma  in  the  Interventricular  Septum,  Am.  J.  M.  Sci.,  Phila.  and  N,  Y., 

1907,  cxxxii,  28. 

Heineke:  Drei  Falle  von  Adams-Stokes'scher  Krankheit,  Berl.  klin.  Wchnschr.,  1907,  xliv,l  125. 
Fahr:  Ueber  die  muskulare  Verbindung  zwischen  Vorhof  und  Ventrikel  (das  His'sche 

Bundel)  im  normalen  Herzen  und  beim  Adams-Stokes'schen  Symptomenkomplex, 

Arch.  f.  path.  Anat.,  etc.,  Ber.,  1907,  clxxxviii,  562. 
Rendu:  Soc.  med.  d.  hop.,  1895.    Quoted  from  James,  W.  B.:  Am.  J.  M.  Sci.,  Phila.  and 

N.  Y.,  1908,  cxxxvi,  469. 
Hay,  J.,  and  Moore,  S.  A.:  Stokes-Adams  Disease  and  Cardiac  Arrhythmia,  Lancet,  Lond., 

1906,  ii,  1271. 

Gibson,  G.  A.:  Heart-block,  Brit.  M.  J.,  Lond.,  1906,  ii,  1113. 

Gibson,  A.  G.:  The  Heart  in  a  Case  of  Stokes-Adams  Disease,  Quart.  J.  M.  Sci.,  Oxford, 

1908,  i,  183. 

Vaquez  and  Esmein:  Presse  m<5d.,  1907,  xv,  57. 

Sendler:  Beitrag  zur  Frage  ueber  Bradycardie,  Centralbl.  f.  innere  Med.,  Leipz.,  1892, 
xiii,  642. 

Jellinek,  Cooper,  Ophuls:  The  Adams-Stokes  Syndrome  and  the  Bundle  of  His,  J.  Am.  M. 
Asso.,  Chicago,  1906,  xlviii,  955. 

MacCallum,  W.  G. :  Stokes- Adams  Disease  with  Infarction.  Read  before  the  Johns  Hop- 
kins Medical  Society,  Nov.  4,  1907. 

Heineke,  A.,  M  tiller,  A.,  and  v.  Hoesslin,  A. :  Zur  Kasuistik  des  Adams-Stokes'schen  Symp- 
tomenkomplexes  und  der  Ueberleitungsstorungen,  Deutsch.  Arch.  f.  klin.  Med., 
Leipz.,  1908,  xciii,  459. 


HEART-BLOCK  AND  ADAMS-STOKES  SYNDROME.        589 

James,  W.  B.:  A  Clinical  Study  of  some  Arrhythmias  of  the  Heart,  Am.  J.  M.  Sci.,  Phila. 

and  N.  Y.,  1908,  cxxxvi,  469. 
Norris,  G.  W. :  Extrasystolic  Arrhythmia  Simulating  Heart-block,  Univ.  Penn.  M.  Bull., 

Phila.,  1910,  xxii,  342. 
Butler,  G.  R.:  Heart-block  (Adams-Stokes  Disease),  Am.  J.  M.  Sci.,  Phila.  and  N.  Y., 

1907,  cxxxiii,  715. 

Gerhardt,    D.:      Ueber    Ruckbildung    des    Adams-Stokes'schen     Symptomenkomplexes, 

Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1908,  xliii,  485. 
Edes,  R.  T.:  Slow  Pulse,  with  Especial  Reference  to  Stokes-Adams  Disease,  Trans.  Asso. 

Am.  Phys.,  Phila.,  1901,  xvi,  521. 
Thanhoffer:  Centralbl.  f.  d.  med.  Wissensch.,  1875,  405.    Quoted  from  His. 
Fleming,  G.  B.,  and  Kennedy,  A.  M.:  A  Case  of  Complete  Heart-block,  with  an  Account 

of  Post-mortem  Findings,  Heart,  Lond.,  1910-11,  ii,  77. 
Peabody,  F.  W. :  Heart-block  Associated  with  Infectious  Diseases,  Arch.  Int.  Med.,  Chicago, 

1910,  v,  252. 
Taylor,  F.  L.:  A  Case  of  Transient  Heart-block  due  to  Intestinal  Toxaemia,  J.  Am.  M. 

Assoc,  1708,  i,  1246. 
Thayer,  W.  S.,  and  Peabody,  F.  W.:  A  Study  of  Two  Cases  of  Adams-Stokes  Syndrome 

with  Heart-block,  Arch.  Int.  Med.,  Chicago,  1911,  vii,  289. 
Tanaka,  T.:  Ueber  die  Veranderungen  der  Herzmuskulatur  vor  allem  des  Atrioventrieu- 

larbundel  bei  Diphtherie,  Arch.  f.  path.  Anat.,  etc.,  Berl.,  1912,  ccvii,  115. 
Krumbhaar,  E.  B.:  Adams-Stokes  Syndrome  with  Complete  Heart-block  without  Destruc- 
tion of  the  Bundle  of  His,  Arch.  Int.  Med.,  Chicago,  1910,  v,  583. 
Neuburger,  Th.,  and  Edinger,  L.:    Einseitiger  fast  totaler  Mangel  des  Cerebellums,  Varix 

oblongata?  Herztod  durch  Accessoriusreizung,  Berl.  klin.  Wchnschr.,  1898,  xxxv,  69. 
Gibson,  G.  A.,  and  Ritchie,  W.  T.:  Further  Observations  on  Heart-block,  Practitioner, 

Lond.,  1907,  i,  587. 
Mackenzie,  James:  New  Methods  of  Studying  the  Affections  of  the  Heart,  Brit.  M.  J., 

1905,  i,  519,  587,  702,  759,  812. 

Saigo,  Y.:  Die  Purkinjeschen  Muskel  fasern  bei  Erkrankungen  des  Myokards,  Verh.  d. 

Deutsch.  path.  Ges.,  Jena,  1908,  xii,  165. 
Dunn,  A.  D. :  Atrioventricular  Dissociation  following  Diphtheria,  J.  Am.  M.  Asso.,  Chicago, 

1908,  1,  1985. 

Strubing:  Deutsch.  med.  Wochnsch.,  Leipz.,  1893.    Quoted  from  Edes. 

Hewlett,  A.  W.:  Digitalis  Heart-block,  J.  Am.  M.  Asso.,  Chicago,  1907,  xlviii,  47. 

Gibson,  A.  G.:  The  Action  of  Digitalis  on  the  Human  Heart,  Quart.  J.  M.  Sc,  Oxford, 

1907,  i,  173. 
Lewis,  T.,  and  Mack,  E.  G.:  Complete  Heart-block  and  Auricular  Fibrillation,  Quart. 

J.  M.,  Oxford,  1909-10,  iii,  273. 
Deneke:  Zur  Rontgendiagnostik  seltener  Herzleiden,  Deutsches  Arch.  f.  klin.  Med.,  Leipz., 

1906,  lxxxix,  39. 
Einthoven,  W.    Quoted  on  page  96. 

Pick,  F.:  Zur  Klinik  des  Elektrocardiogramms  (Discussion),  Verhandl.  d.  Kong.  f.  innere 

Med.,  Wiesbaden,  1909,  xxiv,  653. 
Barker,  L.  F.,  Hirschfelder,  A.  D.,  and  Bond,  G.  S.:  The  Electrocardiogram  in   Clinical 

Diagnosis,  J.  Am.  M.  Ass.,  Chicago,  1910,  lv,  1350. 
Schreiber,  E.:    Ueber  Herzblock  beim  Menschen,  Deutsches  Arch.  f.  klin.  Med.,  Leipz., 

1906,  lxxxix,  277. 
Vigouroux:  Gaz.  d.  h6p.,  Par.,  1876.    Hewan,  A.    Quoted  from  Edes. 
Schmaltz:  Zur  Kenntniss  der  Adams-Stokes'scher  Krankheit,  Munchen.  med.  Wchnschr., 

1905,  lii,  1120. 
Erlanger,   J.:   Ueber  die  Mode  der  Vaguswirkung  auf  die  Kammern  des  Hundeherzens, 

Arch.  f.  d.  ges.  Physiol.,  Bonn,  1909,  cxxvi,  77. 
Bachmann,  G. :  Sphygmographic  Study  of  a  Case  of  Complete  Heart-block;  A  Contribu- 
tion to  the  Study  of  the  Action  of  Strophanthus  in  the  Human  Heart,  Arch.  Int.  Med., 

Chicago,  1909,  iv,  238. 
Hewlett,  A.  W.,  and  Barringer,  T.  B.:    The  Effect  of  Digitalis  on  the  Ventricular  Rate  in 

Man,  Arch.  Int.  Med.,  Chicago,  1910,  v,  93. 
Windle,  J.  D. :  Permanent  Complete  Heart-block,  A  Case  with  an  Exceptionally  Frequent 

Ventricular  Rate,  Heart,  Lond.,  1910-11,  ii,  102. 


XII. 

PERICARDITIS. 

Historical. — The  presence  of  changes  in  the  pericardium  in  animals 
was  known  to  Galen,  and  Senac  in  1749  described  the  condition  in  man. 
Auenbrugger  and  later  Corvisart  were  able  to  make  out  changes  in  dul- 
ness  due  to  pericardial  effusions.  Laennec  detected  the  murmur  of  fibrin- 
ous pleurisy,  and  described  it  as  resembling  the  creaking  of  a  new  saddle, 
but  its  diagnostic  significance  was  positively  established  by  Collin  and  by 
Devilliers  in  1824. 

ETIOLOGY. 

The  frequency  with  which  pericarditis  occurs  varies  greatly  according 
to  various  observers,  and  particularly  according  to  the  age  of  their  patients. 
It  seems  to  be  considerably  more  common  in  children  than  in  adults  with 
cardiac  disease,  as  stated  by  Poynton,  as  it  accompanied  endocarditis 
and  myocarditis  in  94  per  cent,  of  Sturges's  cases  of  heart  disease  (carditis) 
from  the  Great  Ormond  Street  Children's  Hospital.  This  is  in  accordance 
with  the  somewhat  exaggerated  statement  of  Cadet  de  Gassicourt  that  all 
children  who  are  killed  by  rheumatism  die  from  pericarditis;  but  it  applies 
more  to  children  of  the  second  decade  than  of  the  first,  since  death  from 
rheumatic  affections  is  most  common  in  the  second  decade.  Pericarditis 
was  found  in  19  of  Osier's  73  autopsies  upon  cases  of  chorea.  Pericar- 
ditis occurred  in  230  (1  per  cent.)  of  the  cases  admitted  to  the  medical 
service  of  the  Johns  Hopkins  Hospital.  Of  these  53  were  associated  with 
endocarditis;  8  with  myocarditis.  Other  factors  were  pneumonia  39; 
rheumatism  31;  nephritis  33;  tuberculosis  25;  pleurisy  17;  gonorrhoea  3; 
aneurism  2;  leukaemia  2;  syphilis  1.  Rheumatism  occurred  in  51  per  cent, 
of  the  100  cases  reported  by  Sears  from  the  Boston  City  Hospital.  This 
relationship  between  pericarditis  and  rheumatism  has  been  proved  experi- 
mentally by  Wasserman,  Triboulet,  Poynton  and  Paine,  Walker,  Cole  and 
Beattie  (page  387). 

Pneumonia  is  also  one  of  the  common  causes  of  pericarditis  (18  per 
cent,  of  Sears's  series),  and  usually  ranks  next  to  the  rheumatic  cycle  as  an 
etiological  factor.  Pericarditis  was  present  in  4.66  per  cent,  of  the  cases  of 
pneumonia  at  the  Johns  Hopkins  Hospital  (Chatard),  and  in  2-3  per  cent, 
of  Preble's  series  in  Chicago.  According  to  the  latter  observer  its  relative 
frequency  is  about  proportional  to  the  extent  and  severity  of  the  disease. 
This  claim  is  also  borne  out  by  Chatard's  statistics  (frequency  of  15.7  per 
cent,  in  the  cases  coming  to  autopsy).  Moreover,  the  appearance  of  an 
acute  pericarditis  in  the  course  of  the  disease  is  a  very  grave  sign,  for 
only  two  cases  (6.5  per  cent.)  of  Chatard's  series  recovered. 
590 


PERICARDITIS.  591 

Pericarditis  is  also  common  in  scarlatina  (especially  with  strepto- 
coccus infection),  in  severe  measles,  and  in  smallpox.  In  the  latter  it  is 
frequently  purulent. 

Tuberculous  pericarditis  is  quite  common  (8  per  cent,  of  Breitung's 
autopsies),  and  in  contrast  to  the  rheumatic  form  rarely  subsides.  It  often 
ends  in  effusion. 

The  pericarditis  of  chronic  nephritis  and  uraemia  constitutes  a  frequent 
termination  of  this  disease,  though  it  is  by  no  means  always  fatal.  It  is 
usually  due  to  an  intercurrent  infection,  and  the  pyogenic  cocci  can  often 
be  cultivated  from  the  exudate. 

Pericarditis  may  also  result  as  a  secondary  infection  in  septicaemia  and 
in  puerperal  infections  as  well  as  in  gonorrhoea,  especially  when  there  is 
accompanying  arthritis.  It  is  rare  in  typhoid  fever  (3  times  in  McCrae's 
1500  cases) ;  occurs  occasionally  in  influenza;  and  sometimes  results  from 
septicaemias  due  to  B.  coli,  B.  aerogenes  capsulatus,  B.  pyocyaneus,  etc. 

Trauma  without  direct  injury  of  the  pericardium  or  viscera  was  the 
cause  of  pericarditis  in  Blancard's  case  in  1688,  and  a  large  number  of  cases 
due  to  this  cause  were  collected  by  Bernstein  in  1896.  Blows  upon  the  chest, 
wagon  running  over  the  body,  etc.,  are  the  common  causes. 

FORMS    OF    PERICARDIAL    EXUDATION. 

The  exudate  into  the  pericardial  cavity  may  assume  various  forms. 
In  simple  venous  stasis  and  asphyxia  of  the  endothelial  cells  (hydro- 
pericardium)  a  clear  thin  fluid  of  low  specific  gravity,  relatively  poor  in 
proteid  and  especially  in  fibrinogen,  is  secreted.  When  there  is  true  inflam- 
mation of  the  pericardium,  the  exuded  fluid  is  rich  in  fibrinogen  and  of  rela- 
tively high  specific  gravity  (over  1015)  and  contains  nucleo-albumen 
(clouding  with  acetic  acid).  Samuel  has  shown  that  when  the  exudate  is 
poor  in  fibrin  ferment  it  remains  fluid  (pericarditis  with  effusion) ,  whereas 
when  this  is  present  the  fibrinogen  coagulates  (fibrinous  pericar- 
ditis). According  to  Opie,  the  enzymes  are  derived  chiefly  from  the 
leucocytes,  especially  the  polymorphonuclears,  and  hence  the  amount  of 
fibrin'  deposited  depends  largely  upon  the  number  of  these  cells  present. 
Moreover,  since  these  cells  pass  out  from  the  blood-vessels,  the  fibrin  is  first 
and  most  thickly  deposited  in  the  vicinity  of  the  latter, — i.e.,  along  the 
epicardium  above  the  circumflex  and  descending  rami  of  the  large  coronary 
arteries,  where  it  begins  in  the  form  of  strands  passing  out  from  about 
the  leucocytes,  and  hence  gives  the  heart  a  shaggy  appearance  (cor  villosum, 
Fig.  279) .  This  layer  of  fibrin  usually  has  the  appearance  and  consistency 
of  a  yellow  batter.  When  fresh  it  is  not  very  adherent  to  the  heart,  and 
may  reach  a  thickness  of  an  inch  or  more.  There  may  be  no  fluid  in  the 
pericardial  cavity,  but,  as  a  rule,  both  fibrin  and  fluid  are  present,  the 
latter  often  in  large  quantities.  The  fluid  is  usually  thick,  containing 
uncoagulated  fibrinogen  as  well  as  small  flaky  masses  of  fibrin,  which  may 
render  it  too  thick  to  be  removed  by  aspiration.  When  the  exudate  is 
extremely  rich  in  bacteria  and  leucocytes,  the  proteolytic  enzymes  are 
given  off,  which  digest  the  fibrin,  and  the  fluid  becomes  purulent. 

When  the  fibrinous  exudate  of  a  simple  pericarditis  is  absorbed  rapidly, 
it  leaves  no  traces  and  the  pericardium  again  becomes  clear.    But  when  it 


592 


DISEASES   OF   THE   HEART   AND    AORTA. 


lasts  for  some  time  and  the  resolution  is  slow,  organization  takes  place, 
and  white  patches  of  pericardial  thickening  (" milky  spots")  are  found 
over  the  surface  of  the  heart. 

These  may,  however,  result  from  small  perivascular  foci  like  those  of 
chronic  myocarditis,  without  ever  giving  rise  to  the  clinical  picture  of 
pericarditis. 


Fig.  278. — Acute  fibrinous  pericarditis. 


Fig.  279. — Tuberculous  pericarditis  (cor  villosum). 


Organization  and  Adhesion. — The  strands  of  newly  formed  connective 
tissue  may  penetrate  the  fibrin  between  the  two  layers  of  pericardium  and 
completely  bridge  the  cavity  with  fibrous  strands  (Fig.  286).  In  many 
cases  the  tug  of  the  heart  in  systole  stretches  these  out  into  fibrous  cords 
an  inch  or  more  in  length;  in  other  cases,  or  over  other  parts  of  the  same 
heart,  the  adhesions  are  denser,  the  two  surfaces  may  be  completely  glued 
together  and  the  cavity  obliterated  (adherent  pericardium). 

The  division  into  these  forms  of  pericarditis  is,  therefore,  an  arbitrary 
one,  but,  as  will  be  seen,  is  made  necessary  by  the  absolute  difference  in 
both  diagnostic  signs  and  mechanical  effects  upon  the  circulation,  and 
thus  as  regards  indications  for  treatment.  Their  relative  frequency  is 
shown  in  the  following  table,  which  Gibson  quotes  from  Breitung's  autop- 
sies at  the  Berlin  Charite  Hospital  (Virchow's  Department). 

Cases.  Per  cent. 

Serofibrinous 108  33 . 3 

Hemorrhagic 30  9.2 

Purulent 24  7.5 

Tuberculous  (secondary) 24  7.5 

Tuberculous  (primary) 2  0.7 

Partially  adherent Ill  34.3 

Totally  adherent 23  7.3 

Ossified 2  0.7 

324  100 


PERICARDITIS.  593 

Although  the  pathogenesis  is  the  same,  the  clinical  manifestations  of 
fibrinous  pericarditis,  pericardial  effusion,  and  adherent  pericardium  are 
different;  hence  they  are  discussed  separately. 

SIMPLE  FIBRINOUS  PERICARDITIS. 
PATHOLOGICAL    PHYSIOLOGY. 

The  friction  due  to  the  presence  of  the  fibrinous  exudate  imposes  a 
slight  increase  in  the  resistance  to  both  contraction  and  filling  of  the  heart. 
The  exudate  itself  takes  up  a  certain  amount  of  space  in  the  pericardial 
cavity  and  may  thus  somewhat  diminish  the  filling  of  the  heart;  but 
these  factors  rarely  suffice  to  embarrass  the  circulation. 

Either  as  a  result  of  the  accompanying  injury  to  the  heart  muscle  or 
from  irritation  of  the  depressor  nerve,  the  peripheral  vessels  are  dilated 
and  the  blood-pressure  is  low.  The  pulse  also  becomes  small  and  rapid, 
but  is  usually  regular. 

SYMPTOMS. 

Precordial  pain,  palpitation,  shortness  of  breath,  and  weakness  are 
the  common  complaints,  as  well  as  occasional  chilly  feelings.  Fever,  with 
which  these  are  associated,  is  generally,  but  not  always,  present. 

The  onset  is  very  often  insidious,  and  the  disease  may  not  be  recog- 
nized at  all  by' the  patient.  Precordial  pain  is  the  most  striking 
symptom.  Sibson  estimates  that  it  occurs  in  70  per  cent,  of  the  cases. 
Henry  Head  calls  attention  to  the  fact  that  the  pain  of  pericarditis  is  not 
a  referred  pain,  but  a  true  local  pain,  often  limited  to  the  area  over  which 
the  friction  is  audible  and  associated  with  tenderness  on  pressure  and  on 
percussion.  It  does  not  radiate  from  this  site,  and  differs  in  this  respect 
from  the  anginal  pain.  The  other  symptoms,  shortness  of  breath  and  palpi- 
tation, manifest  no  special  peculiarity. 

Occasionally,  especially  when  the  pericarditis  affects  the  posterior 
wall  of  the  pericardium,  there  is  pain  on  swallowing.  This  pain 
is  in  every  way  similar  to  the  tenderness  of  the  interspaces  in  front,  and 
occurs  when  the  bolus  of  food  presses  upon  the  pericardium  as  it  passes 
down  the  oesophagus. 

When  the  recurrent  laryngeal  nerve  is  affected  by  the  inflammation, 
aphonia  or  change  in  the  voice  results.  Involvement  of  the  phrenic 
often  produces  hiccough. 

PHYSICAL    SIGNS. 

The  patients  are  usually  quite  pale,  occasionally  cyanotic.  Except 
for  accompanying  joint  involvement,  fibrinous  pleurisy,  or  pulmonary 
consolidation,  there  are  few  signs  outside  the  heart.  (Edema  of  the  extremi- 
ties is  rare  unless  there  are  accompanying  valvular  lesions.  Over  the  heart 
there  may  be  some  precordial  bulging,  especially  in  children,  but  the  cardiac 
impulse  may  be  less  marked  than  usual,  weak,  diffuse,  and  wavy.  On 
palpation  there  is  sometimes  a  slight  superficial  scratching  felt,  especially 
between  the  left  parasternal  line  and  the  sternum;  but  this  is  by  no  means 
as  marked,  as  frequent,  or  as  regular  as  in  valvular  lesions. 
38 


594 


DISEASES   OF   THE   HEART    AND    AORTA. 


The  area  of  cardiac  dulness  and  flatness  may  or  may  not  be  increased 
in  one  or  both  directions,  dependent  upon  the  amount  of  the  exudate  as 
well  as  upon  the  degree  of  dilatation  of  the  heart,  but  the  outlines  char- 
acteristic of  pericardial  effusion  are  not  present  when  the  exudate 
is  plastic. 

The  pathognomonic  sign  of  fibrinous  pericarditis  is  the  superfi- 
cial scratching  or  churning  murmur  or  friction  sound 
described  by  Laennec  as  resembling  the  rubbing  of  a  new  saddle.  It 
can  be  imitated  more  or  less  closely  by  placing  the  palm  of  the  hand  over 
the  ear  and  then  scratching  to  and  fro  upon  the  back  of  the  hand  with  the 
finger-nail.  The  pericardial  friction  is  exactly  similar  in  character  to  the 
friction  heard  in  pleurisy,  but  its  time  is  coincident  with  the  cardiac  cycle. 
It  does  not,  however,  coincide  sharply  with  either  systole  or  diastole,  but 
is  usually  heard  during  portions  of  both.  It  is  usually  louder  during  systole 
than  during  diastole,  probably  because  the  two  surfaces  are  moved  across 
one  another  with  greater  force.    A  short  pause  usually  occurs  between  the 

systolic  and  the  diastolic  portion 


of  the  friction.  The  diastolic 
friction  is  softer  than  the  systolic, 
occurs  rather  early,  and  ceases 
during  the  latter  half  of  this 
period,  or  in  other  words  as  ven- 
tricular filling  diminishes.  It 
may  also  be  heard  again  at  the 
time  of  auricular  systole,  giving 
a  triple  sound  to  the  friction 
(Broadbent).  Sometimes,  espe- 
cially when  the  pericarditis  is  just 


UlTIUVEimilCUUtR 


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Fig.  280. — Diagram  showing  the  relations  of  the 
pericardial  and  pleural  frictions  to  the  cardiac  and 
respiratory  movements.  The  pericardial  friction  is 
indicated  by  narrow  zigzag  line,  the  pleural  friction 
by  black  triangles,  the  heart  sounds  by  the  usual 
black  bands. 


beginning  and  the  friction  very  soft,  it  is  not  heard  at  all  during  diastole. 

The  friction,  as  a  rule,  does  not  replace  the  normal  heart  sounds,  but 
these,  as  well  as  loud  endocardial  murmurs,  may  be  heard  simultaneously 
with  it.  Their  more  distant  quality  tends  to  accentuate  the  superficiality 
of  the  friction  sound.  Moreover,  the  latter  is  considerably  accentuated 
by  moderate  pressure  of  the  stethoscope  in  the  interspaces.  As  Emerson 
has  shown,  this  is  also  true  of  certain  endocardial  sounds,  but  the  latter 
are  quite  different  in  quality  from  a  fresh  pericarditis. 

As  the  exudate  is  absorbed,  the  friction  softens  gradually  into  a  barely 
distinguishable  roughening  of  the  first  sound,  and,  finally,  disappears 
altogether. 

When  portions  of  the  exudate  become  organized  and  remain  as  thick- 
enings of  the  endocardium,  they  may  still  give  rise  to  some  roughening 
of  the  first  sound,  which  may  be  very  difficult  to  interpret,  and  this  is 
especially  true  when  they  remain  in  the  form  of  fibrous  strands  and  loose 
adhesions  (see  page  598). 

The  friction  is  usually  first  heard  over  the  third  and  fourth  left  inter- 
space near  the  sternum,  over  the  area  at  which  the  exudate  first  appears. 
In  the  cases  which  are  secondary  to  pneumonia  and  pleurisy  there  is  often 
a  "pleuropericardiaT '  friction,  with  respiratory  accentuation 
heard  over  a  considerable  strip  along  the  left  margin  of  the  heart  where 


PERICARDITIS.  595 

the  pleura  overlies  the  pericardium.  The  pleurisy  exists  in  the  layers  of 
pleura  in  front  of  the  pericardium.  The  two  processes  exist  simultaneously 
in  separate  cavities  whose  walls  are  in  contact.  Sears  has  pointed  out 
that  in  recurrent  attacks  of  pericarditis  the  friction  may  be  heard  only 
at  the  back  in  the  left  interscapular  region.  This  occurred  in  a  case  in 
which  the  anterior  portion  of  the  pericardium  was  adherent.  The  pulse 
in  acute  pericarditis  is  usually  small  and  rapid,  the  blood-pressure  low 
(100  mm.  or  under),  and  the  pulse-pressure  small  (10-25  mm.),  but  this  is, 
at  least  in  part,  due  to  the  loss  of  vasodilator  tone,  and  in  part  to  the  myo- 
cardial weakening  brought  about  by  the  same  process. 


DIAGNOSIS. 

Diagnosis  is  usually  simple,  and  the  murmurs  are  rarely  mistaken  for 
endocardial,  although  Osier  mentions  one  case  in  which  a  to-and-fro  aortic 
murmur  was  mistaken  for  a  pericardial  rub. 

When  a  certain  amount  of  fluid  is  present  in  the  pericardium  the 
friction  may  disappear  if  the  heart  is  pushed  backward;  and,  as  a  small  peri- 
carditial  effusion  is  often  overlooked,  the  whole  condition  may  escape 
diagnosis. 

Case  of  Simple  Fibrinous  Pericarditis. 

F.  G.,  a  colored  hod-carrier,  aged  50,  entered  the  Johns  Hopkins  Hospital  on  July  22, 
1904,  complaining  of  pain  around  the  heart.  Except  for  the  fact  that  one  son  died  of  gal- 
loping consumption,  the  family  history  is  negative. 

The  patient  has  been  a  healthy  man,  but  had  measles,  chicken-pox,  whooping-cough, 
mumps,  scarlet  fever  as  a  boy,  and  rheumatic  fever  at  38.  He  is  not  subject  to  sore 
throat.  He  had  a  cough  with  pain  in  the  chest  twenty  years  before  admission,  but 
has  had  no  recurrence.  He  has  had  several  attacks  of  gonorrhoea.  He  has  always 
done  hard  work. 

He  was  perfectly  well  until  six  weeks  before  admission,  when  he  had  severe 
pain  in  the  right  thigh  and  hip  which  lasted  five  weeks,  but  he  kept  at  work 
in  spite  of  the  pain.  Four  days  before  admission  he  began  to  cough,  and  two  days  later 
felt  a  cutting  pain  around  the  heart,  which  was  especially  severe  on  drawing 
a  deep  breath.  This  has  persisted.  He  did  not  notice  any  special  shortness  of  breath,  and 
kept  at  work  for  three  days  after  the  precordial  pain  had  set  in. 

The  examination  note  by  Dr.  Cole  states  that  the  patient  is  a  well-nourished  colored 
man,  mucous  membranes  of  fair  color,  no  glandular  enlargement.  Lungs  clear  throughout 
on  auscultation  and  percussion.  Over  the  heart  a  feeble  impulse  is  seen  in  the  fifth  left 
interspace  8.5  cm.  from  the  midline.  The  impulse  is  localized.  There  is  no  bulging  of  the 
interspaces.  On  percussion  the  area  of  cardiac  dulness  is  found  to  extend 
11.5  cm.  to  the  left  of  the  midline  in  the  fifth  interspace,  3.0  cm.  to  the  right  opposite 
the  fourth  rib.    The  cardiohepatic  angle  is  90°. 

The  heart  sounds  are  distinctly  heard  at  the  apex,  but  there  is  also  aloud 
rough  pericardial  friction  which  is  not  exactly  synchronous  with  the  heart 
sounds  and  is  increased  by  pressure  with  the  stethoscope.  There  are  no  endocardial  mur- 
murs. The  friction  increases  in  intensity  toward  the  base  of  the  heart, 
where  the  heart  sounds  are  distant  and  the  second  pulmonic  is  louder  than  the  second 
aortic.    The  pulse  is  of  fair  volume,  moderate  tension,  regular,  88  per  minute. 

The  sputum  is  mucopurulent,  but  contains  no  tubercle  bacilli  and  no  elastic  fibres. 

Urine,  450  c.c,  amber  colored,  acid,  containing  a  considerable  amount  of  albumin 
and  numerous  hyaline  casts.  Blood  count  shows:  red  blood-corpuscles  3,500,000;  haemo- 
globin 50  per  cent.;  leucocytes  7100.     Temperature  ranges  from  101°  to  102.5°  F. 

An  ice-bag  was  kept  continuously  over  the  precordium,  and  he  was  given  strychnine, 
1.5  mg.  (?V  gr.),  every  four  hours. 


596  DISEASES   OF   THE   HEART    AND    AORTA. 

On  the  second  day  after  admission  the  temperature  fell  to  normal  and  the  patient 
felt  better.  The  pain  in  the  chest  had  gone.  The  pericardial  friction  was  still  heard,  but 
less  intense  than  before,  and  by  the  following  day  could  be  heard  only  over  a 
small  area  in  the  fourth  left  interspace  near  the  sternal  margin. 
It  disappeared  entirely  during  the  course  of  the  following  week,  and  he  became  entirely 
well.  There  were  no  signs  of  pericardial  adhesion.  The  patient  left  the  hospital  on  August 
8,  in  the  third  week  after  his  admission,  and  has  not  sought  admission  since  then. 


TREATMENT. 

,  Absolute  rest  in  bed  is  necessary,  since  the  heart  must  be  spared  as 
much  as  possible,  and,  moreover,  cardiac  strain  and  venous  stasis  tend  to 
increase  the  exudation.  The  diet  should  be  light  or  should  consist  of  milk 
alone  during  the  acute  stages.  If  there  is  much  pain,  morphine  may  be 
freely  given  to  relieve  it,  since  this  symptom  is  not  likely  to  become  chronic; 
and,  on  the  other  hand,  it  is  important  to  keep  the  heart's  action  as  quiet 
as  possible.    For  this  purpose  an  ice-bag  is  usually  applied  to  the  precordium. 

Silva  has  shown  in  dogs  that  by  this  means  the  local  temperature 
within  the  pericardium  may  be  lowered  1°  or  even  3.5°  C.  (1.8° — 7.3°  F.). 
Buxbaum  states  that  the  use,  of  the  ice-bag  in  pericarditis  is  now  quite 
general  throughout  the  world.  In  American  clinics  this  is  certainly  the 
case.  The  clinial  experience  of  the  writer  has  been  one  of  uniform  satis- 
faction in  its  use.  The  fact  that  Rubino  was  able  to  produce  pericarditis 
in  animals  by  the  intravenous  injection  of  cultures  of  pyogenic  cocci  only 
when  ice  was  simultaneously  applied  to  the  chest,  has 
probably  little  bearing  upon  the  therapeutic  use  of  the  latter,  since 
Rubino  probably  chilled  his  animals  severely,  while  in  the  therapeutic 
application  the  cooling,  especially  of  the  deeper  layers,  is  both  localized 
and  mild.  No  doubt  the  local  temperature  of  the  inflamed  pericardium 
is  reduced  to  normal,  but  not  much  below  it. 

Other  methods  of  counterirritation  are  also  useful  and  devoid  of  this 
possible  objection.  Head  cites  a  case  in  which  relief  of  the  pain  within  five 
minutes  was  brought  about  by  the  application  of  three  leeches  to  the 
precordium,  and  Biers's  suction  cups  or  the  old-fashioned  dry  or  wet 
cupping  may  be  resorted  to  with  equal  satisfaction.  This  may  also  be  said 
of  hot  or  warm  poultices,  hot-water  bags,  and  the  modern  electrical  heating 
pads  whose  temperature  can  be  kept  regulated  with  great  accuracy.  Blis- 
ters (cantharides) ,  mustard  plasters,  Paquelin  cautery,  and  Finsen  light 
may  also  be  used  with  great  satisfaction,  or  even  a  ''light  bath'' 
from  a  single  small  incandescent  lamp  with  reflector  placed  near  the  pre- 
cordium! 

Medicines  seem  to  be  of  little  value.  Caton  recommends  potassium 
iodide.  Broadbent  states  that  digitalis  should  be  avoided  in  the  early 
stages,  but  Romberg  recommends  its  use  in  the  cases  with  nephritis.  It 
should  be  used  at  once  and  should  be  preceded  by  intravenous  strophanthin 
if  signs  of  acute  cardiac  failure  manifest  themselves. 

The  pain  is  not  relieved  by  salicylates,  so  that  codeine,  .03  Gm.  (£  gr.), 
heroin,  .005  Gm.  (TVgr.),  dionin,  .02  Gm.  (^  gr.),  or  morphine,  .016  Gm. 
({  gr.),  must  often  be  given. 

The  bowels  should  be  kept  moving  easily  with  saline  purgatives. 


PERICARDITIS.  597 


PROGNOSIS. 

Osier  states  that  "simple  fibrinous  pericarditis  never  kills,"  but  peri- 
carditis is  frequently  seen  as  a  terminal  event  in  other  conditions,  espe- 
cially in  pneumonia,  tuberculosis,  gout,  and  nephritis.  In  any  of  these  it 
is  a  grave  but  not  always  fatal  sign. 

The  main  dangers  accompanying  fibrinous  pericarditis  are  the  develop- 
ment of  effusion  on  the  one  hand  or  of  pericardial  adhesions  on  the  other. 
Sometimes  all  three  conditions  occur  successively  in  the  same  case,  the 
fluid  collecting  within  a  few  days  after  the  fibrinous  exudate,  is  removed 
after  a  few  weeks  by  aspiration  or  absorption,  and  is  followed  by  organi- 
zation of  the  exudate  with  adhesions  which  usually  last  throughout  one  or 
several  years  and  finally  terminate  the  life  of  the  patient.  Fortunately, 
these  complications  are  by  no  means  the  rule,  and  in  many  cases  fibrinous 
exudate  is  absorbed  without  further  trouble. 

It  is  evident  from  both  the  pathological  and  the  clinical  stand-point 
that  the  fresher  the  exudate  the  cleaner  will  be  its  absorption.  Hence  the 
importance  of  vigorous  treatment. 

PERICARDITIS    WITH  EFFUSION. 

Frequently  during  the  course,  and  especially  in  the  second  or  third 
week,  of  an  acute  pericarditis  fluid  collects  within  the  pericardium.  Under 
normal  conditions  there  are  from  twenty-five  to  fifty  cubic  centimetres 
of  serous  fluid  present.  In  pericardial  effusions  from  500  c.c.  to  1  litre  is 
frequent;  as  much  as  4000  c.c.  has  been  found  at  autopsy  by  Verney.  A 
pericardial  membrane  of  the  usual  size  could  not  accommodate  so  large 
an  effusion,  and  stretching  of  the  former  usually  goes  on  simultaneously 
with  increase  in  the  latter.  Hence  it  follows  that  the  actual  size  of  the 
effusion  may  be  of  little  import,  and  a  small  rapidly  exuded  effusion  may 
produce  signs  of  intrapericardial  pressure  sooner  than  a  large  one  arising 
slowly. 

The  character  of  the  fluid  may  vary  as  much  as  its  quantity.  It  may 
be  thin  and  serous  and  free  from  coagula,  especially  when  poor  in  leuco- 
cytes, or  it  may  contain  small  gelatinous  coagula  forming  here  and  there 
about  masses  of  leucocytes;  or  this  process  may  be  so  generalized  that  the 
whole  mass  may  be  converted  into  a  very  thin  jelly.  Diapedesis  of  corpus- 
cles through  the  injured  vessel  walls  may  cause  it  to  become  bloodstained, 
a  condition  which  is  especially  frequent  in  carcinomatosis  or  sarcomatosis 
of  the  pericardium. 

PATHOLOGICAL    PHYSIOLOGY. 

Francois-Franck,  Lagrolet,  and  Cohnheim  have  shown  that  the  injec- 
tion of  fluid  into  the  pericardial  cavity  hinders  the  entrance  of  blood  into 
the  auricles,  and  thus  causes  stasis  of  blood  in  the  venae  cavae  and  fall  in 
the  bloocl-pressure.  Their  experiments  were  repeated  by  Starling,  who 
found  that  on  injecting  successive  amounts  of  20  c.c.  and  10  c.c.  of  oil 
into  the  dog's  pericardium,  the  pressure  in  the  vena  cava  rose  gradually, 
while  that  in  the  aorta  and  pulmonary  vein  remained  constant  for  some 
time.     That  is  to  say,  the  rise  in  venous  pressure  compensated  for  the 


598 


DISEASES   OF   THE   HEART   AND    AORTA. 


increased  pressure  within  the  pericardium,  and  although  some  venous 
stasis  occurred  the  circulation  was  not  retarded.  As  much  as  60  c.c.  of  oil 
could  thus  be  injected  into  the  dog's  pericardium  without  producing  any 
other  change.  But  when  10  c.c.  more  were  injected  the 
condition  changed  suddenly  and  completely.  The  small  excess 
of  fluid  in  the  pericardial  cavity  had  caused  the  pressure  within  it  to  rise 
considerably  above  that  in  the  veins,  and  above  the  level  to  which  the 
venous  pressure  could  rise  during  stasis.  The  walls  of  veins  and 
auricles,  therefore,  collapsed  under  excess  of  pressure 
(Fig.  281),  and,  since  but  little  blood  could  enter  the  ventricles,  the  blood- 


■■  FLUID 


Fig.  281. — The  circulation  in  cases  with  pericardial  effusion.  (Diagrammatic.)  I.  Normal.  II. 
Small  effusion,  showing  the  rise  in  venous  pressure  and  the  increased  difficulty  in  the  filling  of  the  heart. 
III.  Great  increase  in  intrapericardial  pressure,  showing  the  complete  cutting  off  of  venous  inflow  and 
fall  in  arterial  pressure.  The  area  shaded  with  horizontal  broken  lines  indicates  the  height  of  the  pressure 
within  the  pericardium.       (Compare  with  Fig.  26.) 

pressure  in  the  aorta  fell.  The  same  change  occurred  in  Francois-Franck's 
experiments  when  the  intrapericardial  pressure  was  raised  from  10  mm.  to 
20  mm.  Hg.  When  the  pressure  was  not  relieved  death  ensued,  the  heart 
beating  for  a  short  time  after  the  circulation  had  ceased.  On  the  other 
hand,  when  the  small  excess  of  fluid  was  removed,  the 
blood-pressure  quickly  rose  again  and  the  circulation  returned 
to  normal.  This  experiment  exactly  reproduces  the  condition  in  man  when 
a  pericardial  effusion  is  collecting,  illustrates  the  mechanism  of  death  in 
that  condition,  and  also  illustrates  the  beneficial  effect  obtained  from  par- 
acentesis when  even  a  small  amount  of  fluid  is  removed. 


SYMPTOMS    AND    COURSE. 

Pericardial  effusion  is  somewhat  less  frequent  in  children  than  are 
the  other  forms  of  pericarditis,  its  subjects  being  usually  adults  and  often 
persons  past  middle  age.  The  symptoms  of  pericardial  effusion  are  more 
insidious  than  those  of  the  fresher  fibrinous  inflammation,  pain  being 
somewhat  less  common  and  less  intense,  dyspncea  and  weakness  being 
more  intense.  The  patients  are  very  much  more  comfortable  in  the  vertical 
than  in  the  horizontal  position,  the  difference  being  even  more  striking 
than  in  the  ordinary  forms  of  heart  disease.  Few  clinicians  indeed  can 
concur  in  James  Mackenzie's  statement  that  the  presence  of  fluid  in  the 


PERICARDITIS. 


599 


pericardium  does  not  give  rise  to  symptoms  of  circulatory  embarrassment. 
Fainting  spells  and  sudden  death  are  very  common,  occurring  when  the 
inflow  into  the  auricle  is  obstructed. 


PHYSICAL    SIGNS. 

The  patients  are  usually  pale  and  weak  with  rapid  respirations.  The 
veins  of  the  neck  and  extremities  may  be  prominent 
(high  venous  pressure),  and  this  is  especially  marked  when  the  intraperi- 
cardial  pressure  is  approaching  the  danger  point.  There  may  be  inspira- 
tory  distention  of  the  veins. 

Inspection  of  the  thorax  usually  shows  a  fulness  of  the  inter- 
spaces over  the  precorclium,  and  frequently  a  very  diffuse  wavy  impulse 
which  is  lacking  in  the  definiteness  usually  seen  in  both  systolic  impulse 
and  systolic  retraction  over  and  about  the  normal  or  enlarged  heart. 
Neither  this  nor  the  presence 
of  a  cardiac  pulsation  outside 
the  apex  is  of  real  value  in 
establishing  the  diagnosis  of 
pericardial  effusion. 

Palpation,  as  a  rule,  reveals 
nothing  of  importance,  except 
that  the  cardiac  impulse  is 
usually   very  feeble   or   absent. 

Changes  in  Cardiac  Outline. 
—  The  pathognomonic  sign  is 
revealed  by  the  alteration 
of  dulness  on  percus- 
sion. Auenbrugger  in  his  first 
diagnostic  efforts  was  able  to 
demonstrate  a  great  increase  in 
cardiac  dulness  in  pericarditis 
with  effusion,  and  this  obser- 
vation was  confirmed  by  Cor- 
visart,  who  recognized  a  large 
area  of  flatness  in  the  form  of  a  triangle  with  base  downward.  This, 
however,  was  also  encountered  in  numerous  cases  of  dilated  heart  and 
led  to  many  errors  in  diagnosis,  until  T.  M.  Rotch,  of  Boston,  in  1878, 
demonstrated  that  flatness  was  present  in  the  fifth  right 
interspace  early  in  the  disease  and  constituted  an  almost  diagnos- 
tic feature.  He  was  able  to  prove  this  upon  the  cadaver  by  injecting 
various  quantities  of  cocoa  butter  into  the  pericardial  cavity.  Flat- 
ness in  the  fifth  right  interspace  appeared  whenever  more 
than  200  c.c.  of  cocoa  butter  had  been  injected.  Less  than  200  c.c. 
could  not  be  recognized. 

Rotch's  observations  were  confirmed  by  W.  Ebstein  in  1893,  who 
laid  stress  upon  the  obtuseness  of  the  angle  formed  by  cardiac  and  liver 
dulness  (cardiohepatic  angle).  This  dulness  is  particularly 
marked  when  the  patient  leans  forward  and  toward  the  right,  so  that  the 


Fig.  282. — Area  of  cardiac  dulness  from  pericardial 
effusion,  showing  Corvisart's  triangular  area  of  dulness 
and  Sibson's  pear-shaped  area  of  flatness;  Rotch's  area 
of  dulness  (R)  in  the  fifth  right  interspace;  Ebstein's 
obtuse  cardiohepatic  angle  (EB). 


600  DISEASES   OF   THE   HEART   AND    AORTA. 

fluid  gravitates  to  this  point.  The  right  border  of  an  enlarged  heart,  on 
the  other  hand,  always  forms  an  acute,  or  at  most  a  right,  angle  with  the 
liver  flatness,  and  flatness  rarely  extends  to  the  fifth  right  interspace, 
being  most  marked  in  the  fourth.  The  matter  has  been  still  further  investi- 
gated by  Aporti  and  Figaroli,  who  found  that  with  the  subject  in  the  ver- 
tical position  as  little  as  150  c.c.  of  fluid  showed  itself  by  pushing  the  area 
of  dulness  downward  and  outward  at  both  its  lower  angles — at  both  cardio- 
hepatic  angle  and  at  the  apex.  The  lower  border  of  flatness  is,  therefore, 
the  arch  with  concavity  downwards  which  had  already  been 
described  by  Concato.  When  more  fluid  collects,  the  pericar- 
dium becomes  more  tense,  all  the  surfaces  become  convex,  and  Concato's 
arch  disappears.  As  a  diagnostic  sign  the  variations  in  dulness  about  the 
apex  are  much  less  definite  than  in  the  fifth  right  interspace,  and  hence 
they  are  of  little  importance. 

At  the  upper  border  of  dulness  the  usual  slight  resonance  behind  the 
sternum  gives  way  to  a  tongue  of  absolute  flatness  when  the  exudate  is 
large,  so  that  the  dulness  assumes  the  form  of  a  pear  hang- 
ing from  its  stalk  (Sibson). 

Moreover,  the  pericardium  presses  upon  the  lungs  about  its  borders, 
causes  them  to  relax  and  give  rise  to  S k o d a i c  tympany  and  tubu- 
lar breathing  not  only  in  front  but  also  at  the  angle  of  the 
left  scapula  (Ewart.)  Flatness  may  also  be  observed 
over  the  spines  of  the  vertebrae,  especially  from  the  fifth 
to  the  tenth,  where,  as  found  by  Koranyi,  the  note  is  normally  resonant. 
This  sign  may  also  be  present  when  the  left  auricle  is  greatly  dilated,  as 
in  mitral  insufficiency. 

Position  of  the  Heart  in  Pericardial  Effusion. — The  signs  on  auscultation 
may  vary.  Most  commonly,  as  found  by  Pirogoff  and  subsequent  writers, 
the  heart  sinks  in  the  pericardial  fluid  and  comes  to  lie  against  the  vertebral 
column  and  away  from  the  chest  wall,  from  which  it  is  separated  by  a 
thick  layer  of  fluid.  This  fluid  muffles  the  heart  sounds,  which  may  be 
totally  absent,  disappearing  first  about  the  apex,  later  at  the  base. 
Aporti  and  Figaroli  have  shown  that  with  650  c.c.  of  exudate  a  very 
small  area  of  heart  wall  near  the  base  will  still  remain  free  from  fluid,  and 
over  this  the  heart  sounds  and  friction  rub  may  be  heard. 

On  the  other  hand,  the  heart  sounds  and  friction  may  persist  even 
when  a  large  amount  of  fluid  is  present,  as  in  the  case  reported  below,  in 
which  the  pericardium  contained  1200  c.c.  of  fluid.  The  sounds  were  faint 
at  the  apex,  but  became  more  distinct  as  the  base  was  approached,  where 
the  friction  was  also  well  heard.  An  aspirating  needle  introduced  in  the 
sixth  left  interspace  came  at  once  against  the  heart.  At  autopsy  the  heart 
was  found  lying  against  the  chest  wall.  This  anterior  position,  though 
not  the  usual  one,  is,  according  to  Schaposchnikoff,  often  assumed  by  the 
heart  of  a  cadaver  when  fluid  or  paraffin  is  injected  into  the  pericardium. 
Schaposchnikoff  believes  that  the  heart  is  held  in  this  position  in  spite  of 
the  force  of  gravity  by  the  elasticity  of  the  great  vessels. 

Abdomen. — The  liver  may  be  both  enlarged  from  the  venous  stasis 
and  pushed  down  by  the  pericardial  effusion,  so  that  its  lower  edge  is  fre- 
quently palpable,  sometimes  even  as  low  as  the  umbilicus.     The  spleen 


PERICARDITIS. 


601 


may  also  be  somewhat  enlarged.  Ascites  and  movable-  dulness  are  some- 
times present. 

Over  the  extremities  the  veins  may  appear  distended,  and  there  is 
often  oedema. 

BIood=pressure. — The  blood-pressure  is  usually  rather  low,  except  in 
the  cases  with  nephritis,  in  which  it  may  be  above  normal. 

The  pulse  is  usually  small,  frequently  collapsing,  and  often  of  the  type 
of  pulsus  paradoxus — fall  of  blood-pressure  during  inspiration,  with  de- 
crease in  the  size  and  frequency  of  the  pulse,  and,  on  the  other  hand,  inspi- 
ratory swelling  of  the  veins.  This  condition  is  due  to  traction  on  the  walls 
of  the  vena  cava  producing  stasis  during  inspiration. 

i  ii 


Fig.  283. — Positions  of  the  heart  in  pericarditis  with  effusion.  I.  The  fluid  is  in  front  of  the  heart, 
as  described  by  Pirogoff.  II.  The  heart  is  floated  up  against  the  chest  wall,  as  described  by  Schaposchni- 
koff.  ST,  sternum;  OE,  oesophagus;  PV,  pulmonary  veins;  8,  eighth  thoracic  vertebra.  The  arrows 
indicate  the  compression  of  the  auricles.     The  broken  line  indicates  the  outline  of  the  uncollapsed  auricle. 

X=ray  Examination. — Examination  with  the  fluoroscope  shows  the 
exact  size,  form,  and  position  of  the  effusion  (Fig.  283),  and  both  before 
and  after  paracentesis  may  be  of  great  help  in  locating  pockets  of  encapsu- 
lated fluid.  The  relations  to  the  diaphragm  and  the  presence  of  mediastinal 
adhesions  may  sometimes  be  diagnosed  by  this  means,  and  particularly 
by  means  of  permanent  radiographs  made  with  a  tube  of  low  vacuum. 


Case  of  Pericarditis  with  Effusion. 

The  following  typical  case  was  under  the  writer's  care  in  the  Johns  Hopkins  Hospital. 
It  has  been  previously  reported  in  considerable  detail  by  Professor  Thayer. 

R.  C.  W.  B.,  a  German  saloon-keeper,  aged  59,  was  brought  to  the  hospital  at  12.30 
P.M.  on  Sept.  1,  1903,  barely  able  to  speak,  owing  to  shortness  of  breath  and 
weakness.  He  was  too  ill  to  give  a  history,  except  for  the  statement  that  for  several 
years  he  had  been  troubled  with  shortness  of  breath,  which  has  gradually  increased  until 
the  past  few  days,  when  it  suddenly  became  very  much  aggravated. 

Examination  note  by  Dr.  Cole  was  as  follows:  Patient  is  a  moderately  well-nourished 
man,  muscles  flabby.  At  time  of  the  examination  he  is  lying  flat  with  head  slightly  propped 
up  and  looks  very  ill.  Respiration  40  per  minute.  Pupils  are  small,  react  readily  to  light. 
Tongue  dry,  slightly  coated.  No  marked  pyorrhoea;  teeth  not  good.  Veins  of  the 
neck  are  very  full;  no  marked  pulsation  of  the  deeper  vessels.  No  general  glandular 
enlargement.  Chest:  Expansion  fairly  good;  equal;  considerable  respiratory  distress. 
Resonant  throughout  right  front  and  axilla  and  left  upper  front,  but  note  is  markedly 
impaired  in  lower  left  axilla  and  at  lower  right  back,  much  more  markedly  in  lower  left 


602 


DISEASES   OF   THE   HEART   AND    AORTA. 


back  up  to  the  angle  of  the  scapula.  On  auscultation. — Left:  Breath  sounds  are 
clear  throughout  upper  front  and  upper  back  except  for  a  few  mucous  rales  in  interscapular 
space.  Below  they  are  very  distant,  practically  absent  at  the  extreme  base,  except  just 
at  the  angle  of  the  scapula,  where  they  are  a  little  harsher  (Ewart's 
sign).  Right  side:  Breath  sounds  are  quite  clear  throughout  except  in  the  lower  back 
where  there  are  mucous  rales  and  breath  sounds  are  distant. 

Heart.  — There  is  no  impulse  visible  or  palpable.  There  is  a  wide  area 
of  cardiac  d  u  1  n  e  s  s  extending  above  to  the  middle  of  the  third  rib  16.5  cm. 
to  the  left  of  the  midline  in  the  fifth  interspace  when  the  patient  lies  on  his  right  side. 
When  on  his  back,  however,  the  dulness  is  difficult  to  make  out,  as  it  extends  directly  to 

the  dulness  in  the  axilla.  On  the  right 
dulness  extends  apparently  7  cm.  to 
the  right  of  the  midline  in  the  fourth 
interspace.  The  angle  between  the  upper 
limit  of  liver  dulness  and  the  cardiac  dul- 
ness is  very  obtuse.  There  is  quite 
definite  precordial  bulging,  though 
the  intercostal  spaces  seem  no  fuller  than 
on  the  right.  At  the  apex  and  over  the 
entire  precordium  the  heart  sounds 
are  barely  audible  until  one  reaches 
almost  to  the  costal  margin  in  the  fourth 
and  fifth  left  interspace,  where  the  sounds 
are  heard  faintly  with  a  to-and-fro  mur- 
mur, which  is  also  heard  over  the  sternum 
from  the  third  to  the  fifth  rib.  This 
murmur  is  quite  superficial  and 
is  louder  during  expiration  than 
during  inspiration,  apparently  not  increased 
by  pressure  of  the  stethoscope.  It  sounds 
suspiciously  pericardial  in  charac- 
ter, but  not  definitely  so.  The  heart's 
action  is  almost  fetal  in  rhythm  (pulse- 
rate  138  per  minute).  Heart  sounds  are 
heard  more  loudly  in  the  second  left  inter- 
space; neither  aortic  nor  pulmonic  second 
is  specially  accentuated.  Pulse  is  very 
small   and  can  hardly  be  counted. 

The  abdomen  is  full.  There  is  no 
movable  dulness  in  the  flanks.  The  feet 
and  legs  are  markedly  cedematous. 

At  5.45  p.m.  the  patient  was  prepared 
for  paracentesis  pericardii  by  the  method 
of  Delorme  and  Mignon  under  aseptic  precautions.  An  incision  was  made  in 
the  fifth  left  interspace  at  the  sternal  margin,  the  pericardium  ex- 
posed, and  a  trocar  inserted  through  it.  By  means  of  a  Potain  aspirator  25-50  c.c.  of  thick 
serosanguineous  fluid  were  removed,  after  which  no  more  could  be  removed. 
Another  puncture  was  immediately  made  in  the  costoxiphoid  angle  and  a  small  amount 
of  fluid  again  removed.  The  patient's  pulse  and  general  condition  did  not  change.  He 
became  delirious  and  died  at  7.30  p.m. 

The  autopsy  findings  confirmed  the  clinical  observations.  There  were,  how- 
ever, still  1200  c.c.  of  pericardial  fluid  which  lay  behind  the  heart 
both  to  the  left  and  to  the  right.  The  heart  lay  directly  against  the 
chest  wall,  and  therefore  had  come  against  the  point  of  the  needle  and  prevented  the 
removal  of  the  fluid.  As  Dr.  Cole  remarked  in  a  subsequent  note,  "the  fact  that  the  heart 
sounds  were  heard  loudest  over  the  sternum  and  along  the  left  sternal  margin  should  have 
led  me  to  insert  the  needle  either  to  the  right  of  the  sternum  or  far  to  the  left — outside  the 
mammillary  line"  (preferably  the  latter).  The  pericardium  was  lined  with  a  yellow 
fibrinous    exudate.      The  heart  muscle  showed  cardiosclerosis.     The   coronary 


Fig.  284. — Radiograph  of  a  patient  with  pericar- 
dial effusion,  taken  with  the  tube  in  front  of  the 
patient.  (Kindness  of  Prof.  C.  M.  Cooper.)  The 
figure  shows  the  overflowing  of  the  pericardial  cav- 
ity. The  spots  over  the  surface  of  the  lungs  are 
artefacts  due  to  the  presence  of  air-bubbles  in  the 
developer. 


PERICARDITIS.  603 

arteries  were  tortuous.  There  were  thickening  of  the  aortic  valves  and  adhesions  of  the 
cusps,  which  gave  rise  to  slight  aortic  stenosis.  The  left  pleura  contained  700  c.c.  of  slightly 
turbid  straw-colored  fluid.  Both  lungs  contained  small  areas  of  tuberculous  broncho- 
pneumonia. 

PURULENT  PERICARDITIS. 

The  effusion  in  many  cases  is  purulent  and  associated  with  more  or 
less  severe  septic  symptoms,  septicaemia,  chills,  extreme  pallor  and  weak- 
ness, and,  as  a  rule,  a  septic  fever,  though  in  some  cases  the  temperature 
remains  normal. 

The  condition  may  follow  exposure  to  bad  weather,  empyema,  or 
trauma  to  either  the  front,  sides,  or  back  of  the  chest.  The  staphylococci, 
streptococci,  pneumococci,  gonococci,  and  a  great  variety  of  other  bacteria 
may  be  the  infective  agen:s. 

The  symptoms  and  physical  signs  are  very  similar  in  both  simple 
and  purulent  effusions.  The  history  of  trauma  and  the  presence  of  empyema 
or  other  foci  of  pus  speak  in  favor  of  a  purulent  effusion.  Leucocytosis 
may  be  present  in  both  conditions.  The  aspirating  syringe  usually  gives 
the  diagnosis. 

HYDROPERICARDIUM. 

Hydropericardium,  or  simple  serous  effusion  into  the  pericardium, 
may  occur  along  with  ascites,  hydrothorax,  and  general  anasarca  in  chronic 
heart  failure  or  in  nephritis,  or  it  may  occur  alone  as  a  result  of  local  venous 
stasis  from  the  pressure  of  mediastinal  growths,  glands,  or  aneurisms,  or 
from  strangulation  of  the  veins  by  adhesions.  In  this  case  an  afebrile 
course  is  run.  Leucocytosis  is  often  absent  (or  may  be  due  to  simultaneous 
bronchitis  or  bronchopneumonia),  and  the  diagnosis  rests  upon  the  signs 
of  the  intrathoracic  condition  which  is  the  causal  factor. 

The  differential  diagnosis  is  made  from  the  fluid  obtained  on  para- 
centesis, which  is  clear,  thin,  serous,  of  low  specific  gravity  (under  1018), 
and  gives  no  clouding  with  acetic  acid  indicative  of  nucleo-albumin.  It 
is  poor  in  leucocytes  and  fibrin  ferment,  and  there  is  not  much  albumin 
(shown  by  Esbach's  method).  The  presence  of  a  pericardial  friction  at 
any  time  during  the  course  of  the  disease  is  sufficient  to  exclude  a  simple 
hydropericardium. 

H^MOPERICARDIUM. 

Hsemopericardium  is  produced  by  the  effusion  of  pure  or  almost  pure 
blood  into  the  pericardium,  and  occurs  especially  as  a  result  of  direct  or 
indirect  trauma,  stab  or  gunshot  wounds  penetrating  the  cavity,  or  rupture 
of  the  heart  or  of  an  aneurism.  It  may  also  occur  from  erosion  of  a  blood- 
vessel by  a  malignant  growth. 

Hemorrhage  into  the  pericardium  takes  place  much  more  rapidly 
than  the  other  exudations,  so  that  the  pericardium  has  less  opportunity 
to  stretch  and  accommodate  itself  to  its  contents.  The  intrapericardial 
pressure,  therefore,  rises  more  rapidly  than  in  the  other  conditions,  and 
symptoms,  signs,  and  danger  develop  more  rapidly.  Death  may  occur 
at  once.  When  possible  operative  procedures  must  be  begun  promptly 
in  order  to  save  the  patient. 


604  DISEASES   OF  THE   HEART   AND    AORTA. 


PNEUMOPERICARDIUM. 

When  air  or  gas  enters  or  develops  within  the  pericardial  cavity  (as 
from  perforation  after  trauma  or  tuberculosis  or  infection  with  Bacillus 
aerogenes  capsulatus  Welchii  in  a  case  reported  by  Nicholls),  the  condition 
is  termed  pneumopericardium.  Usually  this  is  associated  with  the  pres- 
ence of  purulent  or  serous  fluid  (pyopneumopericardium,  pneumohyclro- 
pericardium) .  Since  there  is  normally  a  negative  pressure  ( — 3  to  — 5  mm. 
Hg)  within  the  cavity,  it  follows  that  air  will  enter,  just  as  into  the  thorax 
(pneumothorax),  whenever  there  is  a  free  perforation  to  the  outside  or  to 
the  air-passages.  This  is  most  frequent  in  perforating  wounds,  but  occa- 
sionally occurs  as  the  result  of  tuberculosis  or  perforation  of  a  purulent 
pericarditis. 

The  signs  of  pneumopericarditis  are  very  characteristic.  The  percus- 
sion note  over  the  cardiac  area  may  vary  from  a  bell-like  tympany 
to  an  absolutely  wooden  flatness,  or  when  there  is  an  open- 
ing of  medium  size  a  cracked-pot  note  may  be  heard.  With  a  free  communi- 
cation to  the  outside  such  as  results  from  operation  upon  the  pericardium, 
however,  the  air  within  the  pericardium  is  not  set  into  vibration  by  the 
percussion  stroke  and  does  not  alter  the  note  at  all. 

On  auscultation,  except  in  the  latter  condition,  a  loud  churning 
''mill-wheel''  murmur  is  heard,  but  when  the  communication  is  a  free 
one  this  may  be  totally  absent. 

TUBERCULOUS  PERICARDITIS. 

Tuberculous  pericarditis  is  a  common  and  severe  condition.  The 
fibrinous  stage  is  somewhat  more  chronic  than  in  the  other  forms  of  peri- 
carditis, lasting  several  weeks  or  months,  and  often  resulting  in  the  forma- 
tion of  deposits  of  fibrin  (Fig.  256)  an  inch  in  thickness,  with  or  without 
the  presence  of  fluid.  Gray  tubercles  of  various  size  may  be  visible  within 
and  upon  the  surface  of  the  exudate,  but  frequently  they  may  not  be  pres- 
ent, and  the  baciiii  must  be  sought  for  histologically  or  by  guinea-pig 
inoculation. 

The  fluid  in  pericardial  effusion  is  frequently  blood  stained.  It  is 
occasionally  purulent  (Kast).  Tuberculous  pericarditis  is  most  commonly 
associated  with  other  tuberculous  processes,  especially  involvement  of 
the  pleurae,  but  it  may  also  occur  as  a  "  primary"  manifestation  by  spreading 
from  caseous  mediastinal  lymph-glands. 

The  course,  though  more  chronic  than  other  pericardial  processes, 
is  quite  similar,  but  the  exudate  is  not  absorbed  completely  and  goes  on 
to  either  fluid  or  adhesive  pericarditis.  Frequently  both  conditions  occur 
and  encapsulated  effusions  result.  There  is  usually  a  considerable  rise  of 
afternoon  temperature. 

The  physical  signs  and  therapy  of  tuberculous  pericarditis  are  about 
the  same  as  in  the  other  forms,  plus  the  general  management  of  a  case  of 
tuberculosis — rest,  fresh  air,  very  liberal  diet  (when  cardiac  symptoms  have 
subsided),  and  sustaining  measures.    The  prognosis  is  bad. 


PERICARDITIS.  605 


TREATMENT  OF  PERICARDITIS  WITH  EFFUSION. 

Palliative  treatment  of  fluid  within  the  pericardium  must  be  limited 
to  the  periods  in  which  intrapericardial  pressure  is  well  below  the  range 
of  venous  pressure,  and  must  be  pursued  with  full  cognizance  of  the  fact 
that  death  may  ensue  whenever  the  pressure  exceeds  this  limit. 

The  palliative  measures  consist  of  counterirritation,  with  ice-bag  or 
poultices,  etc.,  blisters,  and  especially  application  of  Bier's  suction  cups 
or  leeches.  Diuretics, — theocin,  diuretin, — combined  with  digitalis  or 
strophanthus,  and  free  purgation  may  be  resorted  to,  and  the  liquid  intake 
restricted  to  below  1000  c.c.  per  day,  in  the  hope  of  reducing  the  pericardial 
fluid  by  these  means.  However,  these  methods  are  at  best  but  feeble 
palliatives,  and  often  more  risk  is  entailed  in  their  use  than  in  the  more 
radical  procedures. 

Paracentesis  Pericardii. — The  idea  of  removing  fluid  within  by  tapping 
the  pericardium  was  first  suggested  in  1646  by  Riolan,  who  advised  tre- 
phining the  sternum  one  inch  above  the  xiphoid.1  He  did  not  attempt, 
however,  to  carry  it  out,  and  the  first  operation  upon  the  pericardium  was 
performed  in  1819  by  Romero,  of  Barcelona.  Romero  operated  upon  three 
cases  of  pericarditis,  with  two  recoveries,  a  percentage  which  is  above  the 
average  even  for  the  present  day.2 

Puncture  of  the  pericardium  by  means  of  a  trocar  was  first  performed 
by  Jowett,  of  Nottingham,  in  1827.  It  was  brought  into  more  general 
repute  by  Schuh,  of  Vienna,  under  Skoda's  direction  (1839),  in  France 
by  Trousseau  (1854)  and  by  Aran  (1855),  and  in  England  by  Clifford 
Allbutt  (1866).  Paracentesis  pericardii  should,  of  course,  be  undertaken 
with  all  possible  asepsis  of  skin,  hands,  and  instruments. 

The  instrument  used  has  varied  from  a  thick  trocar  several  millimetres  in  diameter 
to  the  finest  aspirating  needle.  The  ideal  cannula  is  one  which  has  a  bore  (about  1  mm.) 
sufficient  to  allow  a  viscous  liquid  to  escape  easily,  and  yet  not  so  great  as  to  permit  the 
entrance  of  air  through  the  perforation.  A  trocar  and  cannula,  especially  one  ending  in 
a  T  and  stop-cock,  is  the  best  form  of  apparatus,  since  it  permits  the  operator  to  clear  the 
lumen  of  the  cannula  at  will  and  at  the  same  time  to  remove  the  fluid  by  suction  through 
an  aspirating  bottle.3 

Various  sites  for  the  paracentesis  are  recommended,  with  four  ends 
in  view: 

1.  To  obtain  the  fluid. 

2.  To  avoid  infecting  the  pleural  cavity  and  puncturing  the  lungs. 

3.  To  avoid  puncturing  the  heart. 

4.  To  avoid  injuring  the  internal  mammary  artery. 

1  "  Si  non  passis  exhaurire  istud  serum  per  hydragoga,  licet  ne  terebra  sternum  aperire, 
intervallo  pallicis  a  cartilagine  xiphoide." 

2  It  is  interesting  that  this  method  has  recently  been  advocated  by  J.  H.  Bacon  (A 
Procedure  for  Opening  the  Pericardium,  Am.  J.  M.  Sc,  Phila.  and  N.  York,  1905,  cxxx, 
652)  as  a  result  of  a  series  of  experiments  upon  the  cadaver.  Bacon  does  not  mention  the 
work  of  these  pioneer  surgeons. 

3  Dr.  Chas.  S.  Bond  has  found  a  curved  aspirating  needle  with  lumen  about 
1  mm.  in  diameter  very  useful  in  tapping  the  pericardium  when  the  fluid  lies  back  or  is 
encapsulated.  The  needle  which  he  uses  has  a  radius  of  about  10  cm.  following  the  curve 
of  the  heart  and  enabling  him  to  pass  around  the  latter  without  injuring  it.  The  danger 
of  entering  the  ventricle  by  a  straight  push  is  also  much  less  with  an  instrument  of  this  form. 


606 


DISEASES   OF   THE   HEART   AND    AORTA. 


Sites  for  Paracentesis. — Trousseau  (1854)  recommended  introducing  the  needle  in  the 
fourth  interspace  just  below  the  mammilla;  Dieulafoy  (1873)  in  the  fifth  about  six  centi- 
metres from  the  sternal  margin.  Puncture  at  these  sites  or  at  the  outer  border  of  absolute 
dulness  (flatness)  has  the  disadvantage  of  always  traversing  and  often  infecting  the  pleural 
cavity,  so  that  occasionally  the  patient  may  be  caused  gratuitous  empyema  or  even  a  fatal 
pneumonia. 

In  order  to  avoid  entering  the  pleural  cavity,  Baizeau  (1868)  and  Delorme  and  Mignon 
advocate  puncturing  the  pericardium  as  near  as  possible  to  the 
sternal  margin  in  the  fifth,  or  if  possible  the  sixth,  left  inter- 
space. In  order  to  render  the  procedure  more  certain,  the  latter  investigators  advise 
making  an  incision  through  the  skin  with  a  bistoury.  The  needle  (of  medium  diameter) 
is  then  introduced  into  the  sixth  interspace  if  possible,  .and  otherwise  into  the  fifth  along 
the  edge  of  the  sternum,  pushed  in  for  a  centimetre  or  two,  and  then  the  point  directed 

downward  and  inward  by  a  slow  con- 

r~MP^"  ' '^H Ml  H . HBHBf      tinuous    movement    until    the    liquid 

^^  ^^^B,';.     ^J'        emerges.    In  order  to  empty  the  peri- 

^^H^-'.v^'        cardial    cavity   the    needle    should    be 
^H  H      connected  with  an  aspirator  bottle  and 
y— >w  ^B-'^.i      *^e  fl11^  collected   by  gentle   aspiia- 

.   /     fcTNy  1 :~i'^       tion.1    When  the  instrument  is  inserted 

/-•    Rtj5^-      \      /        ,BK      slowly  in  the  manner  described,  the 
"^  /       ©ffiST  flj     '       risk  of  injuring  the  heart  (right  ven- 

o   v(|ft-d^ra  !V?>~H      tricle)   is  minimal,  for  the  beating  of 

^ffi&pk,  I  H      the  latter  against  the  point  can  be  felt 

I      ■/\1      as   soon   as   ^   is    touched   and    long 
§        K-",'  I      before  it  can  be  penetrated.     Even 
i    „  'f .'' iH     if   through   lack   of   care   the 

1  If*    ■■   '       right    ventricle    be    penetrated, 

I  I  V  .'•;      harm     rarely     results.      For 

f*  1     "        mJBi      example,   Hulke    mentions    a  case  in 

which  he  penetrated  the  right  ventricle 
and  a  few  jets  of  blood  spurted  out, 
but  the  patient's  condition  improved! 
and  he  cites  several  other  similar  cases. 
Only  one  case  of  death  (from  laceration 
of  the  right  ventricle)  due  to  para- 
centesis is  on  record  (West).  Unques- 
tionably when  all  goes  well  the  technic  of  Delorme  and  Mignon  is  the  most  satisfactory, 
since  the  danger  of  injuring  both  heart  and  pleura  is  minimal.  On  the  other  hand,  the 
chance  of  a  "dry  puncture"  is  great.  At  the  place  selected  the  point  of  the  needle  may 
penetrate  a  great  deal  of  dense  fibrous  tissue  and  even  periosteum  and  the  lumen  may  thus 
become  plugged.  Should  the  fluid  not  appear,  this  source  of  error  may  be  obviated  by 
carefully  inserting  a  wire  through  the  whole  length  of  the  needle  after  it  has  been  pushed 
into  the  cavity  and  then  withdrawing  the  wire.  Another  difficulty  may  lie  in  the  position 
of  the  heart  itself,  as  occurred  in  the  above-mentioned  case  of  the  writer's,  in  which  the 
heart  instead  of  lying  behind  the  fluid  lay  directly  against  the  chest  wall  in  the  position 
described  by  Schaposchnikoff .  When  the  needle  was  introduced  by  Dr.  Cole,  it  encountered 
the  heart  at  once,  and  the  rubbing  of  the  latter  against  the  point  could  be  readily  felt. 
This  might  have  been  prophesied  from  the  fact  that  the  heart  sounds  were  well  heard  over 
the  precordium.  With  the  exception  of  a  few  cubic  centimetres  of  clear  fluid  the  puncture 
was  a  dry  one,  in  spite  of  several  successive  insertions  of  the  needle  both  at  this  point  and 
in  the  costoxiphoid  angle.  The  patient's  condition  became  very  bad,  and  he  died  before  a 
second  paracentesis  could  be  undertaken.  Autopsy  showed  the  heart  lying  directly  against 
the  chest  wall  with  1200  c.c.  of  fluid  above  and  to  the  left.  In  this  case,  as  in  all  those  in 
which  the  heart  sounds  and  pericardial  friction  are  well  heard  at  the  time  of  paracentesis, 


Fig.  285. — Sites  for  paracentesis  pericardii  and  peri- 
carditomy.  Ri,  Riolan  (1646),  trephining  the  sternum; 
D  &  M,  Delorme  and  Mignon  (1895),  paracentesis; 
It,  Romero  (1819),  pericardiotomy;  E,  v.  Eiselsberg's 
pericardiotomy;  TV,  Trousseau  (1854);  Di,  Dieulafoy 
(1873),  paracentesis;    W,  West,  pericardiotomy   (1883). 


1  Sewall,  J.  Am.  M.  Asso.,  Chicago,  1909,  advises  aspirating  the  fluid  into  the  aspirator 
bottle  by  sucking  out  the  air  with  the  mouth  instead  of  with  a  mechanical  aspirator.  The 
procedure  is  simpler  and  mistakes  and  failures  of  the  pump  are  impossible. 


PERICARDITIS.  607 

it  would  have  been  better  to  have  introduced  the  needle  at  the  outer  border  of  cardiac  flat- 
ness in  spite  of  puncturing  the  pleura,  and  to  have  risked  empyema  to  save  the  patient. 

Curschmann  advocates  puncture  from  the  posterior  lateral  area  of  cardiac  flatness 
and  Meog  (Therap.  Monatshefte,  1914,  xviii,  430)  was  able  to  record  600  c.c.  of  fluid  by  this 
method  when  previous  anterior  punctures  had  been  dry. 

Drainage  of  the  Pericardium. — Prof.  Pearson,  of  Cork,  punctures  the  pericardium, 
with  a  large  trocar,  withdraws,  and  then  introduces  a  fine  rubber 
catheter  into  the  pericardial  cavity  through  the  cannula.  The  rubber  catheter  follows 
the  curves  of  the  pericardium  without  danger  of  rupturing  it,  and  thus  enables  him  to  reach 
exudates  which,  as  in  the  case  of  R.  C.  W.  B.  cited  above,  are  located  behind  the  heart. 
He  also  withdraws  the  metal  tube  and  leaves  the  rubber  tube  in  place  as  a  permanent  drain 
for  several  days  at  a  time,  and  states  that  in  this  way  he  has  been  able  to  cure  a  number  of 
stubborn  cases  of  chronic  pericarditis  with  effusion  which  had  resisted  all  other  methods 
of  treatment. 

The  fact  cannot  be  too  greatly  emphasized  that  cases  with  pericardial  effusion  are 
usually  desperate  cases,  and  the  fluid  should  be  gotten  out  at  all  hazards. 

Resection. — As  has  been  seen,  paracentesis  pericardii,  even  in  cases 
of  simple  serous  pericarditis,  may  be  far  from  satisfactory.  In  purulent 
pericarditis  and  hsemo-  and  pneumopericardium  it  is  still  less  so.  In  such 
cases  paracentesis  is  inadequate  and  the  pericardium  must  be  opened 
freely.  Radical  as  this  procedure  may  seem,  its  satisfactory  performance 
by  Romero  antedates  paracentesis.  Romero  made  an  incision  in  the  fifth 
intercostal  space  at  the  level  of  the  costochondral  articulation,  introduced 
his  finger  into  the  wound,  palpated  the  pericardium  with  his  finger,  and 
then  seized  it  with  forceps  and  opened  it  with  curved  scissors.  The  opera- 
tion is  best  performed  under  light  chloroform  anaesthesia.  Though  this 
must  be  carefully  administered  on  account  of  the  cardiac  weakness,  it  is  a 
significant  fact  that  most  of  the  patients  have  stood  the  anaesthetic  well. 

The  site  for  free  incision  has  varied  with  different  operators.  Rosen- 
stein  made  a  free  incision  in  the  fourth  left  interspace  close  to  the  sternum 
and  then  inserted  a  rubber-tube  drain.  West  operated  in  the  fifth  left 
interspace  in  the  nipple  line,  having  previously  introduced  an  aspirating 
needle,  which  he  used  as  director  for  a  long  narrow-bladed  sharp-pointed 
bistoury,  subsequently  enlarging  the  opening  with  a  probe-pointed  bistoury. 
V.  Eiselberg  resected  the  fourth  costal  cartilage  and  then  opened  the  peri- 
cardium. Delorme  and  Mignon  perform  what  is  probably  the  least  danger- 
ous and  most  satisfactory  operation.  They  disarticulate  the  fifth  and  sixth 
costal  cartilages  from  the  sternum  with  a  pointed  bistoury,  draw  them 
forward  one  by  one,  and  fracture  them  about  4  cm.  from  the  sternum. 
They  then  dissect  down  to  the  pericardium,  which  they  pull  forward  with 
forceps,  and  then  slit  it  up  with  scissors  for  several  centimetres. 

Many  observers,  from  Aran  to  the  present,  supplement  the  simple 
drainage  with  irrigation  of  the  pericardium.  Aran  injected 
a  dilute  tincture  of  iodine  at  100°,  a  procedure  which  in  his  case  (though  not 
in  all  others)  did  not  cause  pain;  West  used  warm  1  per  cent,  carbolic 
acid;  others  used  simple  salt  solution.  The  importance  of  irrigation  can- 
not be  too  freely  emphasized,  since  the  treatment  should  aim  not  only  at 
recovery  but  also  at  reducing  the  exudate  and  the  resulting  adhesions  to 
a  minimum. 

Delorme  and  Mignon  operated  upon  all  forms  of  pericardial  effusions. 
Their  conclusions  are  summed  up  in  the  following:     "  100  observations 


608  DISEASES   OF  THE   HEART   AND   AORTA. 

— 82  paracentesis,  18  incision:  82  paracentesis — mortality  65  per  cent.; 
18  incisions — mortality  38  per  cent.  Let  us  do  for  the  pericardium  what 
we  have  done  for  the  peritoneum." 

The  relative  merits  of  palliative  therapy,  paracentesis,  and  free  incision 
are  well  shown  in  West's  case  of  purulent  pericarditis: 

A  van  boy,  aged  16,  was  struck  in  the  back  by  a  truck  and  knocked  down.  No  symp- 
toms for  two  months,  then  shivering  and  pain  in  the  left  side  and  precordium.  Pain  sub- 
sided in  a  few  days.  Three  weeks  later  he  went  out  for  a  short  walk;  became  very  faint 
and  almost  fell  down.  Pain  seized  him  in  the  pit  of  the  stomach.  Became  cyanotic,  dys- 
pnoeic,  and  nauseated.  Admitted  Sept.  7.  Pulse  78;  paradoxic,  losing  2-3  beats  at  each 
inspiration.  Precordial  bulging  and  oedema.  Dulness  from  right  nipple  line  to  three  inches 
outside  left  nipple  line.  Cardiac  sounds  almost  inaudible.  Liver  pushed  down  and  felt  in 
epigastrium.     Slight  oedema  of  feet. 

Twelve  leeches  applied  to  the  precordium  followed  by  poul- 
tices.    Palliative  treatment  for  a  week.    Pulse  and  general  condition  feebler. 

Sept.  14.  Paracentesis  pericardii — fourth  left  interspace  below  nipple; 
90  c.c.  1  per  cent,  carbolic  acid  at  100°  then  introduced  through  the  needle  and  used  to 
wash  out  pericardial  cavity.     No  pain.     Patient  much  relieved. 

Sept.  17.  Patient's  condition  again  bad.  Paracentesis  fails  to  remove  fluid.  Free 
incision  under  chloroform,  as  above  described,  in  fifth  left  interspace;  at  least 
two   quarts   of   pus   removed.     Immediate  improvement.    Uneventful  recovery. 

Left  hospital  Feb.  23,  and  the  following  September  was  perfectly  well  and  had  been 
following  his  usual  work  for  the  past  six  months  as  well  as  ever. 

Rosenstein's  case  and  those  of  Delorme  and  Mignon  show  similar 
results. 

West  gives  the  following  statistics  for  paracentesis : 

Phthisis 

Rheumatic  fever 

Scurvy 

Pleurisy 

Injury.... 

Pneumonia 

General  dropsy: 

Morbus  cordis 

Nephritis 

Chronic  bronchitis 

Mediastinal  tumor 

Unassigned 

67  34  33 

In  spite  of  the  comparative  harmlessness  and  brilliant  results  obtained 
by  the  radical  operation  in  purulent  pericarditis,  it  is  not  probable  that 
this  procedure  can  be  extended  to  the  milder  exudates,  since,  just  as  in 
joints,  free  prolonged  drainage  is  followed  by  complete  obliteration  of  the 
cavity.  Irrigation  of  the  cavity  through  an  aspirating  needle  or  trocar, 
after  tapping,  is  possible  only  when  the  diameter  is  large  and  the  outflow 
is  a  free  one. 


Number. 

Recovery. 

Deat 

13 

4 

9 

11 

7 

4 

9 

6 

3 

6 

5 

1 

3 

2 

1 

2 

2 

2 

2 

2 

2 

m  . 

1 

1 

.  , 

1 

1 

17 

7 

10 

PERICARDITIS.  609 

BIBLIOGRAPHY. 

Pericarditis. 

Historical  data  are  taken  from  G.  A.  Gibson,  Diseases  of  the  Heart  and  Aorta,  Edinb.  and 

Lond.,  1898. 
Poynton,  F.  J.:  Heart  Disease  and  Thoracic  Aneurism,  Lond.,  1907. 
Sturges.     Quoted  from  McPhedran,  A.:  Pericarditis,  Osier's  Mod.  Med.,  Phila.,  1908,  iv. 
Cadet  de  Gassicourt.    Quoted  from  Hochsingers  in  Pfaundler  and  Schlossmann's  "Diseases 

of  Children,"  translated  by  Shaw  and  La  Fetra,  Phila.,  Lippincott,  1908. 
Sears.     Quoted  from  Osier,  Principles  and  Practice  of  Medicine,  4th  edition,  N.  Y.,  1901. 
Chatard,  J.  A.:  Acute  Pericarditis  complicating  Acute  Lobar  Pneumonia,  Johns  Hopkins 

Hosp.  Bull.,  Balto.,  1905,  xvi,  334. 
Breitung:  Ueber  pericarditis  tuberculosa,  Berl.,  1877. 
Head,  Henry:  On  Disturbances  of  Sensation,  with  Especial  Reference  to  the  Pain  of 

Visceral  Disease,  Brain,  Lond.,  1896,  xix,  153. 
Emerson,  C.  P.:  Bull.  Johns  Hopkins  Hosp. 

Silva.     Quoted  from  Buxbaum,  B.;  Lehrbuch  der  Hydrotherapie,  Leipz.,  1903. 
Rubino,  A.:.Les  pericarditis  experimentales  et  bacteriques,  Arch.  Ital.  de  Biol.,  1892, 

xvii,  298,  and  Rif.  Med.,  1892,  viii. 
Romberg,  E.:  Lehrbuch  der  Krankheiten  des  Herzens  und  der  Blutgefasse,  Stuttgart, 

1906. 
Verney:  Gaz.  hebd.  de  med.,  Par.,  1856,  iii,  793.     Quoted  from  Thayer,  W.  S.:  Observa- 
tions on  Two  Cases  of  Pericarditis  with  Effusion,  Bull.  Johns  Hopkins  Hosp.,  Balto., 

1904,  xv,  149. 
Francois-Franck,  A.:  Recherches  sur  la  mode  de  production  des  troubles  circulataires 

dans  les  epanchements  abandons  du  pericard,  Gaz.  hebd.  de  med.,  Par.,  1877. 
Lagrolet:  De  la  compression  du  cceur  dans  les  epanchements  du  pericard,  These,  Paris, 

1878. 
Cohnheim,  J.:  Vorlesungen  ueber  allgemeine  Pathologie,  Berlin,  1882. 
Starling,  E.  H.:  Some  Points  in  the  Pathology  of  Heart  Disease,  Lancet,  Lond.,  1897,  i, 

569,  652,  723. 
Bolton,  C:  The  Experimental  Production  of  Uncomplicated  Heart  Disease,  with  Especial 

Reference  to  the  Pathology  of  Dropsy,  J.  Path,  and  Bacterid.,  Edinb.  and  Lond., 

1904,  ix,  67. 
Auenbrugger,  L.,  and  Corvisart.    Quoted  from  Ebstein. 
Rotch,  T.  M.:  Absence  of  Resonance  in  the  Fifth  Right  Interspace  diagnostic  of  Pericardial 

Effusion,  Bost.  M.  and  S.  J.,  1878,  xcix,  389,  421. 
Ebstein,  W.:  Zur  Diagnose  der  Flussigkeitsansammlung  im  Perikardium,  Virchow's  Arch., 

1893,  cxxx,  418. 
Aporti,  F.,  and  Figaroli,  P.:  Zur  Lage  der  akutentstandenen  Ergiisse  im  Herzbeutel, 

Zentralb.  f.  inn.  Med.,  1900,  xxi,  737;    from  whom  Concato,  Riv.  clin.  di  Bologna, 

Anno  vii,  Fasc.  4,  is  quoted. 
Sibson:  Article  on  Pericarditis  in  Reynolds's  System  of  Medicine,  Lond.,  1877. 
Koranyi,  F.:  Ueber  den  Perkussionsschall  der  Wirbelsaule  und  dessen  diagnostische  Ver- 

wentung,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lx,  295. 
Thayer,  W.  S.:  Observations  on  Two  Cases  of  Tuberculous  Pericarditis  with  Effusion, 

Johns  Hopkins  Hosp.  Bull.,  Baltimore,  1904,  xv,  149. 
Pirogoff .     Quoted  from  Schaposchnikoff. 
Schaposchnikoff,  B.:  Zur  Frage  ueber  Perikarditis,  Mittheil.  a.  d.  Grenzgeb.  d.  Med.  u.  d 

Chir.,  Jena,  1897,  ii,  86. 
Riolan  and  Romero.    Quoted  from  Schaposchnikoff,  Delome  and  Mignon. 
Jowett.     Quoted  from  S.  West. 

Dieulafoy:  Traits  de  l'aspiration  des  liquides  morbides,  Par.,  1873. 
Delorme,  E.,  and  Mignon:  Sur  la  ponction  et  incision  du  pericarde,  Rev.  de  Chir.,  Par., 

1895,  xv,  797,  987,  and  1896,  xvi,  56. 
West,  S.:  A  Case  of  Purulent  Pericarditis  treated  by  Paracentesis  and  by  Free  Incision, 

with  Recovery,  Statistics  of  Paracentesis  pericardii,  Med.  Chir.  Trans.,  Lond.,  1883, 

lxvi,  235. 
39 


610 


DISEASES    OF   THE   HEART   AND    AORTA. 


ADHERENT   PERICARDIUM. 

(Adherent  pericardium, — adhesive  pericarditis,  synechia?  pericardii, 
concretio  pericardii  cum  corde,  chronic  mediastinopericarditis.) 

Whenever  a  pericardial  exudate,  fibrinous  or  fluid,  is  absorbed  slowly 
a  certain  amount  of  organization  takes  place  in  it  and  adhesions  form  just 
as  after  pleurisy  or  peritonitis.  The  form  of  these  adhesions  varies  consid- 
erably, from  long  thin  strands  stretching  like  cords  across  the  pericardial 
cavity  to  short  bands  of  dense  fibrous  tissue,  or  even  to  a  firm  tissue  which 


LONG 


DENSE 


Fig.  286. — Specimen  showing  the  two  layers  of  pericardium  united  in  some  parts  by  long  strands 
and  in  others  by  short  bands  of  dense  adhesions.  (From  a  specimen  in  the  Army  Medical  Museum, 
Washington,  D.  C.) 


knits  the  two  surfaces  together  and  completely  obliterates  the  cavity.  All 
these  forms  may  be  present  in  different  areas  of  the  same  pericardium,  so 
that  the  process  need  not  be  considered  as  perfectly  homogeneous. 

Moreover,  not  only  the  adhesions  within  the  pericardium  but  particu- 
larly the  extrapericardial  adhesions  which  are  formed  simultaneously  on 
the  outer  surface,  are  of  clinical  importance,  since  it  is  the  latter  which 
form  the  tightest  fines  in  the  harness  and  determine  the  strain  upon  the 
heart.  As  shown  by  Manges'  case  cited  below,  complete  obliter- 
ation of  the  pericardial  cavity  may  cause  no  symptoms 
as  long  as  the  extrapericardial  adhesions  remain  unimportant. 


PERICARDITIS. 


611 


The  main  adhesions  do  not  always  occupy  the  same  position,  but  may 
be  divided  into  the  following  groups  (Fig.  288) : 

1.  Chondropericardial — fixing  the  heart  to  the  costal  cartilages  and  chest  wall  in  front. 

2.  PleuTopericardial — gluing  it  to  the  pleurae  and  fixing  the  edges  of  the  lungs. 

3.  Mediastinopericardial — fixing    its    posterior    surface    and    especially    harnessing 
the  auricles. 

4.  Phrenopericardial — fixing  it  to  the  diaphragm. 


Fig.  287. — Sections  showing  adherent  pericardium.  I  Photomicrographs  by  Dr.  C.  S.  Bond.) 
A.  Seen  with  low  power.  B.  Same  specimen  under  high  power.  C.  Another  specimen,  showing  the 
extreme  vascularity  of  pericardial  adhesions. 


Each  of  these  gives  rise  to  a  distinct  group  of  physical  signs;  and.  since 
these  may  occur  separately,  it  is  important  that  they  should  be  consid- 
ered so. 

PATHOLOGICAL    PHYSIOLOGY. 

The  mechanical  effects  upon  the  circulation  due  to  pericardial  adhesions 
may  be  twofold:  1,  the  work  of  the  ventricle  is  increased  by  the  tug  upon 
the  adhesions;  2,  the  filling  of  the  heart  may  be  hindered  by  strangulation 
of  the  vena  cava.  At  each  contraction  the  heart  must  not  only  drive  out 
the  blood,  but  must  pull  on  its  harness  of  adhesions.  The  additional  work 
which  it  thus  has  to  perform  depends  both  upon  the   tightness   of  the 


612 


DISEASES   OF   THE    HEART   AND    AORTA. 


adhesions  and  upon  the  weight  or  rigidity  of  the  structures 
pulled.  The  latter  factor  depends  upon  the  position  of  the  adhesions, 
whether  it  is  the  ribs,  pleura,  mediastinum,  or  the  diaphragm  and  liver  that 
are  tugged  upon,  being  greatest  for  adhesions  to  the  ribs  and  diaphragm. 
3.  The  emptying  of  the  heart  and  the  flow  through  the  aorta  may,  as 
claimed  by  Kussmaul,  be  hindered  by  the  tugging  of  the  adhesions  upon 
the  arch  of  the  aorta.  This  can  readily  be  shown  experimentally  if  such 
traction  be  made  in  a  dog  whose  chest  has  been  opened.  The  pulse  may 
be  made  to  disappear  absolutely  in  spite  of  the  fact  that  the  heart  rate 
remains  unchanged  and  the  heart  dilates  from  overfilling;  enough  blood 
flows  in  from  the  vense  cavse  to  dilate  the  heart. 


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Fig.  288. — Anterior  and  posterior  pericardial  adhesions.  (Semi-schematic.)  A.  Anterior  adhe- 
sions showing  the  stumps  of  adhesions  to  the  ribs.  B.  Mediastinal  adhesions,  showing  a  side  view  of  the 
heart.  PLE.  P.,  pleuro-pericardial  adhesions;  C.  P.,  costo-  (or  cnondro)-pericardial,  P.  P.,  phreno-peri- 
cardial,  M.  P.,  mediastino-pericardial  adhesions. 


When  this  additional  work  is  imposed  upon  a  heart  already  weak,  it 
may  succumb  to  the  strain,  and  death  may  occur  with  all  the  manifesta- 
tions of  broken  compensation.  The  importance  of  adherent  pericardium 
in  causing  death  from  heart  disease  is  shown  by  the  fact  that  it  was  present 
in  almost  all  the  cases  of  Sturges'  series. 

Usually,  however,  the  ventricles  gradually  recover  from  the  strain  and 
simply  undergo  a  gradual  work  hypertrophy  proportional  to  the  additional 
strain,  and  an  additional  amount  of  work  may  be  done  at  each  systole 
sufficient  to  balance  the  amount  required.  During  exercise,  emotion,  dis- 
ease, or  other  strains,  however,  not  only  the  work  of  the  heart  in  the  circu- 
lation is  increased,  but  with  the  increased  systolic  output  and  systolic 
excursion  of  the  walls  the  tug  upon  the  adhesions  is  increased  enormously, 
and  the  heart  is  thus  readily  overstrained.  The  heavy  beating  of  the  heart 
under  emotional  excitement  is  especially  likely  to  bring  this  about. 

Moreover,  the  process  of  hypertrophy  is  not  a  pure  one.  With  the 
fibrosis  of  the  pericardial  adhesions  outward,  the  process  of  fibrosis  also 


PERICARDITIS.  613 

extends  inward  into  the  somewhat  injured  myocardium,  and  this  process 
goes  on  progressively  with  each  moment  of  overstrain  until  the  myofibrosis 
cordis  is  advanced  and  the  heart  failure  complete. 

The  site  of  the  adhesions  determines  not  only  the  degree  but  the  char- 
acter of  the  heart  failure.  If  the  densest  adhesions  are  over  the  left  ven- 
tricle, the  effect  is  to  inhibit  the  action  of  the  latter  alone.  Nature  performs 
the  experiment  of  Welch,  and  gives  rise  to  the  clinical  picture  of  broken 
pulmonary  compensation  with  dyspnoea,  cardiac  asthma,  or  pulmonary 
oedema. 

If  the  chief  adhesions  are  over  the  right  ventricle,  on  the  other  hand, 
broken  systemic  compensation  sets  in  with  venous  stasis,  tricuspid  insuf- 
ficiency, enlargement  of  the  liver,  and  collection  of  fluid  at  various  sites, 
but  particularly  in  the  peritoneal  cavity  (cf.  Pseudocirrhosis,  page  619). 

On  the  other  hand,  the  tugs  of  the  adhesions  on  auricles  and  ventricles 
may  act  as  mechanical  extrastimuli  and  produce  an  extrasystolic  arrhyth- 
mia, which  in  itself  hinders  the  circulation. 

SYMPTOMS. 

Since  the  actual  formation  of  the  adhesions  really  represents  the  sub- 
sidence of  the  acute  pericardial  process,  it  is  not  surprising  that  the  onset  of 
the  pathological  lesion  is  insidious,  and  indeed  may  coincide  with  the  sub- 
sidence rather  than  the  onset  of  symptoms.  This  is  well  illustrated  by  cases 
of  purulent  pericarditis  like  that  reported  by  Manges,  in  which  obliteration 
of  the  pericardial  cavity  accompanied  the  curve  of  the  healing  of  the  incision. 
The  patient  was  free  from  symptoms,  and  a  year  later  was  working  as  a 
messenger  boy.  In  most  cases  the  process  continues  insidiously  during 
months  or  years  before  cardiac  symptoms  and  heart  failure  set  in,  during 
which  the  patient  may  be  apparently  well  or  may  suffer  only  upon  over- 
exertion, over-indulgence  in  venere  et  potu,  or  emotional  excitement. 
Sooner  or  later  the  pump  wears  out  and  symptoms  become  marked. 

The  symptoms  of  adherent  pericardium  are  mainly  those  of  chronic 
heart  failure — palpitation,  weakness,  etc.  Precordial  pain  localized  about 
the  apex  or  the  base  of  the  sternum  is  common  (65  per  cent.-70  per  cent, 
of  cases).  As  stated  above,  the  other  symptoms  may  fall  into  the  category 
of  cardiac  dyspnoea  or  that  of  venous  stasis  and  dropsy,  dependent  upon 
whether  the  failure  of  compensation  is  in  the  pulmonary  or  systemic  circu- 
lation. In  the  former  case  there  are  attacks  of  coughing  and  acute  dyspnoea, 
sometimes  with  smothering  sensations.  The  latter  often  begins  insidiously 
with  weakness,  enlargement  of  the  liver  and  spleen,  swelling  of  the  abdomen 
(Pick's  pericarditic  pseudocirrhosis  of  the  liver,  or  pericarditic  polyse- 
rositis), and  swelling  of  the  feet.  These  symptoms  may  also  set  in  more 
acutely  as  in  the  form  of  simple  heart  failure. 

Delirium  occasionally  occurs  with  adherent  pericardium,  perhaps  due 
to  disturbed  cerebral  circulation.  In  one  case  under  the  writer's  care  the 
patient  was  subject  to  hallucinations  of  vision  during  the  periods  when  his 
cardiac  condition  was  bad.  These  were  probably  due  to  congestion  of  the 
retinal  capillaries,  so  that  he  saw  lions  and  tigers  jumping  over  one  another 
at  the  foot  of  his  bed,  even  though  he  realized  it  was  a  physiological  hallu- 
cination. 


614  DISEASES   OF   THE   HEART   AND   AORTA. 


PHYSICAL    SIGNS. 

Corresponding  to  the  variations  in  the  site  of  adhesions,  the  physical 
signs  of  adherent  pericardium  are  both  multifarious  and  interesting;  The 
patients  are  often  pale  and  pasty,  the  haemoglobin  being  low  and  the  ca- 
pillaries rather  empty  of  blood.  Sometimes  the  opposite  holds  true,  and 
plethoric  cyanosis  prevails.  Inspection  of  the  veins  of  the  neck  may 
show  filling  of  the  latter  during  inspiration  (KussmauTs 
sign),  accompanied  by  inspiratory  diminution  in  the  size  of 
the  pulse  or  even  omission  of  some  beats  during  inspiration  (pulsus 
paradoxus,  Kussmaul)  (see  page  616).  The  sounds  over  the  heart  during 
this  period  may  become  weaker,  but  usually  still  continue. 

The  so-called  Friedreich's  sign  (diastolic  collapse  of  the  vein),  now 
known  to  represent  merely  a  weak  positive  venous  pulse  (see  page  80), 
is  common  to  many  weak  hearts  and  has.  no  diagnostic  or  prognostic  value. 

C.  M.  Cooper  has  recently  added  what  seems  to  be  a  valuable  accessory  sign  of  ad- 
herent pericardium.  He  determines  how  long  the  patient  can  hold  the  breath  in  inspira- 
tion, and,  five  minutes  later,  the  same  for  holding  the  breath  in  expiration.    In  normal 

,      insp.  =40-70     .  ,.      ,    .       25     .  .  ,  ,..,,. 

individuals    _  ;  in  cardiac  lesion  — ±-;  in  persons   with   mediastinal  and   pen- 

exp.  ==  JAj  Zo  lo 

cardial  adhesions    _        (paradoxical  ratio).     Patients  with  bronchial  asthma  also 

showed  _  (paradoxical  ratio) ;    so  that  its  chief   value   is    as   confirmatory 

evidence.    The  presence  of  a  paradoxical  ratio  may  prove  very  useful  in  confirming,  and 
a  normol  ratio  in  excluding,  mediastinopericarditis. 

Broadbent's  Sign. — The  chest  usually  shows  marked  precordial  bulging, 
especially  in  children.  Walter  Broadbent  in  1895  called  attention  to  a 
''visible  retraction,  synchronous  with  the  cardiac 
systole,  of  the  left  back  in  the  region  of  the  eleventh 
and  twelfth  ribs,''  and  " in  less  degree  of  the  same  region  of  the 
right  back "  (Broadbent's  sign) .  Such  retractions  of  the  interspaces 
have  also  been  recognized  in  many  cases  of  cardiac  hypertrophy  by  the 
Broadbents  as  well  as  by  other  observers  (Tallant).  J.  H.  F.  Broadbent 
has  lately  (Heart  Diseases,  4th  edition)  stated  the  facts  more  definitely 
and  more  accurately  in  the  following  words:  "The  systolic  recession  of 
spaces  alone  is,  however,  not  a  trustworthy  indication,  as  it  may  be  due 
to  atmospheric  pressure,  especially  when  the  heart  is  much  hypertrophied. 
When  the  costal  cartilages  or  lower  end  of  the  sternum 
are  dragged  in,  there  can  be  little  doubt  as  to  the  diagnosis,  as  this  could 
not  be  effected  by  atmospheric  pressure."  This  sign  is  often  most  marked 
in  deep  inspiration  when  the  diaphragm  is  tense. 

Broadbent  also  states  that  systolic  retraction  over  the  apex  is  a  valuable 
sign,  but  only  when  the  impulse  is  forcible  on  palpation,  as  it  may  otherwise 
be  due  to  atmospheric  pressure  (over  the  right  ventricle;  cf.  page  143). 
This  is  certainly  true  in  many  cases,  but  in  the  writer's  experience  there 
are  frequent  exceptions  to  this  rule,  and  it  is  of  value  chiefly  as  a  cor- 
roborating sign. 

Percussion. — The  area  of  cardiac  dulness  is  usually  but  by  no  means 
always  enlarged,  owing  to  the  hypertrophy  which  usually  takes  place, 


PERICARDITIS. 


615 


though  fixation  of  the  lung  borders  may  cause  the  area  of  flatness  and  area 
of  dulness  on  the  left  to  almost  coincide.  The  characteristic  features  on 
percussion  are :  Absence  of  the  usual  change  in  the  left 
border  of  flatness  between  deep  inspiration  and  deep  expiration. 
This  movement  of  the  border  of  the  lungs,  which  is  normally  2-3  cm., 
may  be  reduced  to  less  than  1  cm.  or  may  absolutely  disappear.  The 
position  of  the  apex,  as  determined  by  palpation,  auscultation, 
and  percussion,  also  becomes  fixed,  and  may  not  change 
at  all  when  the  patient  turns  from  lying  on  his  right  side  to  lying 
on  his  left.  However,  both  these 
fixations  majr  be  present  with 
simple  pleural  adhesions  and  no 
actual  involvement  of  the  peri- 
cardial cavity.  This  was  well 
exemplified  in  the  case  of  a 
little  girl  who  had  been  a  pa- 
tient in  the  Johns  Hopkins 
Hospital  several  times  during 
the  last  couple  of  years,  and 
who  presented  signs  interpreted 
as  adherent  pericardium.  At 
autopsy  the  pericardial  cavity 
was  free  from  inflammatory 
processes,  but  the  pleurae  were 
everywhere  bound  down  tightly 
around  it.  Practically  the  effects 
were  nearly  the  same  as  if  the 
pericardial  cavity  had  been  in- 
volved, Broadbent's  sign  and 
pulsus  paradoxus  being  present 
to  a  slight  degree.  Such  cases 
are,  however,  extremely  rare,  and  difficult  to  diagnose  when  they  occur. 

Palpation.  —  Sir  William  Broadbent  has  called  attention  to  the  im- 
portance of  an  exaggeration  of  the  diastolic  shock  or  rebound 
(accompanying  the  second  sound)  over  the  greater  part  of  the  pericardium 
as  characteristic  of  adherent  pericardium.  This  is  certainly  a  useful  aid 
especially  in  corroboration  of  other  signs,  but,  unless  the  distinctness  of 
the  shock  is  far  greater  than  would  be  warranted  by  the  loudness  of  the 
sound  at  the  base,  it  is  of  little  value.  Nevertheless,  the  writer  recalls  a 
case  in  which  the  diagnosis  of  adherent  pericardium  (accompanying  a  well- 
defined  aneurism)  was  based  upon  this  sign  alone  and  was  verified  at 
autopsy.  Professor  Thayer  has  found  that  there  is  often  in  addition  a 
protodiastolic  shock  accompanying  the  third  heart  sound,  which  may  be 
the  most  intense  shock  in  the  whole  cardiac  cycle.  Apparently  this  is 
distinctive  of  adherent  pericardium. 

Thrills,  especially  presystolic  in  time,  are  occasionally  felt,  probably 
owing  to  tugs  upon  strands  of  adhesions,  but  these  alone  are  not  typical. 

Auscultation.— Since  pericarditis  is  frequently  (34  per  cent,  of  Sears's 
cases)  accompanied  by  various  forms  of  valvular  disease,  the  presence  of 


Fig.  289. — Cardiac  outline  in  adherent  pericardium. 
The  broken  line  indicates  the  fixation  of  the  left  border 
of  the  heart  (apex)  and  of  the  left  border  of  cardiac 
flatness  (anterior  margin  of  the  left  lung).  The  small 
diagram  at  the  left  shows  the  relation  of  the  heart  sounds 
to  the  cardiac  cycle,  indicating  the  unusually  loud  third 
heart  sound.  BR  BR  indicate  areas  of  systolic  retrac- 
tion of  the  ribs,  xiphoid,  and  interspaces;  R  1,  2,  Riess' 
gastric  sounds  in  adherent  pericardium. 


616 


DISEASES   OF  THE   HEART   AND    AORTA. 


all  varieties  of  valvular  murmurs,  especially  of  mitral  origin,  is  not  sur- 
prising. A  presystolic  rumble,  probably  due  to  the  stretching  of  strands 
of  adhesions  by  the  contraction  of  the  auricle,  is  occasionally  heard  in 
cases  of  adherent  pericardium  in  which  aortic,  mitral,  and  tricuspid  valves 
are  normal.  Sewall  also  reports  several  cases  with  reduplication  of  the 
first  sound,  which  was  shown  at  autopsy  to  be  due  to  old  peripheral  adhe- 
sions. Professor  Thayer  finds  the  third  heart  sound  and  the  corresponding 
protodiastolic  shock  and  wave  very  distinct  in  adherent  pericardium. 
This  may  be  due  to  the  fact  that  they  are  more  easily  transmitted  to  the 
chest  wall,  or  perhaps  because  the  filling  of  the  heart  causes  sudden  stretch- 
ing of  the  adhesions. 


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Fig.  290. — Inspiratory  and  expiratory  dropping  of  beats  (Riegel's  pulse  and  the  pulsus  paradoxus? 
in  adherent  pericardium,  showing  the  position  of  the  adhesions  which  bring  the  condition  about.  VEN., 
jugular  pulse;  CAROT.,  carotid  pulse;  RESP.,  respiration  (downstrokes  represent  inspiration;  upstrokes 
represent  expiration).  In  cases  with  Riegel's  phenomenon  (anterior  costo-pericardial  adhesions)  the 
conditions  are  as  shown  in  the  diagram  (upper  respiratory  tracing,  venous  pulse,  carotid  pulse);  those 
with  pulsus  paradoxus  correspond  to  the  conditions  shown  by  venous  pulse,  carotid  pulse,  and  lower 
respiratory  tracing. 


>:\MEDIASTIN0 
PERIC 


Riess'  Gastric  Sounds. — A  very  interesting  sign  was  described  by  Riess 
in  1879,  and,  since  it  has  been  verified  by  so  excellent  an  observer  as  Fran- 
<;ois-Franck,  merits  attention.  On  listening  over  the  stomach  in  some 
cases  of  adherent  pericardium,  observers  have  been  able  to  hear  the  heart 
sounds  loud  and  metallic  in  quality.  These  sounds  are  not  much  influenced 
by  changes  of  position,  by  respiration,  nor  by  inflation  or  filling  of  the 
stomach.  They  are  probably  due  to  adhesions  to  the  diaphragm  only,  and 
hence,  as  originally  stated  by  Riess,  are  not  present  in  all  cases  of  adherent 
pericardium. 

Variations  in  the  Pulse. — The  pulse  in  adherent  pericardium  is  usually 
small  and  rapid,  generally  regular,  but  often  showing  an  extrasystolic 
irregularity  which  is  probably  due  to  tugs  upon  the  strands  of  adhesions. 

The  striking  and  characteristic  feature  is  the  marked  diminution  of 
the  pulse-wave  during  inspiration,  amounting  sometimes  to  the  dropping 
of  a  beat  during  that  phase.  This  was  first  noticed  by  Griesinger  in  1854 
in  a  case  in  which  autopsy  showed  strands  of  adhesions  about  the  arch  of 
the  aorta,  causing  kinks  and  stenosis  in  its  lumen  when  pulled  upon  by  the 
descent  of  the  diaphragm.     The  vense  cavse  were  also  caught  in  dense 


PERICARDITIS. 


617 


adhesions  which  strangulated  them  in  similar  manner  during  inspiration. 
Both  inflow  and  outflow  of  blood  were  therefore  hindered  in  that  phase, 
hence  the  diminution  of  the  pulse.  The  same  condition  was  studied  by 
Hoppe  and  later  by  Kussmaul  (1873),  since  whose  report  it  is  known  as 
the  pulsus  paradoxus.  It  is  not  entirely  pathognomonic  of  adhe- 
rent pericardium  or  even  of  pericarditis  in  general,  occurring  with  open 
ductus  arteriosus  Botalli  (Francois-Franck,  see  page  554)  and  in  many 
normal  or  neurasthenic  individuals  (Reichmann),  though  in  these  the  dimi- 
nution does  not  amount  to  complete  dropping  of  beats  during  inspiration. 


ADHES- 


Fig.  291. — A.  Radiograph  of  a  case  of  adherent  pericardium.  (Kindness  of  Prof.  C.  M.  Cooper.) 
B.  Diagram  illustrating  the  condition  seen  in  A,  showing  the  pericardium  pulled  outward  to  the  right  and 
a  portion  of  the  diaphragm  pulled  upward  by  the  adhesions  {ADHES). 


The  occurrence  of  exactly  the  opposite  condition  of  the  pulse,  namely  diminution 
of  the  wave  and  impulse  during  expiration,  has  been  described  by  Riegel  in  cases 
in  which  autopsy  showed  pleuropericardial  adhesions  upon  the  anterior  surface  of  the 
heart.  Riegel  believes  that  the  relaxation  of  the  lung  during  expiration  pulls  the  heart 
upward  and  produces  a  fall  of  pressure  from  displacement  of  the  latter. 

Rosenbach  has  been  able  to  show  experimentally  .that  when  the  heart  was  displaced 
by  an  inflated  rubber  bulb  the  vena?  cava?  became  kinked  and  the  pulse  became  smaller 
and  blood-pressure  fell.  When  this  displacement  occurs  during  inspiration  from  downward 
traction,  a  pulsus  paradoxus  results;  when  it  occurs  during  expiration,  Riegel's  phenom- 
enon occurs. 

Apart  from  these  respiratory  variations  the  blood-pressure  shows  no 
special  features,  being  usually  low  in  uncomplicated  cases;  but  it  is  fre- 
quently normal  from  compensatory  vasoconstriction  and  increased  cardiac 
effort,  and  occasionally  high  in  the  nephritic  and  ursemic  cases. 

X=ray  Examination.  —  The  demonstration  of  pericardial  adhesions 
by  means  of  the  Rontgen  rays  was  first  made  by  Moritz  Benedikt  in  1897. 
Some  question  was  thrown  upon  his  methods  by  the  criticism  of  F.  Moritz 
(1900),  showing  that  normal  shadows  along  the  edge  of  the  cardiac  and 
liver  shadows  may  simulate  adhesions.  These  objections  were  obviated 
by  Stuertz,  who  reported  five  cases  in  which  the  presence  of  adhesions  was 
demonstrated  not  only  by  suspicious  shadows  through  the  lungs  and  along 
the  edge  of  the  pericardium,  but  also  by  the  fact  that  the  margin  of  the 
pericardium  at  these  points  was  pulled  downward  or  outward  when  the 
structures  were  rendered  tense  in  inspiration.    Some  areas  were  also  shown 


618  DISEASES   OF  THE   HEART   AND    AORTA. 

to  be  quite  fixed  during  respiration.  Stuertz's  observations  have  been 
confirmed  by  Lehmann  and  Schmoll  and  by  Dr.  C.  M.  Cooper,  to  whom 
the  writer  is  indebted  for  the  X-ray  shown  in  Fig.  291. 

The  special  value  of  the  X-ray  examination  lies  in  the  fact  that  it 
reveals  the  mediastinal  and  diaphragmatic  adhesions  with  accuracy,  and, 
by  demonstrating  the  points  at  which  the  fixation  and  tension  are  greatest, 
points  out  the  path  for  operative  interference. 

Abdomen. — The  abdomen  is  often  negative,  but  enlargement  of  the 
liver  and  spleen  and  ascites  are  frequent,  as  has  been  shown  by  Weiss  in 
1876. 

Case  op  Adherent  Pericardium. 

The  following  very  typical  case  was  under  the  writer's  care  in  the  City  and  County 
Hospital  of  San  Francisco.  (As  the  original  history  was  lost,  these  notes  are  taken  from 
the  article  of  Lehmann  and  Schmoll,  who  have  previously  published  the  case.) 

L.  A.,  engineer,  23  years  old,  entered  the  hospital  complaining  of  headache,  nausea, 
and  shortness  of  breath.  He  had  had  rheumatism  six  years  before  admission,  and  then  had 
pain  over  the  heart.  Since  then  he  had  had  two  attacks.  During  the  past  few  years  he 
has  been  subject  to  periods  of  heart  failure  with  dyspnoea,  during  which  he  is  frequently 
depressed  and  sometimes  even  maniacal. 

The  patient's  lips,  ears,  and  extremities  are  deeply  cyanotic.  The  pulse  is  irregular, 
with  numerous  extrasystoles,  many  of  them  ineffectual.  The  apex  impulse  (systolic  pro- 
trusion) is  visible  in  the  sixth  interspace  3  cm.  outside  the  mammillary  line,  beyond  which 
there  is  a  well-marked  systolic  retraction  of  the  interspaces  in  front  and  back.  There  is 
also  systolic  retraction  of  the  ribs  and  costal  margin  (Broadbent'a  sign).  The  apex  is 
fixed  and  does  not  move  with  change  of  position,  but  the  area  of  flatness  changes  during 
respiration  (movement  of  the  lung  border).  There  is  well-marked  pulsation  over  the  right 
ventricle.  Dulness  extends  above  to  the  third  rib  and  3  cm.  to  the  right  of  the  right  para- 
sternal line.  A  loud  presystolic  rumble  and  a  loud  systolic  murmur  are  heard  over  the  apex. 
The  second  pulmonic  is  markedly  accentuated.  Both  sounds  are  heard  with  the  extra- 
systoles. 

The  lungs  are  clear  except  for  dulness  and  bronchovesicular  breathing  at  the  left 
base  behind. 

The  liver  is  greatly  enlarged  and  readily  palpable,  but  there  is  no  pulsation.  There 
is  some  cedema  of  the  feet. 

Clinical  diagnosis:  Left-sided  pleurisy,  adhesion  of  the  pericardium  with  the  pos- 
terior surface  of  the  heart,  mediastinum,  and  diaphragm,  mitral  stenosis  and  insufficiency. 

Examination  with  the  fluoroscope  showed  the  heart  to  be  dilated  to  right  and  left. 
There  was  a  marked  angular  protrusion  along  the  right  border  of  the  cardiac  shadow. 
In  this  region  the  outlines  of  the  shadow  are  less  sharply  defined  than  usual,  merging  into 
the  liver  and  vertebral  shadows.  The  diaphragm  is  equally  high  on  left  and  right,  moving 
less  on  the  latter. 

The  patient's  condition  did  not  improve  under  rest  and  digitalis.  He  often  had  in- 
tense precordial  pains.  On  one  occasion  he  was  subject  to  definite  hallucinations,  imagin- 
ing that  he  saw  lions,  tigers,  and  other  brightly  colored  wild  animals  springing  to  and  fro 
upon  the  floor  of  the  ward  and  over  his  bed,  though  he  was  at  the  time  otherwise  rational, 
and  even  realized  that  it  was  an  hallucination.  He  was  placed  in  a  solitary  cell  for  twenty- 
four  hours  at  his  own  request,  for  fear  of  doing  personal  violence  to  the  persons  about  him. 

His  condition  became  so  much  worse  that  cardiolysis  was  decided  upon  as  a  last 
resort  and  was  performed  by  Professor  Stillman.  The  ribs  were  resected  over  the  pre- 
cordium  and  the  pericardium  opened  in  exploration.  The  heart  was  everywhere  covered 
with  adhesions,  which  over  the  anterior  surface  of  the  heart  consisted  of  strands  about  an 
inch  long.  There  was  no  fibrinous  exudate  and  no  fluid.  The  patient  took  the  ether  badly 
and  became  extremely  cyanotic.  The  shock  of  the  operation  did  him  evident  harm,  for 
during  his  entire  sojourn  after  that  he  felt  even  worse  than  before.  The  wound  itself  caused 
him  no  trouble  and  healed  per  primum.  The  patient  left  the  hospital  three  weeks  after 
the  operation,  in  spite  of  advice. 


PERICARDITIS. 


619 


Pericardiac  Pseudocirrhosis  of  the  Liver  (Pick),  and  Polyserositis  from 
Adherent  Pericardium  (Cabot). — Hutinal  in  1895  described  a  form  of 
liver  cirrhosis  of  cardiac  origin  (cirrhose  cardiaque).  Friedel  Pick  (1896) 
in  Pribram's  clinic  called  attention  to  a  very  interesting  clinical  condition 
which  is  not  infrequently  encountered,  but  whose  nature  is  often  over- 
looked. This  is  seen  in  certain  cases  which  run  the  course  of  a  primary 
hepatic  cirrhosis,  beginning  with  asci- 
tes, enlargement  of  the  liver,  slight 
jaundice,  general  weakness  and 
dyspnoea,  but  devoid  of  any  special 
cardiac  features.  Occasionally  there 
were  also  enlargement  of  the  super- 
ficial veins  of  the  abdomen  and  oedema 
of  the  feet.  The  first  and  second 
cases  were  considered  clinically  to  be 
primary  cirrhosis  of  the  liver,  and  the 
discovery  of  adherent  pericardium  at 
autopsy  came  as  a  surprise.  In  his 
third  case  adherent  pericardium  was 
carefully  sought  for  and  found,  and 
the  diagnosis  was  correctly  made. 
Death  occurred  in  two  to  four  years 
after  onset  of  symptoms.  The  peri- 
cardia in  these   cases  were  found   to 

be  completely  or  almost  completely  adherent,  the  rest  of  the  heart  normal. 
The  livers  showed  both  interlobular  cirrhosis  and  chronic  perihepatitis 
(iced  liver,  Curschmann),  the  peritoneum  was  thickened,  and  chronic 
perisplenitis  was  present.  An  example  of  this  condition  is  found  in  the 
case  of  J.  M.  C.  cited  on  page  370,  in  whom  the  presence  of  adherent  pericar- 
dium was  not  suspected  during  life. 

In  1898  R.  C.  Cabot  described  a  similar  case.  Flesch  and  Schossberger  find  the  con- 
dition not  infrequent  in  children,  presenting  the  superficial  manifestations  of  a  primary 
cirrhosis  without  the  presence  of  alcohol  and  syphilis  as  etiological  factors.  On  careful 
examination  the  presence  of  adherent  pericardium  is  readily  detected  by  its  usual  signs. 

Flesch  and  Schossberger  were  able  to  reproduce  the  condition  experimentally  in  dogs. 
They  produced  pericarditis  by  injections  of  tincture  of  iodine  into  the  pericardial  cavity 
and  allowed  the  animals  to  recover,  during  which  period  adherent  pericardium  occurred. 
After  a  few  months  ascites  and  cedema  set  in  and  the  animals  died.  Their  results  have 
been  confirmed  by  O.  Hess,  who  has  also  produced  cyanosis  and  cirrhosis  of  the  liver  by 
suturing  the  inferior  vena  cava  to  the  diaphragm. 

Another  point  in  the  differential  diagnosis  from  true  primary  cirrhosis  is  the  fact  that 
the  veins  of  the  arms  and  neck  are  usually  enlarged  to  almost  the  same  extent  as  those  of 
the  portal  system,  showing  that  the  stasis  is  not  confined  to  the  latter.  There  is  no 
caput  medusae. 


Fig.  292. — Case  of  pericardiac  pseudocir- 
rhosis. (After  Cabot,  Bost.  M.  and  S.  J.,  1898, 
cxxxviii.) 


TREATMENT. 

The  treatment  of  adherent  pericardium  may  be  both  palliative  and 
operative.  The  palliative  treatment  is  simply  the  general  treatment  for 
cardiac  weakness:  rest,  diet,  and  cardiac  stimulants,  strychnine  and  digi- 
talis, during  the  onset  and  acute  stages;  careful  graduated  exercises  and 
training  during  the  period  of  relative  freedom  from  symptoms. 


620  DISEASES   OF   THE   HEART   AND    AORTA. 

It  is  impossible  to  remove  the  condition,  and  the  therapy  must  be 
simply  so  directed  that  that  which  cannot  be  cured  may  best  be  endured. 

Anaemia  should  be  treated  with  iron,  exposure  to  infection  avoided, 
and  general  hygienic  conditions  maintained.  For  reasons  mentioned  above, 
these  precuations  should  be  carried  out  even  more  carefully  than  for  simple 
valvular  disease. 

Surgical  Treatment  (Cardiolysis) .  —  In  1902  Brauer,  of  Heidelberg, 
introduced  a  simple  method  of  treatment  which  promises  to  revolutionize 
the  therapy  of  adherent  pericardium.  Brauer  proposed  ''to  relieve 
the  heart  functionally  by  breaking  the  strong  bony 
ring  of  ribs,  not  by  a  severe  operation  with  the  breaking  up  of  exten- 
sive adhesions  but  only  by  substituting  a  soft  covering  for  the  natural  bony 

covering  of  the  heart On  account  of  the  tremendous  strain  upon 

the  heart,  due  to  traction  on  the  chest  wall,  we  foresaw  a  danger  in  opera- 
tion under  narcosis The  operation  was  tried  upon  a  patient  with 

adherent  pericardium,  broken  compensation,  ascites,  and  oedema.  Seg- 
ments of  the  third,  fourth,  and  fifth  ribs  7  to  9  cm.  in  length  were  resected 
under  light  narcosis,  the  periosteum  being  carefully  removed.  The  patient 
made  an  uninterrupted  recovery.  His  pulse  soon  became  stronger  and 
more  regular,  the  ascites  and  oedema  disappeared,  and  he  was  able  to  do 
heavy   work  without  symptoms.     The  pulse  still  remained  irregular." 

Brauer  reported  two  other  cases  with  equally  good  results,  and  these 
have  been  confirmed  by  Beck,  Umber,  Meyer,  Westfeld,  Wenckebach, 
and  others.  Brauer  particularly  states  that  he  does  not  attempt  to  break 
up  the  adhesions,  as  Delorme  and  Carl  Beck  have  proposed,  since  he  believes 
that  this  operation  is  too  severe  and  that  the  adhesions  would  form  again 
too  rapidly,  although  he  states  that,  in  individual  cases,  this  might  be 
done  besides  his  operation. 

As  regards  the  indications  for  cardiolysis,  it  would  appear  that,  since 
the  adherent  pericardium  cannot  otherwise  be  relieved,  this  operation  is 
worthy  of  trial  whenever  symptoms  of  cardiac  weakness  occur  and  recur 
in  a  patient  with  well-marked  adhesions  to  the  chest  wall  (tugging  in  of 
the  lower  ribs,  fixation  of  the  left  border  of  flatness  on  inspiration,  immo- 
bility of  the  apex)  and  recur  in  spite  of  general  cardiac  hygiene.  It  is  not 
necessary  to  wait  for  the  complete  cardiac  break-down  to  prophesy  that 
this  must  sooner  or  later  occur  in  such  a  case,  and  to  see  that  the  sooner 
the  work  of  the  heart  is  relieved  the  longer  will  be  the  life  of  .the  patient. 
Moreover,  it  is  evident  that  if  the  operation  is  performed  between  attacks 
of  cardiac  overstrain,  the  patient  is  in  better  condition  to  withstand  the 
shock  of  the  operation  and  the  danger  of  the  latter  is  diminished.  If  the 
cardiolysis  is  not  performed  until  the  patient's  heart  has  almost  completely 
given  way,  as  in  the  case  of  the  patient  with  the  visual  hallucinations 
referred  to  above,  he  can  scarcely  fail  to  suffer  from  the  shock  of  the  opera- 
tion; but  even  in  such  cases  Brauer's  results  have  been  striking,  and,  since 
there  is  no  other  mode  of  relief,  operation  is  warranted. 

It  must  be  confessed  that  in  such  cases  the  manner  in  which  the  anaes- 
thesia is  administered  determines  a  large  part  of  the  shock  from  the  opera- 
tion, and  may  prove  a  decisive  factor  in  the  outcome.  The  selection  of  the 
anaesthetist  constitutes  no  small  part  in  the  management  of  the  case. 


PERICARDITIS.  621 

The  question  also  arises  whether  operation  should  be  advised  in  chil- 
dren or  adolescents  whose  pericardia  are  adherent  to  the  chest  wall,  but  in 
whom,  owing  to  the  flexibility  of  the  latter,  the  symptoms  do  not  as  yet 
demand  operative  interference.  In  this  regard  each  case  must  of  course 
be  decided  upon  its  own  merits,  but  it  is  evident  that  as  age  advances  the 
rigidity  of  the  ribs  is  bound  to  increase  and  the  strain  upon  the  heart  pro- 
portionately. If  the  case  remains  relatively  free  from  symptoms  as  age 
advances,  it  should  be  left  alone;  but  if  the  progress  of  the  second  or  third 
decade  brings  with  it  increasing  cardiac  symptoms  or  the  signs  of  pericardi- 
tic  pseudocirrhosis,  the  question  of  early  cardiolysis  should  be  seriously 
considered.  Since  there  is  no  hope  that  children  will  "outgrow"  an  adhe- 
rent pericardium,  it  should  be  relieved  as  much  as  possible  before  the  strain 
has  ruined  the  heart  muscle.  When  valvular  lesions  are  present,  especially 
mitral  stenosis,  the  danger  from  operation  is  of  course  greater,  but  in  the 
hands  of  a  skilful  surgeon  this  is  much  less  than  might  be  expected  and  is 
probably  less  than  that  in  pericardiotomy  for  purulent  pericarditis. 

BIBLIOGRAPHY. 
Adherent    Pericardium. 

Manges,  M.:  Adherent  Pericardium,  Internat.  Clin.,  Phila.,  1905,  15  ser.,  i,  1. 

Hoppe,  F. :  Ueber  einen  Fall  von  Aussetzen  des  Radialpulses  wahrend  der  Inspiration  und 

die  Ursachen  des  Phanomens,  Deutsche  Klinik,  1854,  No.  3. 
Kussmaul:    Ueber   schwielige    Mediastino-pericarditis    und    paradoxen  Puis,   Berl.   klin. 

Wchnschr.,  1873,  x,  433,  445,  461. 
Friedreich,  N.:  Ueber  den  Venenpuls,  Deutsches  Arch.  f.  klin.  Med.,  Leipz.,  1865-6,  i,  241. 
Cooper,  C.  M.:  The  Respiratory  Ratio;    a  Preliminary  Note,  J.  Am.  M.  Assoc,  Chicago, 

1909,  lii,  1182. 
Broadbent,  Walter:  An  Unpublished  Physical  Sign,  Lancet,  Lond.,  1895,  ii,  200. 
Broadbent,  Wm.  H.:  Adherent  Pericardium,  Trans.  M.  Soc,  Lond.,  1897-8,  xxi,  109. 
Broadbent,  Wm.  H.  and  J.  H.  F.:  Heart  Disease  and  Aneurism  of  the  Aorta,  New  York, 

4th  ed.,  1906. 
Camac,  C.  N.  B.:  Broadbent's  Sign,  Johns  Hopkins  Hosp.  Bull.,  Balto.,  1898,  ix,  271. 
Tallant,  A.  W.:  Some  Observations  on  the  Occurrence  of  Broadbent's  Sign,  Boston  M. 

and  S.  J.,  1904,  cli,  457. 
Sewall,  H.:  On  a  Common  Form  of  Reduplication  of  the  First  Heart  Sound  due  to  Extra- 
cardiac  Causes,  Contrib.  Sci.  Med.,  Vaughan,  Ann  Arbor,  1903,  29. 
Riess,  L.:  Ueber  ein  neues  Symptom  der  Herzbutelverwachsung,  Berl.  klin.  Wchnschr., 

1878,  xv,  751.    Weitere  Beobachtungen  ueber  einer  die  Herztone  begleitende  Magen- 

consonanz  bei  Herzbeutelverwachsungen,  ibid.,  1878,  xvi,  333. 
Francois-Franck,   A.:  Des  bruits  extracardiaques  in  general,   en  particulier  des  bruits 

gastrique  rhythmes  avec  le  coeur;    contribution  au  diagnostic  de  l'adherence  au  peri- 

carde,  Gaz.  hebd.  de  Med.,  Par.,  1885,  2  ser.,  xxii,  757. 
Griesinger's  observation  (1854),  reported  by  A.  Widenmann,  Beitrag  zur  Diagnose  der 

Mediastinitis,  Diss.,  Tubingen,  1856. 
Hoppe,  F.:  Ueber  einen  Fall  von  Aussetzen  des  Radialpulses  wahrend  der  Inspiration, 

u.s.w.,  Deutsche  Klinik;  1854,  No.  3. 
Reichmann,  E.:  Die  inspiratorische  Yerkleinerung  des  Pulses  (sogen  Pulsus  Paradoxus), 

Ztschr.  f.  klin.  Med.,  Berl.,  1904,  liii,  112. 
Riegel,  F.:  Ueber  extrapericardiale  Verwachsungen,  Berl.  klin.  Wchnschr.,  1877,  xiv,  657. 
Rosenbach,  O.:  Experimentelle  Untersuchungen  Ueber  die  Einwirkung  von  Raumbesch- 

rankungen  in  der  Pleurahohle  auf  den  Kreislauf  apparat,  Arch.  f.  path.  Anat.,  etc., 

Berl.,  cv,  215. 
Benedikt,  M.:  Wien.  med.  Wchnschr.,  1897. 
Moritz,  F.:  Munchen  med.  Wchnschr.,  1900.    Quoted  from  Lehmann  and  Schmoll. 


622  DISEASES    OF   THE    HEART   AND    AORTA. 

Stuertz:  Zur  Diagnose  der  Pleuraadhasionen  aus  Pericard  und  Zwerchfell,  Fortschr.  a.  d. 
Geb.  d.  Rontgenstr.,  Hamb.,  1904,  vii,  215. 

Lehmann  and  Schmoll:  Pericarditis  adhesiva  im  Rontgenogramm,  ibid.,  1905,  ix,  196. 

Cooper,  Charles  Miner:  Personal  communication. 

Pick,  F.:  Ueber  chronische  unter  dem  Bilde  der  Lebercirrhose  verlaufende  Pericarditis 
(pericarditische  Pseudolebercirrhose),  Ztschr.  f.  klin.  Med.,  Berl.,  1896,  xxix,  385. 

Cabot:  Bost.  M.  and  S.  J.,  1898. 

Flesch  and  Schossberger:  Diagnose  und  Pathogenese  der  in  Kindesalter,  haufigsten  Form 
der  Concretio  Pericardii  cum  Corde,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lix,  1.  Con- 
firmed also  by  Hess,  O.:  Diagnose  und  Pathogenese  der  im  Kindesalter  haufigsten 
Form  der  Concretio  Pericardii  cum  Corde,  Ztschr.  f.  klin.  Med.,  Berl.,  1906,  lx,  174. 

Brauer,  L.:  Cardialyse,  Miinchen.  med.  Wchnschr.,  1902,  xlix,  982.  Untersuchungen  an 
Herzen  Cardiolysis  und  ihre  Indikationen,  Arch.  f.  klin.  Chir.,  Berl.,  1903,  lxxi,  258. 

Beck.     Quoted  from  Brauer. 

Umber:  Perkiarditis  und  mediastinale  Verwachsungen  und  Cardiolysis,  Therap.  d.  Gegen- 
wart.,  1905. 

Wenckebach,  K.  F. :  Remarks  on  Some  Points  in  the  Pathology  and  Treatment  of  Adherent 
Pericardium,  Brit.  M.  J.,  Lond.,  1907,  i,  63.    Ueber  pathologische  Beziehungen  zwi- 
schen  Atmung  und  Kreislauf,  Samml.  klin.  Vortr  ,  Leipz.,  1907,  No.  465,  466. 
For  a  review  of  the  subject  see  also  Delatour,  H.  B.:  Surgery  of  the  Pericardium 

and  Heart,  Am.  J.  Surg.,  N.  York,  1909. 


XIII. 

WOUNDS  OF  THE  HEART  AND  CARDIAC  TRAUMA. 

Hippocrates  and  Celsus,  Paul  of  iEgina,  Roland,  Lanfranc,  and  other 
writers  of  antiquity  taught  that  wounds  of  the  heart  were  followed  immedi- 
ately by  death;  but  Ambroise  Pare  (1552)  saw  a  gentleman  of  Turin  "who, 
although  wounded  in  the  heart  during  a  duel,  was  able  to  pursue  his  antag- 
onist 700  feet  before  he  dropped  to  the  ground  and  died."  Muler  (1641) 
treated  a  soldier  who  lived  for  fifteen  days  after  sustaining  a  wound  of  the 
heart, — an  observation  so  unheard  of  at  the  time  that  he  had  the  autopsy 
protocols  signed  by  the  commander  of  the  garrison!  Aprilis  (1680)  de- 
scribes a  wound  of  the  right  auricle,  after  receiving  which  the  man  had  lived 
for  five  days. 

The  results  of  modern  times  were  summed  up  by  G.  Fischer  in  1867 
(351  cases)  and  Loison  (1899)  (277  cases).  Fischer  found  the  wounds 
occurring  with  the  following  frequency: 

Death  within  a  few 

minutes.  Recovery. 

Right  ventricle 107 — 21 . 9  per  cent.  6 

Left  ventricle 95 — 25 .  per  cent.  6. 

Both  ventricles 24 — 34 .  per  cent.  2 

Right  auricle 28 — 25 .  per  cent. 

Left  auricle 13 — 38 .  per  cent. 

Apex 12  4 

Base 1  1 

Septum  ventriculorum 6  1 

Whole  heart 15 — 62 .  per  cent.  1 

Left  heart : 5 

Right  heart 3  11 

Coronary  artery 1  1 

Pulmonary  artery 1 

Not  specified 40  17 

351  50  (11.2%) 

In  452  cases  there  were  50  (12  per  cent.)  of  spontaneous  recovery. 

EXPERIMENTAL    SURGERY. 

Elsberg  in  1899  made  a  very  careful  study  of  wounds  experimentally 
produced  in  the  rabbit's  heart.  He  found  that  those  produced  during 
systole,  when  the  heart  fibres  are  shortened,  become  enlarged  during  dias- 
tole and  hence  bleed  more  than  wounds  of  corresponding  size  produced 
during  the  latter  phase.  Wounds  that  completely  penetrate  the  heart  wall 
bleed  more  than  those  which  do  so  partially.  Those  which  enter  perpen- 
dicularly bleed  more  than  those  which  penetrate  obliquely,  for  in  the  latter 
case  the  walls  form  a  valve-like  approximation  during  systole.  Indeed 
Prof.  Barker  and  the  writer  have  produced  oblique  wounds  penetrating  the 
entire  wall  of  the  dog's  ventricle,  which  scarcely  bled  at  all. 

623 


624 


DISEASES   OF   THE   HEART   AND    AORTA. 


Even  the  smallest  incised  wounds  made  by  Elsberg  in  the  rabbit's 
auricle  were  always  fatal  unless  sutured,  while  those  of  the  right  ventricle 
were  more  fatal  than  those  of  the  left.  Wounds  of  2  mm.  or  less  in  the  left 
ventricle  frequently  healed  spontaneously.  However,  when  suture  was 
employed  a  large  part  of  the  ventricles  could  be  cut  through  and  the  ani- 
mal's life  saved.    , 

The  size  of  the  instrument  producing  the  injury  plays  little  role,  for, 
although  in  general  large  wounds  bleed  more  and  are  more  uniformly  fatal 
than  small  ones,  nevertheless  large  and  fatal  wounds  have  been  produced 
by  even  ordinary  needles.  For  example,  Thiemann  describes  the  case  of  a 
man  who  in  pressing  against  a  heavy  beam  accidentally  drove  a  sewing 
needle  through  his  chest  wall,  where  it  became  imbedded  and  stuck  into  the 


Fig.  293. — Wounds  of  the  left  ventricle.  (From  specimens  in  the  Army  Medical  Museum,  Wash- 
ington, D.  C.)  A.  Bullet  wound  in  the  heart  of  a  soldier  who  lived  for  two  days  after.  B.  Stab  wound  in 
the  left  ventricle  ;  death  within  two  hours. 


heart  wall,  ripping  one  hole  1.5  cm.  long  in  the  wall  of  the  right  auricle  and 
another  smaller  hole  in  the  wall  of  the  right  ventricle.  His  life  was  saved  by 
operation  four  and  one-half  hours  later. 

A  single  small  puncture  of  the  heart  wall  with  a  needle  with  prompt 
withdrawal  of  the  needle  and  no  laceration,  as  is  occasionally  done  in  para- 
centesis pericardii,  as  a  rule  causes  no  marked  disturbance  and  does  not 
require  operative  interference. 

Death  from  penetrating  wounds  of  the  heart  results  either  from  bleed- 
ing, or,  as  was  already  shown  by  Morgagni  and  by  Cohnheim,  from  accumu- 
lation of  blood  within  the  pericardium  (see  page  598),  compressing  the 
auricles  and  preventing  the  entry  of  blood  into  the  heart. 

It  is  possible  that  in  the  rare  cases  of  instantaneous  death  the 
trauma  may  cause  the  ventricles  to  pass  into  a  state  of  fibrillation  and 
the  circulation  abruptly  cease.  There  is  no  proof  that  this  is  frequent, 
however,  and  the  cases  of  instantaneous  death  from  wounding  the  heart 
are  less  common  than  might  be  expected. 


WOUNDS   OF   HEART   AND   CARDIAC  TRAUMA.  625 


SYMPTOMS. 

The  symptoms  accompanying  a  wound  in  the  thorax  which  suggest  a 
wound  of  the  heart  (intrapericardial  pressure)  are  those  of  angina  pec- 
toris—  pain  down  the  left  arm,  a  feeling  of  precordial  oppression  and 
precordial  pain,  especially  marked  on  expiration.  Pressure  upon  the  pre- 
cordium  increases  these  pains.  There  is  shortness  of  breath.  Occasionally 
there  are  abdominal  pain  and  spasm  of  the  abdominal  muscles  (Rehn).  As 
Fischer  pointed  out,  pain  is  also  felt  about  the  external  wound,  but  as  a 
rule  not  in  the  heart  itself.  Even  probing  of  the  heart  wound, 
while  it  may  give  rise  to  weakness  and  syncope,  is  not 
accompanied  by  pain.  Thus,  one  patient  whose  left  ventricle  had 
been  wounded  thought  that  the  knife  had  only  gone  through  his  clothes. 
Blood  is  often  found  spurting  from  the  wound  with  a  well-defined  pulsa- 
tion. Sometimes  it  is  foamy  and  mixed  with  air,  indicating  that  the  lung 
has  been  penetrated. 

PHYSICAL    SIGNS. 

The  area  of  cardiac  dulness  is  increased  or  is  replaced  by  tympany 
(pneumo-hsemopericardium) .  The  heart  sounds  are  replaced  by  loud 
churning  or  water-wheel  murmurs.  The  blowing  murmur  caused 
by  the  jet  of  blood  passing  out  of  the  heart  may  also  be  distinguished. 

The  pulse  becomes  small,  weak,  rapid,  and  finally  imperceptible. 

Whenever  time  warrants,  an  X-ray  examination  should  be  done  at 
once,  and  the  bullet  or  foreign  body  located.  This  may  sometimes  be  very 
exactly  done  by  means  of  stereoscopic  pictures  and  greatly  simplifies  the 
operation. 

TREATMENT. 

Operative  interference  in  the  treatment  of  wounds  of  the  heart  was  first 
proposed  by  Rose,  who  confined  himself  to  opening  the  pericardium  and 
removing  the  blood  that  compressed  the  auricles.  This  procedure  was  often 
of  benefit  and  even  effected  cure  in  cases  where  bleeding  ceased  spontane- 
ously, but  when  the  heart  continued  to  bleed  it  was  of  no  avail. 

Up  to  this  time  it  had  been  thought,  in  spite  of  the  experiments  of 
physiologists,  that  suture  of  the  heart  wall  itself  would  be  accompanied  by 
instant  death.  But  in  1895  Salomoni  and  Del  Vecchio  demonstrated  that 
wounds  in  the  heart  of  the  dog  could  be  successfully  treated  in  this  manner; 
and  in  1896  Cappelen,  Farina,  and  Rehn  sutured  the  heart  wall  in  man. 
The  passing  of  the  sutures  had  no  ill  effects.  Cappelen's  and  Farina's 
patients  died  a  few  days  later  from  secondary  causes,  but  Rehn's  patient, 
who  had  received  a  stab  wound  in  the  right  ventricle,  operated  on  forty- 
eight  hours  after  the  injury,  recovered,  and  thus  a  revolution  in  cardiac 
surgery  was  made.  Rehn  had  demonstrated  that  wounds  of  the  heart 
could  and  should  be  successfully  explored  and  sutured  like  wounds  of 
other   viscera. 

If  the  patient  is  in  severe  collapse  from  loss  of  blood,  an  intravenous 

infusion  of  warm  salt  solution  (37°  C.)  should  be  begun  at  once  while  the 

operators  are  hastily  cleaning  and  disinfecting  the  field  of  Operation.     As 

a  last  resort  a  direct  arteriovenous  transfusion  into  the  veins  of  the  arm 

40 


626 


DISEASES   OF  THE   HEART   AND    AORTA. 


may  be  made  from  another  individual  by  the  method  of  Crile,  Buerger, 
or  Hartwell  while  the  operation  on  the  heart  is  going  on,  and  some  exsan- 
guinated patients  may  thus  be  saved. 

Operative  Procedure.  —  The  incision  should  be  sufficiently  large  to 
admit  of  a  satisfactory  exposure.  A  flap  is  made  in  the  chest  wall  over 
the  point  of  penetration,  usually  including  two  ribs  and  three  interspaces. 
The  flap  adopted  by  most  operators  is  horizontal  U  shaped  with  bifurca- 
tions pointing  to  either  left  or  right,  the  connecting  bar  passing  through 
either   sternochondral   or   costochondral   articulations.     Occasionally  the 


Fig.  294. — Exposure  of  the  heart  for  suturing  a  wound.  (After  G.  T.  Vaughan,  J.  Am.  M.  Assoc, 
1909,  lii.)  1,  heart;  2,  deep  sutures;  3,  superficial  sutures;  4  and  5,  retractors  on  the  pericardium;  0, 
left  pleural  line;  7,  flap  of  chest  wall  including  the  fourth,  fifth,  and  sixth  ribs;  8,  heart,  outlined  by 
broken  outline. 


form  is  that  of  an  upright  or  an  inverted  U,  a  H  ,  or  an  H.  If  the  wound 
is  near  the  sternum  and  has  not  already  penetrated  the  pleura,  that  cavity 
should  not  be  opened,  and  the  el  or  EH  shaped  flap  is  the  best;  but  if  the 
wound  has  pierced  the  pleura,  any  convenient  exposure  may  be  adopted. 
The  incision  through  the  pectoralis  major  should  be  parallel  to  its  fibres 
which  may  be  retracted.  The  sternochondral  or  costochondral  articula- 
tions are  cut  through,  the  ends  of  the  incision  prolonged  along  parallel  to 
the  ribs,  and  the  flap  forcibly  reflected  back,  fracturing  the  costal  cartilages 
to  permit  a  wide  opening.  If  the  pleura  has  not  been  penetrated,  it 
should  be  pulled  toward  the  outer  edge  of  the  wound  with  retractors.  A 
free  incision  should  be  made  into  the  pericardium,  the  pericardial  cavity 
emptied  of  clots,  the  wound  in  the  heart  located,  and  sutured  with  a  fine 
curved  needle  and  silk  thread.    In  passing  the  sutures  the  heart  wall  may 


WOUNDS   OF   HEART   AND   CARDIAC   TRAUMA.  627 

be  grasped  with  forceps  without  danger,  the  irregularity  which  accom- 
panies the  passing  of  the  needle  representing  merely  a  few  extrasystoles 
resulting  from  the  irritation,  and  passing  off  rapidly.  Elsberg  never  ob- 
served sudden  stoppage  of  the  heart  and  fibrillation  following  the  inser- 
tion of  sutures.  The  writer,  after  several  hundred  experiments  upon  ex- 
posed clogs'  hearts,  is  able  to  confirm  these  statements  of  Elsberg.  Elsberg 
states  that  the  interrupted  suture  is  preferable  to  the  continuous,  for, 
though  it  takes  longer  to  apply,  it  injures  fewer  muscle  fibres  and  is  more 
certain  to  hold.  The  sutures  should  be  tied  during  diastole;  these 
do  not  tear  out  as  readily  as  sutures  tied  during  systole.  In  tightening  the 
sutures  the  two  serous  surfaces  of  the  wound  should  be  pushed  in  so  as  to 
be  brought  into  apposition.  The  surfaces  unite  by  the  usual  growth  of 
fibrous  tissue.  The  nuclei  of  the  muscle  cells  near  the  wound  seem  to  be 
increased  in  number,  and  there  is  some  amitotic  and  mitotic  division  but 
no  definite  regeneration  of  muscle. 

Control  of  Hemorrhage.  —  When  the  bleeding  was  so  profuse  that 
death  seemed  imminent,  Elsberg  found  it  necessary  to  adopt  provisional 
means  for  stopping  bleeding  while  putting  in  the  sutures.  For  this  he  used 
a  hastily  placed  tobacco-pouch  suture,  or  even  a  ligature  about  the  whole 
heart  just  above  the  wound.  (This  does  not  apply,  of  course,  to  wounds 
in  the  upper  half  of  the  ventricles.)  He  was  then  able  to  place  the  sutures 
bloodlessly,  after  which  the  provisional  ligature  was  removed.  In  this 
way  he  was  able  to  suture  tremendous  wounds  (2  cm.  in  a  rabbit's  heart, 
corresponding  to  about  10  cm.  in  the  human  heart),  with  66  per  cent, 
of  recoveries. 

Large  wounds  of  the  auricle  may  be  more  difficult  to  control.  Sauer- 
bruch  recommends  stopping  the  bleeding  by  gently  compressing  the  auricle 
between  the  middle  and  ring  fingers  while  grasping  the  point  to  be  sutured 
between  the  index  finger  and  thumb.  Rehn  finds  that  with  some  care  a 
ligature  may  be  placed  about  the  auricle  to  still  the  bleeding  while  the 
sutures  are  rapidlj'-  put  in,  but  there  is  danger  of  death  from  fibrillation  if 
the  circulation  is  completely  cut  off.  The  writer  has  been  able  to  control 
the  hemorrhage  from  quite  large  wounds  in  the  dog's  heart  for  over  ten 
minutes  by  holding  his  finger  gently  against  the  wound.  The  heart's  action 
was  not  weakened  by  this  procedure,  nor  did  it  become  irregular;  and  suffi- 
cient time  was  gained  to  lay  the  sutures  carefully.  This  was  found  to  be 
more  bloodless,  and  for  large  wounds  more  convenient,  than  Elsberg's 
method  of  laying  temporary  sutures. 

If  possible  the  bullet  should  be  removed  unless  it  is  too  deeply  imbedded 
in  the  cavity  of  the  heart.  Under  these  circumstances  it  may  be  left  at 
least  for  a  subsequent  operation,  as  it  often  becomes  encapsulated  and  may 
do  no  further  harm.  All  operators  agree  that  operation  in  the  Sauerbruch 
negative  pressure  chamber  or  with  Brauer's  positive  pressure  lessens  the 
danger  of  pneumothorax,  and  is  therefore  advisable  when  it  requires  no 
delay.  It  is  particularly  useful  when  the  wound  is  about  to  be  closed,  to 
prevent  the  continuance  of  the  pneumothorax. 

As  regards  the  question  of  drainage,  each  individual  case  must  be  de- 
cided on  its  own  merits.  It  is,  of  course,  important  to  prevent  sepsis, 
purulent  pericarditis,,  and  pyopneumothorax.     When  the  pleura  has  not 


628  DISEASES   OF   THE   HEART   AND    AORTA. 

been  pierced,  the  pericardium  may  be  closed  in  a  large  number  of  cases 
without  drainage  (Rehn's  statistics  show  4  cases — 3  cures,  1  death — with- 
out drainage  of  pericardium;  with  drainage,  5  cases — 5  deaths,;  perhaps, 
however,  drainage  was  used  in  only  the  more  severe  cases).  When  the 
pleura  has  been  pierced,  it  should  usually  be  drained.  Whenever  bits  of 
cloth,  dirt,  etc.,  have  entered  the  wound,  it  should  always  be  drained. 

Before  closing  the  wound  the  pericardial  cavity  should  again  be 
explored  to  see  that  no  other  wounds  in  the  heart  wall  or  vessels  have 
been  overlooked. 

Occasionally  large  branches  of  the  coronary  arteries  are  found  to  be 
pierced  and  must  be  ligatured.  This  is  necessary,  and,  as  shown  by  Porter 
and  Baumgarten  (see  page  366),  is  not  always  fatal,  as  there  is  a  certain 
amount  of  collateral  circulation,  but  sudden  death  may  result  during 
subsequent  excitement,  so  that  in  such  cases  more  prolonged  rest  is  advisa- 
ble than  in  cases  of  simple  suture.  It  is  worthy  of  note,  however,  that 
this  complication  is  not  mentioned  in  the  twelve  cases  of  late  results  com- 
piled by  Rehn. 

After  closure  of  the  wound,  with  or  without  drainage,  administration 
of  urotropin  is  probably  advisable,  since  Crowe  has  found  that  it  is  excreted 
in  the  pleural  and  pericardial  fluids  in  a  concentration  sufficient  to  inhibit 
the  growth  of  bacteria;  and  Bernheim  believes  that  its  use  increases  the 
resistance  of  these  membranes  (in  dogs  at  least)  to  infection.  It  has, 
moreover,  no  harmful  effects. 

Results  of  Operation. — Since  Rehn's  first  operation  a  large  number  of 
cases  have  been  reported.  In  1907  he  was  able  to  collect  statistics  of  124 
cases — 49  recoveries  (39.5  per  cent.),  75  deaths  (60.5  per  cent.).  In  this 
series  there  were  only  15  cases  of  gunshot  wound,  but  in  a  series  of  30 
cases  of  the  latter  compiled  from  the  series  of  Ricketts,  Borchardt,  and 
Rehn,  there  were  14  recoveries  (46.6  per  cent.)  and  16  deaths  (53.4  per 
cent.).  Of  the  75  deaths  in  Rehn's  series  16  died  on  the  operating  table, 
17  died  of  loss  of  blood  and  collapse  within  two  days,  30  died  of  infection 
(purulent  pericarditis  and  empyema) .  In  many  cases  the  haste  of  operation 
prevented  disinfection  of  the  field.  One  patient  (Gerzen's)  died  of  sudden 
hemorrhage  on  the  fifty-third  day.  Rehn  also  collected  reports  of  12  cases 
from  nine  months  to  ten  and  one-half  years  after  operation.  In  nine  exam- 
ination of  the  heart  was  negative;  in  three  there  was  slight  dilatation. 
There  were  costopericardial  adhesions  in  5;  9  were  absolutely  free  from 
symptoms;  2  had  pains  down  left  arm;  1  precordial  pain.  Only  one  had 
symptoms  of  definite  cardiac  weakness. 

G.  T.  Vaughan  has  recently  summarized  and  tabulated  150  cases 
operated  on  between  1896  and  1909,  of  which  51  (34  per  cent.)  recovered, 
a  striking  contrast  to  the  12  per  cent,  of  recoveries  in  the  earlier  years  from 
which  Fischer's  series  was  taken. 


NON-PERFORATING   INJURIES. 

Injuries  of  the  chest  wall  which  do  not  enter  the  pericardium,  such  as 
blows  upon  the  chest,  frequently  produce  secondary  lesions  of  the  heart 
and  pericardium,  which  have  been  mentioned  in  previous  chapters. 


WOUNDS   OF   HEART   AND   CARDIAC   TRAUMA.  629 

The  first  case  of  cardiac  disease  from  contusion  was  recorded  by  Blan- 
card  in  1688  and  is  very  typical.  The  patient  was  a  peasant  45  years  of 
age,  previously  healthy,  who  was  run  over  by  a  hay-cart.  He  did  not 
sustain  any  fracture,  but  suffered  from  pain  in  the  chest,  dyspnoea,  then 
fever,  delirium,  and  died  11  days  later  of  purulent  pericarditis  and  myo- 
carditis. Similar  cases  were  recorded  by  Bonetus  (1700),  Akonside  (1766), 
and  numerous  other  writers  both  ancient  and  modern. 

Bernstein  in  1896  was  able  to  collect  126  cases  from  the  literature. 
In  autopsies  upon  42  of  these  cases  there  was  found 

Endocarditis  alone 16  times 

Myocarditis        "     0 

Pericarditis        "    10 

Endo-  and  myocarditis 4 

Peri-    and  myocarditis 5 

Endo-  and  pericarditis 5 

The  signs  and  symptoms  appeared: 

Immediately  after  the  trauma 67 . 6  per  cent. 

Within  one  month 17.5   "       " 

Within  one  year 4.7    "       " 

Later  than  one  year 7.1    "       " 

Time  not  given 3.1    "       " 

G.  Fischer  gives  a  list  of  the  causes  of  traumatic  rupture  of  the  heart 
in  his  series: 

Run  over  by  or  crushed  between  wheels  of  wagon 21 

Crushed  by  machinery 4 

Falls  from  considerable  heights 13 

Falls  from  heights  of  10  feet  or  less 7 

Struck  by  falling  objects 6 

Kicked  in  chest 4 

Hurled  against  wall 2 

.Kulbs  has  recently  investigated  the  subject  experimentally.  The 
results  in  23  animals  within  12  days  of  the  injury  were: 

Hemorrhages  into  the  heart  valves 17  times 

(1  rupture  of  an  aortic  valve) 

Subendocardial  or  sub  pericardial  hemorrhages 10  times 

extensive  hemorrhage  into  the  septum 3  times 

Pericardial  hemorrhages. 10  times 

Hemorrhages  from  lungs 6  times 

There  was  polymorphonuclear  infiltration  and  disintegration  of  muscle  fibres  in  the 
vicinity  of  the  hemorrhages. 

The  symptoms  and  signs  of  these  conditions  following  trauma  do 
not  differ  from  those  in  similar  lesions  due  to  other  causes,  and  have 
been  considered   under  those   heads. 


630  DISEASES    OF   THE    HEART   AND    AORTA. 

BIBLIOGRAPHY. 

Wounds  of  the  Heart  and  Cardiac  Trauma. 

For  historical  data  see — 
Ricketts,  B.  M.:  The  Surgery  of  the  Heart  and  Lungs,  New  York,  1904. 
Borchardt,  M.:  Ueber  Herzwunden  und  ihre  Behandlung.     Pfahlungs  verletzungen  von 

Herz  und  Lunge,  Samml.  klin.  Vortrage,  No.  411-412;    Chir.  No.  113-114,  Ser.  xiv, 

Heft  21-22,  Leipz.,  1906. 
Elsberg,  C.  A.:  An  Experimental  Investigation  of  the  Treatment  of  Wounds  of  the  Heart 

by  Means  of  Suture  of  the  Heart  Muscle,  J.  Exp.  Med.,  N.  Y.,  1899,  iv,  479. 
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1868,  ix,  571. 
Loison,  E.:  Des  blessures  du  pericarde  et  du  cceur  et  de  leur  traitement,  Rev.  de  Chir., 

Paris,  1899,  xix,  49,  205,  774;    1899,  xx,  37. 
Rehn,  L.:  Zur  Chirurgie  des  Herzens  und  des  Herzbeutels,  Arch.  f.  klin.  Chir.,  Berl.,  1907, 

lxxxiii,  723. 
Rose:  Deutsch.  Ztschr.  f.  Chir.,  xx.     Rosenthal:  Deutsch.  med.  Wchnschr.,  1895.     Del 

Vecchio:  Rif.  Med.,   1895;    Zentralbl.  f.  Chir.,   1895,   574.     Salomoni:    ibid.,   1896. 

Farina:  ibid.,  1896,  1224.     Quoted  from  Rehn. 
Rehn,   L.:  Ueber  penetrirende  Herzwunden  und  Herznaht,  Arch.  f.  klin.  Chir.,  Berl., 

1897,  lv,  315. 
Buerger,  L.  A:  Modified  Crile  Transfusion  Cannula,  J.  Am.  M.  Asso.,  Chicago,  1908,  li,  1233. 
Hartwell,  J.  A. :  A  Simple  Method  of  Blood  Transfusion  without  Cannula,  ibid.,  1909,  lii,  297. 
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Chir.,  Berl.,  1907,  lxxxiii,  565. 
Sauerbruch,  E.  F.:  Die  Verwendbarkeit  des  Unterdruckverfahrens  bei  der  Herzchirurgie, 

ibid.,  1907,  lxxxiii,  537;    also  The  Present  Status  of  Surgery  of  the  Thorax  and  the 

Value  of  the  Sauerbruch  Negative  Pressure  Procedure  in  the  Prevention  of  Pneumo- 
thorax, J.  Am.  M.  Asso.,  Chicago,  1908,  li,  808. 
For  discussion  of  the  positive  pressure  methods  see  Robinson,  S.:    Artificial  Intrapul- 

monary  Positive  Pressure;  Experimental  Applications  in  the  Surgery  of  the  Lungs, 

ibid.,  1908,  li,  803;   and  Green,  N.  W.,  and  Maury,  J.  W.  D.:  The  Positive  Pressure 

Method  of  Artificial  Respiration,  with  its  Experimental  Application  to  the  Surgery  of 

the  Thoracic  (Esophagus,  ibid.,  1908,  li,  805. 
Vaughan,  G.  T.:  Surgery  of  Wounds  of  the  Heart,  J.  Am.  M.   Asso.,  Chicago,    1909, 

lii,  429. 
Bernstein:  Ueber  die  durch  Kontusion  und  Erschtitterung  entstandenen  krankheiten  des 

Herzens,  Ztschr.  f.  klin.  Med.,  Berl.,  1896,  xxix,  519. 
Kiilbs:  Experimentelle  Untersuchungen  ueber  Herz  und  Trauma,  Verhandl.  d.  deutsch. 

path.  Gesellsch.,  Jena,  1908,  xii,  172. 


XIV. 
ANEURISM. 


Aneurism  (aneurysm)  (Greek  avevpi<a/ia  a  widening  out)  =  a  dilatation  of  artery  or 
veins  (Galen). 

An  aneurism  is  a  blood-containing  tumor  whose  walls  are  formed  by  the 
walls  of  a  blood-vessel  and  whose  cavity  is  in  direct  connection  with  the 
blood-vessel  from  which  it  arises  (Osier). 

Historical. — Hippocrates  (430  B.  C.)  and  the  early  Greek  writers  do  not  seem  to  have 
been  familiar  with  aneurism,  but  its  occurrence  and  nature  were  well  known  to  Rufus  and 
Galen  (A.D.  131-201),  who  recognized  two  forms:  "one  from  dilatation,  the  other  from 
wounding  of  a  vessel,"  usually  from  venesection  followed  by  sepsis. 


Fig.  295. — Specimen  of  a  large  aneurism.     (After  Hough.) 

Vesalius  (1543)  was  the  first  to  recognize  aneurisms  within  the  thorax  and  abdomen 
and  was  even  able  to  make  the  diagnosis  of  thoracic  aneurism  during  life.  Ambroise  Pare 
(sixteenth  century)  recognized  the  existence  of  "aneurism  by  anastomosis,  rupture,  erosion, 
and  wound,  along  with  the  frequency  of  thrombosis  within  the  sack."  He  was  also  the  first 
to  suggest  that  venereal  disease  was  a  factor  in  the  genesis  of  aneurism.  The  role  of  syphilis 
was  demonstrated  definitely  by  Lancisi  (1728).  The  next  great  step  was  made  by  Scarpa 
(1805),  who  demonstrated  that  the  most  important  mechanical  factor  was  weakening  of  the 
middle  layer  of  the  arterial  wall,  a  fact  which  has  furnished  a  basis  for  the  more  modern 
pathology  of  aneurism. 

CLASSIFICATION  OF  ANEURISM. 

It  is  extremely  difficult  to  make  a  satisfactory  classification  of  aneu- 
risms, but  the  following,  which  is  based  upon  that  of  Osier,  may  suffice  for 
most  purposes: 

631 


632  DISEASES   OF  THE   HEART   AND    AORTA. 

1.  True  aneurism  (aneurysma  verum,  aneurysma  spontaneum),  in  which  one  or 
more  of  the  coats  of  the  artery  form  the  walls  of  the  tumor. 

A.  Dilatation   aneurism. 

(a)  Sacculated,  in  which  the  bulging  or  out-pocketing  of  the  walls  does  not 

embrace  the  whole  circumference  of  the  artery  and  is  sharply  localized. 
(6)  Fusiform  (or  cylindroid)  aneurism,  in  which  the  dilatation  occurs  over  a 
larger  area  of  artery  whose  entire  circumference  is  involved  in  the  dilatation. 

2.  Dissecting  aneurism,  in  which  the  coats  of  the  artery  are  separated  and  a 
new  cavity  (sometimes  lined  with  endothelium)  is  formed  between  these  layers  (usually 
between  media  and  adventitia). 

3.  False  aneurism,  following  wound  or  rupture  of  an  artery,  consisting  of  a  peri- 
arterial haematoma,  all  the  coats  of  the  artery  having  been  penetrated. 

4.  Cirsoid  aneurism  or  telangioma,  a  tumor  consisting  of  a  large  number  of 
tortuous  arteries  which  are  continuous  with  the  artery  from  which  they  arise. 

5.  Arteriovenous  aneurism,  a  communication  between  artery  and  vein,  either 
direct,  aneurismal  varix,  or  with  the  intervention  of  a  sac,  varicose  aneurism. 

ARTERIES    AFFECTED. 

By  far  the  most  common  forms  are  the  true  aneurisms,  fusiform  and 
sacculated.  The  relative  frequency  in  the  various  arteries  is  shown  in  the 
following  statistics  of  530  cases  (Crisp) : 

Thoracic  aorta 175 

Popliteal  artery 137 

Femoral  artery 66 

Abdominal  aorta 59 

Carotid  artery 25 

Subclavian  artery 23 

Axillary  artery 18 

External  iliac  artery 9 

Cerebral  artery 7 

Common  iliac  artery 2 

Posterior  tibial  artery 2 

Gluteal  artery 2 

Pulmonary  artery 2 

Brachial  artery 1 

Subscapular  artery 1 

Ophthalmic  artery 1 

OCCURRENCE. 

According  to  a  large  set  of  statistics  compiled  by  Richter  and  by  Arn- 
sperger,  aneurism  of  the  aorta  represents  one  of  the  not  infrequent  causes 
of  death,  0.6  per  cent,  of  total  mortality  (Emmerich),  Brodier  1.2  per  cent., 
Miiller  1.49  per  cent.;  in  American  cities  0.6  per  cent.,  Philadelphia  0.6  per 
cent.,  St.  Louis  0.2  per  cent. 

According  to  Gibbons  and  Richter  the  percentage  of  deaths  from  aneurism  in  San 
Francisco  from  1866  to  1870  (1.35  per  cent.)  was  much  greater  than  elsewhere  in  the 
United  States.  Dr.  Gibbons  has  informed  the  writer  that  aneurism  at  that  time  was  par- 
ticularly common  among  stevedores,  who  formed  a  considerable  percentage  of  the  popula- 
tion, and  in  whom  syphilis,  alcohol,  and  hard  work  were  ever-present  factors.  With  the 
passing  of  the  adventurer  and  the  stevedore  as  important  elements  in  the  population,  the 
percentage  of  aneurism  in  San  Francisco  has  diminished,  being  0.90  per  cent,  in  1880-1884, 
0.42  per  cent,  in  1890-1894,  0.33  per  cent,  in  1900-1904  (Gibbons). 

On  the  other  hand,  in  communities  where  syphilis  is  common  the  fre- 
quency of  aneurism  increases.  Thus,  it  is  eleven  times  more  common  in  the 
British  Army  in  India  than  in  the  civilians  at  home,  and  much  more  common 


ANEURISM.  •  633 

in  the  British  than  in  the  Austrian  and  German  armies,  where  venereal  dis- 
ease is  five  times  less  prevalent. 

Aortic  aneurism  is  much  more  common  in  men  than  in  women. 

Crisp 67  women  out  of  551  cases 

Agnew 26  women  out  of  269  cases 

Lisfranc 13  women  out  of  154  cases 

Richter 58  women  out  of  736  cases 


164  women  out  of  1810  cases 
9.05  per  cent.,  or  1  in  11. 

On  the  other  hand,  48  per  cent,  of  cases  of  carotid  aneurism  and  66  per 
cent,  of  dissecting  aneurisms  occurred  in  women. 

As  regards  age  Crisp's  cases  were  distributed  as  follows: 

1  to  10   1         50  to  60  65 

10  to  20   71         60  to  70  25 

20  to  30   51         70  to  80   8 

30  to  40 198         80  to  90   2 

40  to  50  .129         90  to  101 1 

59  per  cent,  between  the  ages  of  thirty  and  fifty. 

As  regards  site  Lawson  gives  the  following  figures : 

Ascending  aorta 34 .     per  cent. 

Arch  of  aorta 34 . 8  per  cent. 

Descending  aorta 17.4  per  cent. 

Abdominal  aorta 13.8  per  cent. 

Hare  and  Holder  find  in  953  cases  collected  indiscriminately: 

Ascending 570  =  60.     per  cent. 

Transverse  arch 104  =  10.6  per  cent. 

Descending '. 110  =  11.5  per  cent. 

Unclassified 169  =  17.5  per  cent. 

figures  which  are  certainly  unusually  high  for  the  ascending  portion. 

Aneurisms  are  by  no  means  always  single,  but  may  sometimes  be  mul- 
tiple. Two,  three,  "  or  even  a  score  "  may  appear  along  the  course  of  the 
aorta,  or  numerous  aneurisms  may  be  present  in  the  peripheral  arteries. 
The  condition  is  simply  the  manifestation  of  the  generalized  action  of  the 
factors  of  sclerosis  and  blood-pressure  on  the  arterial  walls,  and  multiple 
aneurism  formation  is  one  of  the  features  of  experimental  adrenalin 
aortitis  (Erb,  Jr.). 

The  symptoms,  signs,  and  diagnosis  present  no  specific  features,  except 
the  ease  with  which  the  other  aneurisms  may  be  overlooked  after  one  is 
diagnosed.  Careful  examination  and  especially  fluoroscopic  examination 
will  prevent  this  error. 

PATHOLOGICAL  ANATOMY  AND  PATHOGENESIS. 

No  change  of  pressure  that  can  occur  during  life  is  sufficient  to  dilate 
an  artery  to  the  proportions  of  even  the  smallest  aneurism.  According  to 
the  elasticity  curve  of  Roy,  the  dilatation  occurring  between  the  blood- 
pressure  of  120  and  170  mm.  Hg  is  about  20  per  cent,  of  the  diameter  of  the 
artery,  and  the  results  of  Grehant  and  Quinquaud  show  that  very  little  fur- 
ther dilatation  occurs  if  pressure  is  raised  until  the  artery  ruptures  (at  a  pres- 
sure of  1680  to  4630  mm.  Hg;  10  to  20  times  the  blood-pressure  during  life). 


634 


DISEASES   OF   THE   HEART   AND    AORTA. 


Fig.  296. — Aneurism  arising  just  above  a  sinus 
of  Valsalva.  (From  a  specimen  in  the  Army  Medi- 
cal Museum,  Washington,  D.  C.)  OR.,  orifice  through 
which  the  aneurism  is  connected  with  the  aorta; 
AN.,  aneurismal  sac. 


Fig.  297. — Aneurism  of  the  ascending  arch  and 
innominate  artery.  (From  a  specimen  in  the  Army 
Medical  Museum.) 


D.  AOR. 


Fig.  298. — Aneurism  of  the  transverse  portion 
of  the  aortic  arch  penetrating  through  the  sternum. 
(From  a  specimen  in  the  Army  Medical  Museum.) 
INNOM.,  innominate  artery;  L.  CAR.,  left  carotid 
artery;  L.  SUB.,  left  sublavian  artery;  D.  AOR., 
descending  aorta. 


Fig.  299. — Aneurism  of  the  descending  aorta  eroding 
the  vertebra;.   The  sac  contains  a  laminated  clot. 


ANEURISM. 


635 


Changes  in  Arterial  Wall  in  Aneurism. — On  the  other  hand,  as  was 
first  shown  by  Scarpa  (1805),  aneurismal  dilatation  is  always  preceded  by 
changes  in  the  arterial  coats  and  especially  by  weakening  of  the  media. 
In  1875  Koester  showed  that  this  was  due  to  localized  degeneration  of  the 
elastic  fibres  as  the  result  of  certain  inflammatory  changes  in  the  vasa 
vasorum  of  the  media.  "The  inflammatory  process  begins  in  the  vasa 
vasorum  on  the  exterior  of  the  blood-vessel,  follows  them  perpendicularly 
into  the  muscularis  (media) ,  and  distributes  itself  within  this  layer,  being 
most  intense  at  the  places  where  the  vasa  vasorum  break  up  into  capillaries. 
As  a  result  of  this  chronic  multilocular  mesarteritis,  the  media  (muscle 
fibres  and  elastic  fibres)  degenerate.  The  intima  (which  may  be  thickened) 
and  the  adventitia  unite  to  form  a  thick  and  very  vascular  membrane 
which  forms  the  wall  of  the  aneurism."  Since  these  studies  of  Koester, 
writers  are  practically  agreed  that  the  degeneration  of  elastic  tissue  result- 
ing from  mesarteritis  is  the  underlying  cause  of  aneurism  formation. 


WALL 


ELAS 


WALL 


Fig.  300. — Sections  through  the  wall  of  an  aneurism.  (Photomicrographs  made  by  Dr.  C.  S.  Bond.) 
A.  Section  through  the  wall  of  an  aneurism  showing  the  clot  unorganized.  B.  Orcein  stain  showing  the 
destruction  of  elastic  tissue  in  the  aneurism  wall.     Elastic  tissue  (ELAS)  stained  dark. 


Simple  arteriosclerosis  in  which  thickening  of  the  intima  is  the  essential 
feature  does  not  weaken  the  wall  of  the  artery  and  plays  no  role  unless  the 
media  be  destroyed.  This  fact  is  further  borne  out  by  the  experimental 
changes  in  the  artery  produced  by  injection  of  adrenalin  (see  page  343). 
The  resulting  lesion  is  a  mesarteritis  without  changes  in  the  intima,  quite 
dissimilar  to  the  ordinary  arteriosclerosis  of  man;  but  aneurisms,  and  even 
multiple  aneurisms,  are  present  in  a  large  percentage  of  the  animals.  Other 
toxic  substances,  bacterial  toxins,  lead,  alcohol,  nicotin,  lactic  and  other 
acids,  etc.,  produce  these  changes. 

Fabris  has  also  produced  aneurisms  by  external  cauterization  of  the 
arterial  wall  with  silver  nitrate.  A  local  inflammation  was  thus  set  up  in 
the  adventitia  and  media,  which  resulted  in  degeneration  of  the  fibres  of 
the  latter  and  their  replacement  with  young  fibrous  tissue  devoid  of  elastic 


636  DISEASES   OF   THE   HEART   AND    AORTA. 

fibres.  In  a  few  cases  there  was  slight  intimal  thickening.  The  resistance 
of  such  a  fibrous  tube  is  less  than  that  of  an  elastic  tube,  and  aneurismaj 
dilatation,  sometimes  localized,  sometimes  fusiform,  took  place  in  from 
20  to  25  days. 

Etiological  Factors. — In  man  the  etiological  factors  of  aneurism  are 
those  that  produce  mesarteritis.  Chief  among  these  is  syphilis,  which,  as 
first  noted  by  Ambroise  Pare  and  Lancisi,  is  concerned  in  a  very  large  per- 
centage of  the  cases  (Klemperer  25  per  cent.,  Fraenkel  36  per  cent.,  Puppe 
36  per  cent.,  Trier  40.5  per  cent.,  Heiberg  41.87  per  cent.,  Bramwell  50  per 
cent.,  Thieberge  50  per  cent.,  v.  Noorden  54  per  cent.,  Gerhardt  56  per  cent., 
Schutz  64.7  per  cent.,  Welch  66  per  cent.,  Etienne  69  per  cent.,  Malmsen 
80  per  cent.,  Hanpeln  82  per  cent.,  Backhaus  85  per  cent.,  Heller  85  per 
cent.,  Rasch  92  per  cent.).  This  is  especially  true  of  aneurisms  occurring 
in  young  men  and  women,  when  the  other  factors  of  arteritis  play  a  rela- 
tively less  marked  role  than  in  later  life;  so  that,  as  stated  by  Professor 
Osier,  the  presence  of  an  aneurism  in  a  man  or  woman  under  thirty  is 
almost  to  be  regarded  as  presumptive  evidence  of  syphilis.  Moreover, 
syphilitic  aortitis  is  often  most  intense  in  the  first  part  of  the  ascending 
aorta,  hence  the  commonness  of  the  lesion  at  this  site  (Heller).  It  must 
be  added,  however,  that,  though  the  careful  researches  of  OpMils  have 
failed  to  substantiate  this  general  belief,  a  positive  Wassermann  reaction 
is  usually,  obtained  in  such  cases. 

Other  factors  are  alcohol,  hard  work,  lead  poisoning,  tobacco,  gout, 
nephritis,  and  especially  the  infectious  diseases.  Trauma  (blows,  gunshot 
and  knife  wounds,  etc.)  furnishes  a  frequent  cause  for  aneurisms  of  the 
peripheral  arteries  and  abdominal  aorta,  but  is  much  rarer  in  thoracic 
aneurisms.  Cases  like  that  described  by  Hirsh  and  Robins  show,  however, 
that  it  is  a  factor  to  be  reckoned  with.  The  relative  importance  of  these 
factors  is  shown  by  the  figures  of  Etienne,  who  found  syphilis  as  a  cause 
of  166  out  of  230  aneurisms,  while  alcoholism  was  present  in  only  28.  More- 
over, according  to  Hamilton,  aneurisms  are  extremely  rare  in  sanitaria 
for  alcoholics.  They  are,  however,  most  important  contributory  causes, 
not  only  increasing  the  arteriosclerosis  but,  by  raising  the  blood-pressure, 
increasing  the  liability  to  dilatation.  Thus,  aneurisms,  according  to  most 
writers,  are  particularly  common  in  syphilitics  who  perform  hard  work. 
This  is  exquisitely  shown  in  the  colored  patients  at  the  Johns  Hopkins 
Hospital,  in  whom  syphilis  is  very  common  and  who,  as  a  rule,  perform 
hard  work.  Among  these  persons  aneurisms  are  between  five  and  ten  times 
as  common  as  in  the  patients  in  the  white  wards  of  the  same  hospital.  The 
sudden  rise  of  blood-pressure  which  occurs  during  lifting  and  heavy  strains 
(cf.  page  188)  is  a  particularly  important  predisposing  factor,  and  the 
patient  often  notices  that  his  first  symptoms  occurred  at  the  time  of  a 
heavy  muscular  strain  or  began  just  afterwards. 

EMBOLIC  AND  MYCOTIC  ANEURISMS. 

A  somewhat  rarer  form  of  aneurism,  described  by  Tufnell  (1853),  Ogle 
(1866),  Church  (1870),  Smith  (1870),  Ponfick  (1873),  and  Weinberger 
(1907),  is  the  so-called  embolic  or  mycotic  aneurism,  which  arises  especially 


ANEURISM.  637 

during  the  course  of  acute  septicemias,  of  puerperal,  arthritic,  and  influen- 
zal origin.  Septic  emboli  become  lodged  astride  of  the  bifurcation  of  the 
smaller  arteries,  causing  necrosis  of  the  neighboring  portions  of  the  arterial 
wall,  which  may  protrude  or  form  a  true  aneurism,  or  may  rupture  into 
the  surrounding  tissues,  forming  a  false  aneurism.  These  arise  acutely 
during  the  course  of  the  febrile  diseases.  They  are  usually  multiple  and 
are  confined  to  the  smaller  arteries,  while  the  sclerotic  aneurisms  are  more 
common  in  the  larger  arteries. 

DEVELOPMENT    OP    THE    ANEURISM. 

Once  formed,  the  aneurismal  sac  expands  progressively,  usually  pushed 
outward  from  the  artery  along  the  lines  of  the  least  resistance  until  it 
meets  with  some  obstruction.  The  higher  the  blood-pressure  the  more 
rapid  is  the  dilatation.  When  pointing  freely  into  the  thoracic  cavity,  it 
may  expand  until  it  fills  almost  the  entire  half  of  the  cavity  before  ruptur- 
ing. On  the  other  hand,  if  the  proliferation  of  connective  tissue  in  the  wall 
of  the  aneurism  does  not  keep  pace  with  its  growth,  or  if  local  necrosis 
from  infection,  pressure,  or  irritation  takes  place,  a  secondary  bulging  will 
take  place  at  this  point,  and  it  finally  ruptures  there.  A  rupture  is  especially 
precipitated  by  high  blood-pressure,  such  as  occurs  on  exertion,  and  sud- 
den deaths  from  this  cause  are  quite  common  in  aneurism. 

When  the  wall  of  the  sac  presses  upon  neighboring  tissues  it  begins 
to  erode  them.  The  pressure  acts  in  the  following  way:  First,  it  cuts  off 
the  blood  supply  to  the  neighborhood  because  the  pressure  within  it  (aortic 
pressure)  is  greater  than  that  in  the  smaller  blood-vessels.  Secondly, 
necrosis  of  these  tissues  results  from  this  compression.  Thirdly,  the  products 
of  necrosis  are  absorbed  by  the  cells  in  the  tissues  of  the  very  vascular  wall 
of  the  aneurism  as  fast  as  they  are  produced.  Bone  tissue  too  is  absorbed 
by  the  activity  of  the  osteoclasts,  and  the  wall  of  the  sac  thus  advances 
gradually  through  the  chest  wall  very  much  as  a  tumor  might  do,  though 
without  the  intervention  of  abnormal  cells.  Thus,  the  aneurism  eats  its 
way  through  muscle,  cartilage,  bone,  nerves,  and  skin,  and  also  through 
the  walls  of  the  other  vessels  (pulmonary  artery,  vena  cava,  etc.),  bronchi, 
and  oesophagus,  always  forced  onward  in  a  straight  line  by  the  arterial 
pressure  in  the  aorta.  Hence,  aneurisms  usually  point  in  the  direction 
given  them  by  the  impact  of  the  blood  stream;  those  of  the  ascending  aorta 
pointing  to  the  right,  those  of  the  arch  pointing  upward,  those  of  the 
descending  arch  pointing  backward  and  to  the  left  (Fig.  301).  However, 
resistance  of  surrounding  tissues,  and  especially  local  thinning  of  the  aneu- 
rismal wall,  may  cause  its  course  to  be  deflected  somewhat  from  these 
typical  directions. 

Rupture. — The  excessive  thinning  which  results  in  perforation  fre- 
quently occurs  when  the  sac  has  just  penetrated  the  wall  of  one  of  the  sur- 
rounding structures, — bronchus,  oesophagus,  etc., — no  doubt  from  the  pres- 
ence of  local  infections  within  their  lumina,  and  sudden  death  may  result 
from  hemorrhage.  Or,  on  the  other  hand,  small  hemorrhages  may  occur 
from  the  erosion  of  smaller  bronchial  or  oesophageal  arteries  (see  page  639) 
or  through  the  wall  of  the  aneurism  without  any  such  immediate  results. 
40 


638 


DISEASES    OF   THE    HEART    AND    AORTA. 


The  growth  of  an  aneurism  after  penetrating  the  chest  wall  is  well 
shown  by  the  outlines  in  Fig.  302.  The  sac  becomes  larger  and  larger, 
secondary  sacculations  appear  upon  its  surface  (Fig.  302),  and  over  these 
the  thinned  skin  becomes  smooth,  tense,  glossy,  and  finally  of  a  reddish 


Fig.  301. — Composite  figure  showing  the  relations  of  various  aneurisms  to  surrounding  structures^ 
<Schematic.)  OES,  oesophagus;  AN  SUBCL,  aneurism  of  the  subclavian  artery;  SUP.  V.  C,  superior 
vena  cava;  AN  INNOM,  aneurism  of  the  innominate  artery,  pointing  through  the  skin;  AN  TR,  aneu- 
rism of  the  transverse  portion  of  the  arch;  PIIREN,  phrenic  nerve;  REC  LAR,  recurrent  laryngeal; 
L.  VAG,  left  vagus;  DA,  ductus  arteriosus  (Botalli);  AN,  P.A.,  aneurism  of  the  pulmonary  artery;  LBR, 
left  bronchus;  AN.  SIN  VALS,  aneurism  arising  from  a  sinus  of  Valsalva;  AN.  R.  COR  and  AN.  L.  COR., 
aneurism  of  right  and  left  coronary  arteries;  AN  RA,  aneurism  of  right  auricle;  AN.  L.V.,  aneurism  of  left 
ventricle.     The  arrows  show  the  directions  in  which  the  aneurisms  usually  point. 


or  brawny  hue.  The  whole  process  usually  requires  a  few  months,  but  it 
may  occur  more  rapidly.  On  the  other  hand,  in  a  case  described  by  Hirsh 
and  Robins  the  pulsating  tumor  upon  the  chest  remained  practically 
unaltered  in  size  for  twenty-five  years,  during  which  the  patient  continued 
to  do  heavy  work.  Finally,  however,  a  stage  is  reached  at  which  a  small 
perforation  appears,  oozing  blood,  and  soon  after,  with  a  rush  of  blood  like 


ANEURISM.  639 

the  bursting  of  a  dam,  the  aneurism  ruptures  and  the  patient  bleeds  to 
death  within  a  few  minutes. 

The  rupture  into  the  bronchus,  trachea,  or  oesoph- 
agus proceeds  in  the  same  way.  There  is  usually  a  slight  premonitory 
haemoptysis.  This  generally  occurs  a  few  days  before  death,  but  may  not 
occur  until  a  few  hours  before  the  final  rupture;  or,  as  in  the  case  reported 
by  Clarke,  it  may  be  present  for  months.  At  the  final  rupture  the  blood 
spurts  out  of  the  patient's  mouth  and  nose  and  may  even  be  projected 
several  feet  away  from  the  bed. 

On  the  other  hand,  when  the  aneurism  ruptures  inter- 
nally into  one  of  the  cavities  of  the  body,  the  symptoms  are  quite  differ- 
ent. The  patient  feels  something  giving  way  within.  Sudden  collapse, 
asthmatic  attack,  and  gradual  exsanguination  mark  rupture  into  the 
pleura.  Rupture  into  the  pericardium  is  attended  with  intense  pain, 
breathlessness,  collapse,  an  anginal  attack,  and  occasionally  a  con- 
vulsion. In  rupture  into  the  pericardium 
death    is    accelerated    by    cutting    off    the  /^\M 

venous    inflow,    just    as    in  simple   pericar-  J^^^^& 

dial  effusion,  only  within  a  minute  or  two.  /^M1'   " 

Of    course,   under   these    circumstances  no 
blood   appears  externally. 

Rupture    of    the    aneurism    into 
the  pulmonary  artery,  vena   cava, 

.      ,    .  .      ,  •    i.  >    •    i  Fig.  302.— Tracings  of  the  outlines 

Or    right    auricle    Or  right  Ventricle  SOme-       of  an  aneurism  of  the  innominate  artery, 

times  occurs.      The  symptoms  are  usually     swing  the  progress  of  its  growth  and 

i  i  «  the  formation  of  secondary  prominences 

Sudden    Onset    Of    dyspnoea,    Weakness,    Often       upon  its  surface.     (Tracings  made  on 

collapse,  and  extreme  cyanosis,  which  ends     g£  ^^^2  and  DeC'  2-)    °ne" 
in  death  after  a  period  varying  from  sev- 
eral hours  to  several  months,  the  heart  being  unable   to  accommodate 
itself  to  the  sudden  changes  in  the  distribution  of  blood. 

However,  in  a  large  percentage  of  cases  (863  cases — 47  per  cent. — of 
Arnold's  1829  cases)  death  from  aneurism  is  not  due  to  rupture 
of  the  sac  but  "from  pressure  of  the  sac  upon  important  nerves  and  blood- 
vessels, or  from  secondary  changes  which  take  place  in  these  tissues  and  in 
other  vital  organs,  as  a  direct  or  indirect  result  of  such  pressure."  In  154 
cases  without  rupture  the  causes  of  death  were: 

Obstruction  to  air-passages 66 

Exhaustion 50 

Affections  of  lungs  and  pleura 28 

Pericardial  affections 8 

Pressure  on  the  vena  cava  superior 1 

Collapse 1 

Clotting  within  an  Aneurism. — The  healing  of  an  aneurism  occurs  by 
clotting  within  the  sac.  Since  the  latter  is  lined  by  arterial  intima,  there 
is  under  ordinary  circumstances  no  more  reason  for  clotting  to  take  place 
there  than  elsewhere  in  the  artery.  As  shown  by  Mall  and  Welch,  arterial 
thrombosis  occurs  quite  suddenly  when  the  circulation  is  slowed  and  pulsa- 
tion disappears,  especially  if  there  is  some  injury  to  the  wall  of  the  artery, 
and  this  is  a  most  important  factor  in  bringing  about  thrombosis  within 


640  DISEASES    OF   THE   HEART    AND    AORTA. 

an  aneurism,  though  some  fibrin  ferment  must  be  present.  As  a  rule,  in 
fusiform  aneurisms  the  circulation  is  too  strong  and  rapid  for  coagulation 
to  set  in,  but  in  sacculated  aneurisms  a  certain  amount  of  fibrin  collects 
along  the  wall.  Each  layer  of  fibrin  serves  as  a  filter  for  leucocytes,  from 
which  more  fibrin  ferment  is  generated  and  a  second  layer  laid  down,  and 
so  on  until  occasionally  the  entire  aneurism  may  be  filled  spontaneously 
by  a  laminated  clot. 

Owing  to  the  large  area  and  great  thickness  of  the  fibrin  deposited, 
and  to  the  fact  that  the  intimal  endothelium  is  in  most  places  still  intact, 
there  is  little  entrance  of  fibroblasts  into  the  clot  and  little  organization 
goes  on.  The  aneurismal  clot  is,  therefore,  not  converted  into  a  solid  mass 
of  connective  tissue  as  in  endarteritis  or  thrombo-angeitis  obliterans,  but 
remains  simply  laminated  fibrin.  Deposits  of  calcium  salts  sometimes 
occur  upon  them,  however,  and  tend  to  convert  the  obliterated  aneurism 
into  a  solid  tumor. 

SYMPTOMS. 

The  signs  and  symptoms  produced  by  aneurisms  vary  greatly,  and 
depend  upon  the  site  at  which  they  occur  along  the  aorta,  so  that  Broad- 
bent  has  been  "led  to  divide  thoracic  aneurisms  into  two  classes, — namely, 
aneurisms  of  physical  signs  and  aneurisms  of  symp- 
toms, from  the  predominance  of  physical  signs  and  symptoms  respec- 
tively,— the  former  term  applying  to  aneurisms  of  the  ascending. aorta 
and  first  part  of  the  arch,  the  latter  to  aneurisms  of  the  transverse  and 
descending  portions  of  the  arch." 

The  symptoms  produced  by  aneurisms-  arise  secondarily  as  the 
result  of  pressure  upon  surrounding  structures.  Shortness  of 
breath  is  frequent,  resulting  both  from  pressure  on  the  trachea  and 
bronchi  and  from  concomitant  disturbances  in  the  circulation  (embarrass- 
ment of  heart  action,  stasis  from  pressure  on  veins) .  C  o  u  g  h  is  a  common 
symptom,  from  pressure  upon  the  recurrent  laryngeal  nerves  as  well  as 
from  bronchitis .  as  a  result  of  pressure  (occasionally  from  tuberculosis) . 
The  pressure  on  the  laryngeal  nerve  causes  paralysis  of  the  corresponding 
vocal  cord  and  gives  the  cough  a  peculiar  metallic  quality  known  as  "the 
goose  cough,  brassy  cough,  stenotic  cough,  paretic  cough/' 
etc.  It  is  really  the  cough  characteristic  of  paralysis  of  one  vocal  cord,  and 
it  is  characteristic  of  aneurism  only  in  so  far  as  that  the  latter  is  the  com- 
monest circulatory  disturbance  in  which  laryngeal  paralysis  is  a  symptom. 

Paroxysmal  dyspnoea  may  occur,  and  especially  in  certain 
postures  in  which  the  trachea  and  bronchi  are  pressed  upon  by  the  aneurism. 
This  ''asthma''  is  the  most  common  symptom  of  patients  presenting 
themselves  for  treatment,  and  careless  physicians  often  accept  its  presence 
as  the  final  verdict,  remaining  oblivious  to  the  true  nature  of  the  disease. 
Attacks  of  dyspnoea  or  suffocation  very  commonly  come  on  during  sleep 
when  the  laryngeal  muscles  relax  and  narrow  the  laryngeal  slit.  They 
occur  especially  when  the  patient  falls  into  an  unpropitious  position,  so 
that  he  soon  finds  it  most  convenient  to  sleep  bolstered  upright  and  leaning 
slightly  forward  with  chin  depressed.  This  position  affords  the  maximum 
space  about  the  air-passages  with  the  minimum  of  tension  upon  them. 


ANEURISM.  641 

Not  infrequently  a  small  aneurism  of  the  arch  pointing  backward 
and  pressing  upon  the  trachea  or  bronchi  may  cause  actual  suffoca- 
tion, for  which  tracheotomy  may  be  necessary.  In  some  cases,  however, 
the  aneurism  may  be  situated  so  low  that  it  may  be  impossible  to  do  the 
tracheotomy  below  the  area  compressed.  The  only  possible  means  of  relief 
is  then  to  dissect  or  pull  the  aneurism  away  from  the  trachea,  or  to  intro- 
duce a  metal  tube  into  the  latter  and  thus  hold  the  trachea  open  at  the  point 
compressed.  This  procedure  is,  of  course,  extremely  difficult,  and  under 
all  circumstances  great  dyspnoea  from  pressure  on  the  trachea  is  in  itself 
a  dangerous  symptom. 

P  ai  n  is  a  common  symptom  in  aneurism,  and  may  be  of  three  kinds: 

1.  Angina  pectoris — reflex  referred  pain  over  the  heart  or  down  the  arm. 
This  is  especially  common  in  early  aneurism  at  the  beginning  of  the  ascending  aorta  and 
from  the  sinus  of  Valsalva,  and  is  probably  due  to  changes  in  or  pressure  upon  the  aortic 
plexus.    After  these  changes  have  been  long  established  this  pain  may  disappear  (Osier). 

2.  Sharply  localized  pain  may  arise  in  or  about  the  aneurism  itself  when 
its  walls  are  pressed  upon,  or  even  spontaneously,  and  especially  when  it  begins  to  erode 
the  chest  wall. 

3.  A  second  form  of  referred  pain  arises  without  reflex  mechanism  directly 
from  pressure  upon  the  intercostal  nerves  and  those  of  the  brachial  plexus,  especially  in 
aneurisms  of  the  transverse  and  descending  aorta.  The  latter  may  give  rise  to  pain  in  the 
back,  shoulder-blades,  and  sides  and  also  down  the  arm,  and  may  for  a  while  be  mistaken 
for  intercostal  neuralgia  or  for  the  pain  of  pleurisy.  Pain  down  the  arm  is  especially  com- 
mon when  the  aneurism  involves  the  innominate  or  subclavian  arteries,  particularly  when 
the  return  of  venous  blood  is  interfered  with  by  pressure  on  the  veins. 

Difficulty  in  swallowing  and  the  feeling  of  a  lump  in  the 
throat  may  result  from  pressure  upon  the  oesophagus,  especially  when  the 
aneurism  is  adherent  to  it  or  is  infiltrating  its  walls.  This  is,  of  course, 
characteristic  of  aneurisms  of  the  descending  portions  of  the  arch  and  to  a 
less  degree  of  the  descending  aorta.  It  is  not  at  all  a  rare  symptom,  and 
yet  is  by  no  means  as  common  as  might  be  expected  even  when  the  aneurism 
is  large. 

PHYSICAL   SIGNS. 

1.  The  presence  of  a  visible  mass  upon  the  chest  wall  or  elsewhere 
showing  a  pulsation  of  an  elevation  which  begins  about  0.05-0.10  second 
later  than  the  ventricular  systole  (or  the  first  heart  sound),  and  which  on 
palpation  is  felt  to  be  forcible  and  expansile  in  character  (i.e.,  presses 
outward  in  all  directions).  The  shock  with  the  first  sound  is  usually  well 
felt  and  often  accompanied  by  a  thrill;  and  a  diastolic  shock  accompanying 
the  second  sound  is,  when  present,  almost  characteristic.1  On  auscultation 
there  is  usually  a  systolic  murmur  heard  over  the  aneurism,  and  occasionally 
a  diastolic  murmur  when  the  blood  flows  back  into  the  aorta  during  diastole, 
especially  through  a  narrow  opening.  This  is,  of  course,  most  common 
and  most  marked  when  aortic  insufficiency  is  present,  either  organic  or 
relative,  resulting  from  the  general  dilatation  of  the  aorta. 

Long  before  an  aneurism  perforates,  and  in  many  cases  when  it  is 
not  pointing  outward  but  upward  toward  the  episternal  notch  or  clavicles, 

1  The  writer  has  seen  one  case  of  hypernephroma  of  the  thigh  in  which  a  diastolic 
shock  was  palpable,  but  this  is  rare  even  in  the  most  vascular  tumors,  such  as  the  vascular 
mediastinal  sarcomata. 
41 


642  DISEASES   OF  THE   HEART    AND    AORTA. 

there  may  be  seen  a  diffuse  systolic  lifting  of  the  whole  chest 
wall  or  of  the  parts  above  the  tumor.  The  localized  heaving  is,  of  course, 
most  marked  when  the  aneurism  is  in  the  vicinity  of  cartilages  or  articu- 
lations in  the  chest  wall  and  in  younger  individuals;  while  the  most  diffuse 
heaving  occurs  in  the  portions  and  persons  where  the  ribs  and  sternum 
are  most  rigid.  The  impulse  thrill  and  shocks,  systolic  and  diastolic,  are 
also  frequently  present  when  no  heave  or  pulsation  can  be  seen. 

For  discerning  and  timing  slight  pulsations  the  writer  has  fre- 
quently found  it  convenient  to  hold  the  index  finger  a  few  millimetres 
away  from  the  chest  wall,  and  watch  for  either  a  periodic  narrowing  of 
the  slit  between  the  finger  and  the  chest  or  for  a  visible  movement  of  the 
shadow  cast  by  the  finger  upon  the  chest.    For  the  latter  purpose  the  light 

should  strike  as  nearly  as  possible  paral- 

E**/  lei  to  the  chest  so  as  to  magnify  the 

^V  movement  of  the  shadow  (Fig.  303). 

%v  When  aneurism  is  suspected,  it  is 

*^5^^  particularly    important    to   ex- 

"1\  i ^tofeSSy  amine    the    patient's    back    as 

^A^-^^gNy  well  as  to  inspect  carefully  the  front  of 

^^^  *^^v         *^e  cnes^-     This  precaution  was  always 

^rV     particularly  emphasized  by  one  of  the 

great  teachers  of  medicine  who  also  un- 

Fig.  303. — Method  of  inspecting  for  pulsa-       .  .  ..       „.  .    . 

tions.    e,  eye  of  observer  looking  down  from     intentionally  illustrated  its  importance. 

above;    E',  eye  of  observer  upon  level  with        Qn    one    occasion    he    and    another    prO- 
pulsating  area;  finger  above  pulsating  area;  ...  ..... 

S  and  S',  shadows  thrown  by  the  finger  upon       feSSOr,  who  Was  VlSltmg  the   clmiC,  dem- 

Zr^TZrZJo1t:t£Zt^::;     onstrated  to  the  junior  students  a  case 

arrows  indicate  the  extent  of  movement  seen.        of  SUSpected   aneurism,   but   Sent  him  to 

the  wards  for  X-ray  examination  with- 
out having  examined  the  back.  The  absolute  diagnosis  was  at  once  made 
by  the  house  officer,  who  in  the  routine  examination  discovered  a  well- 
marked  pulsation  at  the  back  at  the  level  of  the  third  thoracic  vertebra. 
Dulness  on  percussion  is  of  course  present  over  an  aneurism  as 
over  other  tumors,  the  note  being  flat  when  the  tumor  is  near  the  surface, 
slightly  improved  when  it  is  deep.  This  improvement  is  often  very  slight 
in  deeply  situated  aneurisms  of  the  arch,  and  percussion,  especially  in 
the  first  right  and  left  interspaces  and  over  the  manubrium,  should  be 
very  carefully  carried  out  when  aneurism  is  suspected.  The  exact  outlining 
of  an  aneurism  by  percussion  may  be  very  difficult.  The  area  of  dulness 
on  even  the  lightest  percussion  may  be  considerably  greater  than  that  of 
the  aneurism  itself  (just  as  is  true  of  the  cardiac  dulness,  see  page  147). 
The  uniform  dilatation  of  the  aortic  arch  (to  about  twice  its  normal  diame- 
ter) which  is  so  frequent  in  aortic  insufficiency  may  give  an  area  of  dulness 
over  and  on  both  sides  of  the  sternum  which  may  lead  to  a  diagnosis  of 
aneurism  (Fig.  311).  The  true  nature  of  the  condition  can  be  shown  only 
by  the  X-ray  (Fig.  308). 

In  large  and  in  deeply  situated  aneurisms  direct  percussion  of  the  ver- 
tebral spines  by  Koranyi's  method  may  show  an  unusual  dulness  over  the  corre- 
sponding area  (especially  between  the  third  and  the  sixth  thoracic  spines)  and  may  prove 
of  assistance  in  establishing  the  diagnosis.    It  is,  of  course,  of  no  value  in  those  aneurisms 


ANEURISM.  643 

of  the  arch  in  which  the  trachea  is  interposed  between  vertebrae  and  the  tumor.  The  heart 
is  occasionally  very  much  displaced  by  an  aneurism  which  may  itsejf  come  to  occupy  the 
usual  site  of  the  heart,  so  that  on  casual  examination  it  may  be  mistaken  for  the  latter. 
With  careful  auscultation,  however,  this  error  may  be  excluded. 

Pressure  upon  the  sympathetic  on  either  side  may  give  rise  to  inequality 
of  the  pupils,  usually  with  a  dilatation  upon  the  affected  side.  In 
late  stages,  however,  the  sympathetic  on  that  side  may  be  completely 
destroyed  and  the  pupil  then  becomes  smaller  on  the  affected  side. 
The  dilatation  is  best  seen  when  there  is  moderate  illumination,  for  in  strong 
lights  the  reflex  pupillar  constriction  may  overcome  the  dilator  action  of 
the  sympathetic. 

Tracheal  Tug. — W.  S.  Oliver,  who  described  the  sign  in  1878,  gave 
the  following  directions:  "Place  the  patient  in  the  erect  position  and 
direct  him  to  close  his  mouth  and  elevate  his  chin  to  the  fullest  extent; 
then  grasp  the  cricoid  cartilage  between  the  finger  and  thumb  and  use 
gentle  upward  pressure  upon  it;  when  if  dilatation  or  aneurism  exist  the 
pulsation  of  the  aorta  will  be  distinctly  felt  transmitted  through  the  trachea 
to  the  hand."  This  tracheal  tug  is  no  absolute  sign  of  aortic  dilatation. 
It  is  as  readily  produced  when  solid  mediastinal  tumors  or  enlarged  bron- 
chial glands  adhere  to  both  aorta  and  air-passages  as  from  aneurism. 

Sewall  finds  that  in  a  large  percentage  of  tuberculous  individuals 
(91  out  of  212 — 43  per  cent.)  a  slight  twitch  of  the  trachea  may  be  felt 
during  inspiration,  due  to  contraction  of  the  accessory  muscles,  but  this  is 
not  continuous,  not  synchronous  with  the  pulse-beat,  and  should  not  be 
mistaken  for  the  true  tracheal  tug.  Moreover,  in  his  large  series  of  obser- 
vations this  tracheal  twitch  of  non-aneurismal  origin  was  always  confined 
to  inspiration.  Sewall  found  it  particularly  common  in  cases  of  tuberculo- 
sis or  old  pleurisies  in  which  there  was  adhesion  to  the  left  pleura.  Medias- 
tinal adhesions  anchoring  the  aorta  to  the  air-passages  can  produce  it. 
Wenckebach  has  also  called  attention  to  the  fact  that  it  may  occur  in  cases 
of  enteroptosis,  in  which  the  heart  is  pulled  downward  with  the  liver,  and 
the  arch  of  the  aorta  thus  made  to  pull  upon  the  bronchi.  (This  is  well 
illustrated  by  the  patient  mentioned  on  page  703.)  The  tracheal  tug  is 
most  marked  in  inspiration. 

Tracheal  Percussion  Shock  (Smith). — H.  L.  Smith  has  found  that  if 
one  lightly  taps  the  chest  wall  (direct  percussion)  over  an  aneurismal  area 
one  feels  a  sudden  increase  in  the  impulse  as  soon  as  the  aneurismal  area 
is  reached,  a  shock  resembling  "the  sensation  experienced  by  one  when  a 
rubber  bag  filled  with  water  is  simultaneously  palpated  and  percussed  "  (semi- 
fluctuation).  The  fact  that  he  has  been  able  to  elicit  it  in  62  per  cent,  of  his 
cases  of  which  only  46  per  cent,  gave  a  tracheal  tug  indicates  the  usefulness 
of  the  sign.     In  certain  cases  it  is  undoubtedly  of  considerable  assistance. 

THE    PULSATION    AND    ARTERIAL    PULSE    IN    ANEURISM. 

The  pulsation  over  the  aneurism  resembles  the  form  of  the  arterial 
pulse  except  that  owing  to  the  elasticity  of  the  sac  the  rise  and  fall  are 
usually  more  gradual.  It  is  sometimes  of  importance  to  determine  whether 
the  pulsation  corresponds  to  an  aortic  aneurism  or  an  aneurism  of  the 
ventricle.    This  requires  the  most  carefully  timed  tracings  simultaneously 


646 


DISEASES   OF  THE   HEART   AND    AORTA. 


in  cases  where  it  is  necessary  to  determine  whether  an  aneurism  is  confined 
to  the  innominate,  subclavian,  or  carotid  artery,  or  whether  it  also  involves 
the  aorta.  These  relations  often  cannot  be  shown  by  the  X-ray  and  rest 
upon  this  differentiation  alone. 


aneurism  in  20  per  cent.;   and  an 
been   discovered   with   the 


X-RAY    EXAMINATION. 

Most  of  the  things  which  are  inferred  from  physical  examination 
can  be  actually  seen  with  the  fluoroscope,  and  an  exactness  of  diagnosis 
can  be  reached  which  is  utterly  impossible  with  the  ordinary  methods.  In 
104  cases  of  aneurism  thus  examined  by  Baetjer,  the  clinical  diagnosis  had 
been  correctly  made  in  70  per  cent.;  there  had  been  tentative  diagnosis  of 

unsuspected  aneurism  had 
X-ray  in  10  per  cent.  ' These 
findings  are  particularly  important, 
since  it  is  just  in  these  early  cases 
when  the  physical  signs  are  still 
indefinite  that  treatment  may  be 
profitably  instituted. 

However,  unless  certain  precau- 
tions are  taken  in  the  examination 
an  aortic  shadow  may  be  seen  which 
may  be  diagnosed  an  aneurism  even 
though  none  be  present.  This 
rounded  shadow  is  cast  by  the  arch 
of  the  aorta  just  to  the  left  of  the 
sternum,  and  it  may  be  specially 
marked  if  the  aorta  is  somewhat 
tilted,  as  sometimes  takes  place  in 
enteroptosis  (Wenckebach) .  Holz- 
knecht  has  shown,  however,  that 
this  error  will  not  be  made  if  the 
patient  is  also  turned  so  that  the 
rays  pass  from  left  back  to  right  front  (Fig.  81).  The  normal  aorta  thus 
lies  in  a  plane  parallel  to  the  rays  and  is  seen  as  a  narrow  nearly  vertical 
band,  with  the  light  spaces  of  anterior  and  posterior  mediastinum  in  front 
and  behind  it.  The  uniformly  dilated  aorta  appears  as  a  wide  but  uni- 
form band.  The  aneurism  of  the  ascending  aorta  appears  as  a  battledore 
or  tennis  racket  with  handle  up,  the  aneurism  of  the  arch  as  a  racket  with 
handle  down.  Aneurisms  of  the  innominate  are  separated  from  the  aortic 
shadow  by  a  clear  space  which  is  bridged  by  the  narrow  shadow  of  the 
artery. 

As  Baetjer  states,  it  is  most  important  to  examine  the  chest  for  mal- 
formations and  for  misplacement  of  the  aorta  which  might  be  mistaken 
for  aneurism.  Persistence  of  the  ductus  arteriosus  (Botalli)  must  also  be 
considered  in  shadows  near  that  of  the  descending  arch.  The  shadow  of 
enlarged  mediastinal  glands  is  usually  speckled  or  blotchy  with  occasional 
lighter  areas,  rather  than  uniformly  dark,  while  the  edges  of  sarcomata 
and  other  solid  tumors  are  often  irregular  and  may  fade  away  gradually 


Fig.  307. — Radiograph  of  a  patient  with  a  large 
aneurism  of  ascending  aorta  and  the  arch,  viewed 
from  behind.      (Kindness  of  Prof.  C.  M.  Cooper.) 


ANEURISM. 


647 


into  the  surrounding  tissues.  Moreover,  unless  there  is  a  considerable 
degree  of  intrasaccular  clotting,  an  aneurism  will  be  seen  to  expand  during 
systole  and  to  contract  in  diastole,1  whereas  a  solid  tumor  will  at  most 
rotate  upon  its  axis. 

CHARACTERISTIC    FEATURES    OF    ANEURISMS    AT    DIFFERENT    SITES. 

Characteristic  features  of  thoracic  aneurisms  are  given  in  the  table 
below.  It  must  be  borne  in  mind,  however,  that  these  represent  the  con- 
ditions only  while  the  aneurisms  remain  relatively  small,  for  with  their  fur- 
ther growth  they  may  press  upon  other  structures  and  so  present  the  picture 
of  an  aneurism  affecting  a  different  part  of  the  aorta.  Large  aneurisms  also 
displace  the  heart,  and  may  even  occupy  the  usual  position  of  the  latter. 


Fig.  308. — Radiograph  of  a  patient  with  dif- 
fuse dilatation  of  the  arch  of  the  aorta.  (Kind- 
ness of  Prof.  C.  M.  Cooper.)  The  figure  also  shows 
dilatation  of  the  left  ventricle  and  slight  dilatation 
of  the  left  auricle. 


Fig.  309. — Diagram  of  the  radiograph  shown 
in  Fig.  308.  The  broken  lines  indicate  the  nor- 
mal outlines.  AO,  aorta;  OES,  oesophagus;  LV, 
left  ventricle. 


Aneurism  of  the  Heart. — Symptoms. — Indefinite  signs  of  cardiac  weak- 
ness. Physical  signs. — Two  points  of  maximal  impulse  over  which  tracings 
show  exactly  synchronous  pulsations  (this  point  is  far  from  pathogno- 
monic). Irregular  outline  of  cardiac  dulness  (encapsulated  pericarditis, 
pleurisy,  and  tumors  must  be  excluded) .  Sometimes  systolic  and  diastolic 
murmurs  over  heart  and  aneurism  not  present  over  aorta.  Pulse. — Feeble 
but  equal  and  not  delayed.  X-ray. — Bulging  of  shadow  of  ventricle  or 
auricle  with  enlargement  of  shadow  synchronous  with  systole  of  correspond- 
ing chamber.  Rupture. — Into  pericardium.  Death  often  from  cardiac 
weakness  or  coronary  sclerosis. 

Aneurism  of  Coronary  Arteries. — Symptoms. — No  characteristic  symp- 
toms. Occasional  cardiac  pain.  Physical  signs.  —  Arteriosclerosis.  No 
characteristic  signs  or  even  signs  of  illness.  (Aneurism  usually  size  of 
pigeon's  egg.)  X-ray.  —  No  abnormal  shadows.  Rupture.  —  Into  peri- 
cardium in  19  out  of  21  cases.     In  one  case  into  pulmonary  artery. 

Ascending  Aorta;  Intrapericardial  (Aneurism  of  Symptoms). — Symp- 
toms.— Angina  pectoris.     Attacks  of   cardiac   asthma.     Precordial  pains. 


1  Holzknecht  particularly  emphasizes  the  importance  of  using  the  lead   diaphragm 
in  examining  the  edges  of  the  shadow  for  pulsation. 


646 


DISEASES   OF  THE   HEART   AND    AORTA. 


in  cases  where  it  is  necessary  to  determine  whether  an  aneurism  is  confined 
to  the  innominate,  subclavian,  or  carotid  artery,  or  whether  it  also  involves 
the  aorta.  These  relations  often  cannot  be  shown  by  the  X-ray  and  rest 
upon  this  differentiation  alone. 


aneurism  in  20  per   cent.;   and  an 
been   discovered   with   the 


X-RAY    EXAMINATION. 

Most  of  the  things  which  are  inferred  from  physical  examination 
can  be  actually  seen  with  the  fluoroscope,  and  an  exactness  of  diagnosis 
can  be  reached  which  is  utterly  impossible  with  the  ordinary  methods.  In 
104  cases  of  aneurism  thus  examined  by  Baetjer,  the  clinical  diagnosis  had 
been  correctly  made  in  70  per  cent. ;  there  had  been  tentative  diagnosis  of 

unsuspected  aneurism  had 
X-ray  in  10  per  cent.  ' These 
findings  are  particularly  important, 
since  it  is  just  in  these  early  cases 
when  the  physical  signs  are  still 
indefinite  that  treatment  may  be 
profitably  instituted. 

However,  unless  certain  precau- 
tions are  taken  in  the  examination 
an  aortic  shadow  may  be  seen  which 
may  be  diagnosed  an  aneurism  even 
though  none  be  present.  This 
rounded  shadow  is  cast  by  the  arch 
of  the  aorta  just  to  the  left  of  the 
sternum,  and  it  may  be  specially 
marked  if  the  aorta  is  somewhat 
tilted,  as  sometimes  takes  place  in 
enteroptosis  (Wenckebach).  Holz- 
knecht  has  shown,  however,  that 
this  error  will  not  be  made  if  the 
patient  is  also  turned  so  that  the 
rays  pass  from  left  back  to  right  front  (Fig.  81).  The  normal  aorta  thus 
lies  in  a  plane  parallel  to  the  rays  and  is  seen  as  a  narrow  nearly  vertical 
band,  with  the  light  spaces  of  anterior  and  posterior  mediastinum  in  front 
and  behind  it.  The  uniformly  dilated  aorta  appears  as  a  wide  but  uni- 
form band.  The  aneurism  of  the  ascending  aorta  appears  as  a  battledore 
or  tennis  racket  with  handle  up,  the  aneurism  of  the  arch  as  a  racket  with 
handle  down.  Aneurisms  of  the  innominate  are  separated  from  the  aortic 
shadow  by  a  clear  space  which  is  bridged  by  the  narrow  shadow  of  the 
artery. 

As  Baetjer  states,  it  is  most  important  to  examine  the  chest  for  mal- 
formations and  for  misplacement  of  the  aorta  which  might  be  mistaken 
for  aneurism.  Persistence  of  the  ductus  arteriosus  (Botalli)  must  also  be 
considered  in  shadows  near  that  of  the  descending  arch.  The  shadow  of 
enlarged  mediastinal  glands  is  usually  speckled  or  blotchy  with  occasional 
lighter  areas,  rather  than  uniformly  dark,  while  the  edges  of  sarcomata 
and  other  solid  tumors  are  often  irregular  and  may  fade  away  gradually 


Fig.  307. — Radiograph  of  a  patient  with  a  large 
aneurism  of  ascending  aorta  and  the  arch,  viewed 
from  behind.     (Kindness  of  Prof.  C.  M.  Cooper.) 


ANEURISM. 


647 


into  the  surrounding  tissues.  Moreover,  unless  there  is  a  considerable 
degree  of  intrasaccular  clotting,  an  aneurism  will  be  seen  to  expand  during 
systole  and  to  contract  in  diastole,1  whereas  a  solid  tumor  will  at  most 
rotate  upon  its  axis. 

CHARACTERISTIC    FEATURES    OF    ANEURISMS    AT    DIFFERENT    SITES. 

Characteristic  features  of  thoracic  aneurisms  are  given  in  the  table 
below.  It  must  be  borne  in  mind,  however,  that  these  represent  the  con- 
ditions only  while  the  aneurisms  remain  relatively  small,  for  with  their  fur- 
ther growth  they  may  press  upon  other  structures  and  so  present  the  picture 
of  an  aneurism  affecting  a  different  part  of  the  aorta.  Large  aneurisms  also 
displace  the  heart,  and  may  even  occupy  the  usual  position  of  the  latter. 


Fig.  308. — Radiograph  of  a  patient  with  dif- 
fuse dilatation  of  the  arch  of  the  aorta.  (Kind- 
ness of  Prof.  C.  M.  Cooper.)  The  figure  also  shows 
dilatation  of  the  left  ventricle  and  slight  dilatation 
of  the  left  auricle. 


Fig.  309. — Diagram  of  the  radiograph  shown 
in  Fig.  308.  The  broken  lines  indicate  the  nor- 
mal outlines.  AO,  aorta;  OES,  oesophagus;  LV, 
left  ventricle. 


Aneurism  of  the  Heart. — Symptoms. — Indefinite  signs  of  cardiac  weak- 
ness. Physical  signs. — Two  points  of  maximal  impulse  over  which  tracings 
show  exactly  synchronous  pulsations  (this  point  is  far  from  pathogno- 
monic). Irregular  outline  of  cardiac  clulness  (encapsulated  pericarditis, 
pleurisy,  and  tumors  must  be  excluded) .  Sometimes  systolic  and  diastolic 
murmurs  over  heart  and  aneurism  not  present  over  aorta.  Pulse. — Feeble 
but  equal  and  not  delayed.  X-ray. — Bulging  of  shadow  of  ventricle  or 
auricle  with  enlargement  of  shadow  synchronous  with  systole  of  correspond- 
ing chamber.  Rupture. — Into  pericardium.  Death  often  from  cardiac 
weakness  or  coronary  sclerosis. 

Aneurism  of  Coronary  Arteries. — Symptoms. — No  characteristic  symp- 
toms. Occasional  cardiac  pain.  Physical  signs.  —  Arteriosclerosis.  No 
characteristic  signs  or  even  signs  of  illness.  (Aneurism  usually  size  of 
pigeon's  egg.)  X-ray.  —  No  abnormal  shadows.  Rupture.  —  Into  peri- 
cardium in  19  out  of  21  cases.     In  one  case  into  pulmonary  artery. 

Ascending  Aorta;  Intrapericardial  (Aneurism  of  Symptoms). — Symp- 
toms.— Angina  pectoris.     Attacks  of  cardiac   asthma.     Precordial  pains. 


1  Holzknecht  particularly  emphasizes  the  importance  of  using  the  lead  diaphragm 
in  examining  the  edges  of  the  shadow  for  pulsation. 


648  DISEASES    OF   THE   HEART    AND    AORTA. 

Pain  down  right  or  left  arm.  Shortness  of  breath.  Symptoms  of  cardiac 
failure  predominate.  Physical  signs. — Distention  of  veins  of  head,  neck, 
upper  chest,  arms;  oedema  of  these  parts.  Tracheal  tug  absent  while 
aneurism  is  small.  Pupils  equal  if  aneurism  is  small.  Aneurism  usually 
small,  situated  in  second  and  third  right  interspaces.  Pulsation  in  second 
and  third  right  interspaces.  Often  signs  of  aortic  insufficiency.  General 
oedema  from  aortic  insufficiency.  Pulse. — Delay  of  pulse-wave  uniform. 
Pulses  may  be  equal  in  both  radials  or  may  be  smaller  in  either.  X-ray. — 
Inverted  racket-shaped  shadow  in  left  post,  to  right  ant.  illumination. 
Arch  of  aorta  clear.  Rupture. — Into  pericardial  cavity.  Pulmonary  artery. 
Right  auricle.  Superior  vena  cava.  (Esophagus.  Left  auricle.  Right 
ventricle.  Left  lung.  Right  lung.  Other  causes  of  death.  —  Dyspnoea. 
Exhaustion.  Hydrothorax.  Hydropericardium.  Bronchitis  and  pneu- 
monia.    Pulmonary  infarction.     Suffocation. 

Aneurism  of  the  Ascending  Aorta  between  Pericardium  and  Innominate 
Artery  (Aneurism  of  Physical  Signs). — Symptoms. — Slight  dyspnoea.  Pain 
when  aneurism  presses  on  or  erodes  chest  wall.  Often  an  accidental  finding. 
Physical  signs. — Flushed  face  with  dilated  veins;  sometimes  oedema.  Di- 
lated veins  of  arms.  Pulsation  in  second,  third,  and  fourth  right  interspaces 
(occasionally  shifting).  Dulness  to  the  right  of  the  sternum,  not  over  the 
manubrium.  Systolic,  sometimes  diastolic  murmur,  thrill  and  diastolic 
shock  over  aneurism.  Tracheal  tug,  if  aneurism  is  large.  Pulse. — Uni- 
form delay  of  pulse,  both  sides  synchronous.  Right  radial  usually  smaller 
than  left.  X-ray. — To  right  of  sternum  in  second  to  fourth  interspaces; 
best  made  out  in  post. -ant.  or  right  post,  to  left  ant.  illumination.  In  left 
post,  to  right  ant.  illumination  inverted  racket-shaped  shadow.  Compli- 
cations.— Often  aortic  insufficiency.  Bronchitis.  Tuberculosis  of  right 
lung.  Hemorrhage.  Right  hydrothorax.  Rupture. — Into  pericardium. 
Right  pleural  cavity.    Right  bronchus.    Right  auricle.    Superior  vena  cava. 

Aneurism  of  the  Innominate  Artery. — Symptoms. — Like  those  of  an- 
eurism of  arch  except  that  there  is  no  dysphagia  in  small  aneurisms.  Pain 
and  numbness  down  right  arm  and  to  right  shoulder.  Physical  signs. — 
Dilated  veins  and  swelling  over  right  arm  and  right  side  of  face.  Dulness 
extends  out  under  right  clavicle.  Pulsating  tumor  may  be  felt  under  the 
right  clavicle.  Paralysis  of  right  vocal  cord.  Right  pupil  in  early  stages 
larger  than  left.  Pulse. — Right  radial  pulse  smaller  and  definitely 
later  than  left.  X-ray. — A  ^-shaped  shadow  is  seen  upon  the  left 
arm  of  the  V  which  the  shadow  of  the  innominate  artery  makes  with  that 
of  the  aorta  on  left  post,  to  right  ant.  illumination.  Complications.— Right- 
sided  bronchitis.  Bronchopneumonia.  Tuberculosis.  Hydrothorax. 
Rupture. — Usually  points  upward  and  outward  toward  the  clavicle,  but 
may  point  downward  to  pleura  or  bronhci. 

Aneurism  of  the  Arch  of  the  Aorta  (Aneurism  of  Symptoms). — Symp- 
toms.— Change  in  voice,  especially  high  notes.  Brassy  cough.  Difficulty 
in  swallowing.  Pain  in  throat.  Dyspnoea,  sometimes  amounting  to  suffo- 
cation. Physical  signs. — Inequality  of  pupils.  Usually  dilatation  of  left 
pupil.  Dilated  veins,  flush,  and  sometimes  swelling  over  left  side  Of  face, 
chest,  and  left  arm,  or  changes  bilateral.  Tracheal  tug  early.  Pulsation 
palpable  in  suprasternal  notch.     Pulsation  in  suprasternal  and  supraclavic- 


ANEURISM.  649 

ular  fossae.  Lifting  of  manubrium;  later  perforation  of  manubrium  or 
sternoclavicular  articulation.  Palpable  heaving,  systolic  and  diastolic 
shocks,  and  often  thrill  over  manubrium.  Heart  sounds:  usually  systolic 
murmur  and  sometimes  diastolic  murmur  over  the  tumor.  In  aneurism 
beyond  the  innominate,  the  systolic  murmur  may  be  heard  in  the  left  car- 
otid and  brachial  but  not  in  the  right.  Bronchoscopy  may  show  tumor  per- 
forating bronchus.  X-ray. — Shadow  racket  shaped,  especially  seen  in  left 
post,  to  right  ant.  illumination.  Post. -ant.  or  ant, -post,  illumination  seen 
as  massive  shadow  above  that  of  the  heart.  Complications. — Bronchitis. 
Tuberculosis.  Suffocation  (asphyxia).  Inanition.  Rupture. — Externally 
(anteriorly  through  manubrium  or  above  clavicle).  Into  left  bronchus. 
Trachea.  (Esophagus.  Lungs  and  pleural  cavity,  pericardium,  mediasti- 
num. Pulmonary  artery.  Other  causes  of  death. — Exhaustion.  Pericarditis. 
Collapse.    Suffocation.    (Edema  of  larynx.    Pneumonia.    Tuberculosis. 

Aneurism  of  the  Descending  Aorta.1 — Symptoms. — Lancinating  and  bor- 
ing pains  in  back,  left  shoulder,  left  side,  and  left  side  of  abdomen.  Stiffness 
of  back.  Shortness  of  breath.  When  the  aneurism  is  near  the  diaphragm, 
abdominal  pains  may  be  present  and  the  condition  may  be  considered  to  be 
abdominal.  Physical  signs. — Visible  pulsation  just  to  left  of  spinal  column. 
Dulness  on  percussion.  Heart  sounds  and  corresponding  shocks  over 
aneurism  and  tenderness  over  corresponding  spines.  Areas  of  hyper- 
esthesia or  analgesia  in  corresponding  spinal  segments.  Pulse. — Pulses 
synchronous;  smaller  and  more  gradual  in  left  than  right.  X-ray. — 
^-shaped  shadow  to  left  of  sternum,  especially  in  right  posterior  to  left 
anterior  illumination.  Complications. — Left-sided  bronchitis,  broncho- 
pneumonia, tuberculosis,  hydrothorax,  paraplegia  from  erosion  of  vertebrae. 
Rupture. — Backward  and  externally;  into  oesophagus,  left  pleural  cavity, 
right  pleural  cavity,  bronchi  and  lungs,  pulmonary  artery.  Other  causes  of 
death. — Pressure  on  trachea  and  bronchi,  exhaustion,  pneumonia,  and 
tuberculosis. 

The  following  histories  illustrate  typical  cases  of  aneurism: 

Ascending  Arch  above  Pericardium  (Aneurism  of  Physical  Signs). 

D.  N.  L.,  aged  45,  married.  Except  for  a  well-compensated  aortic  insufficiency  for 
the  past  eight  years,  with  slight  shortness  of  breath,  he  has  been  quite  healthy.  In 
November,  1903,  his  aneurism  was  discovered  accidentally  by  his 
brother,  who  is  a  physician. 

Examination  by  Dr.  Osier  revealed  a  well-nourished  man  who  does  not  appear  ill. 
Face  a  little  congested,  veins  of  neck  and  arms  full;  pulse  48  per  minute,  both  apparently 
synchronous,  a  little  larger  on  left  than  on  right  (maximal  pressure:  left  arm  140;  right 
arm  125).  There  is  no  tracheal  tug.  Over  the  thorax  a  wavy  impulse  is  seen  in  all 
the  right  interspaces  above  the  liver,  and  an  area  of  dulness  as  outlined  in  Fig.  310,  A.  Rela- 
tive cardiac  dulness  in  fourth  interspace  extends  16.5  cm.  to  left  and  15  cm.  to 
right  of  midline.  Over  the  aneurismal  area  there  is  a  marked  systolic  thrill  and  murmur; 
over  the  heart  a  systolic  and  diastolic  murmur. 

1  In  120  cases  of  aneurism  of  the  descending  aorta  collected  from  the  literature  Milanoff 
found  pain  in  72,  dysphagia  in  20,  hsematemesis  13,  haemoptysis  21,  left-sided  pleural  effu- 
sion in  a  few  cases.  Andreef  found  only  8  cases  of  paraplegia  from  aneurism  in  the  litera- 
ture.   The  duration  is  often  from  10  to  15  years;  longer  than  that  of  aneurisms  elsewhere. 

The  condition  is  very  well  discussed  in  English  by  Osier  and  more  recently  by  Hewlett 
and  Clark,  who  give  excellent  radiographs  and  a  very  useful  summary  of  the  literature. 


650 


DISEASES   OF   THE   HEART   AND    AORTA. 


X-ray  examination  by  Dr.  Baetjer  showed  the  pulsating  shadow  of  an  aneurism  of 
size  corresponding  to  the  area  obtained  on  percussion,  arising  from  the  ascending  arch  of 
the  aorta. 

Patient  left  the  hospital,  and  one  month  later  died  without  warning  while  asleep. 
The  only  signs  of  the  approaching  end  were  fifteen  minutes  of  stertorous  breathing. 
Autopsy  revealed  a  large  aneurism  corresponding  to  that  diagnosed  clinically,  as  well  as 
arteriosclerosis  and  aortic  insufficiency.    There  is  no  note  of  rupture  of  the  aneurism. 


Fig.  310. — Cardiac  dulness  in  cases  of  aneurism.  A.  Ascending  aorta  (D.  N.  L.).  B.  Subclavian 
artery  (J.  B.):  the  shaded  area  indicates  the  tumor,  the  curve  indicates  the  pulsation.  C.  Second  part 
of  the  transverse  portion  of  the  arch  (K). 


Aneurism  op  Innominate  Artery. 

J.  B.,  aged  44.    Had  syphilis  13  years  ago,  otherwise  healthy. 

Two  years  ago  complained  of  aching  in  right  shoulder  and  right  side  of 
neck  down  arm  to  hand.  No  pain  in  chest.  There  were  swelling  of  feet  and  ankles  and 
shortness  of  breath.  About  this  time  he  began  to  have  troublesome  paroxysms  of 
coughing.  In  May,  1903,  noticed  that  his  voice  was  "cracked."  In  August, 
1903,  he  noticed  a  pulsating  swelling  above  the  right  clavicle.  This  was 
diagnosed  as  aneurism  of  the  innominate,  and  the  right  carotid  was  ligated 
above  the  tumor.     The  subclavian  could  not  be  ligated,  as  the  patient  took  chloroform 


ANEURISM.  651 

b.ldly.  After  the  ligation  the  tumor  rapidly  increased  in  size.  When  he  entered  the  Johns 
Hopkins  Hospital  two  months  later,  his  voice  was  husky,  the  right  pupil  was  larger  than 
the  left  (irritation  of  the  right  sympathetic  ganglia),  and  a  large  rounded  pulsating  tumor 
was  seen  occupying  the  position  of  the  manubrium  and  extending  out  along  the  right 
clavicle  (Fig.  310,  A,  B).  The  prominence  of  this  tumor  is  shown  in  Fig.  302.  Over  tne 
tumor  a  well-marked  systolic  and  diastolic  shock  may  be  felt.  The  two  heart  sounds  are 
heard  over  the  tumor.  There  is  some  resonance  on  percussion  between  the  tumor  and  the 
heart.  The  area  of  cardiac  dulness  is  not  enlarged,  but  a  soft  diastolic  murmur  is  heard 
at  apex  and  base.  The  right  radial  pulse  is  smaller  than  the  left  and  a  little  delayed.  The 
blood-pressure  varied,  at  first  being  160  in  left  arm,  140  in  the  right  brachial,  later  reach- 
ing 150  in  right  and  130  in  left. 

Patient  was  seen  by  Dr.  Finney,  but  wiring  and  other  operative  procedures  were 
considered  impracticable.  He  was  kept  at  rest  in  bed  on  restricted  diet,  but  nevertheless 
the  aneurism  grew  rapidly,  as  shown  by  the  successive  elevations  in  Fig.  302. 

On  Dec.  2,  at  4.00  a.m.,  he  felt  a  severe  throbbing  in  the  aneurism,  and  a  couple  of 
smaller  bulgings  (Fig.  302)  appeared  upon  its  surface,  which  had  not  been  present  the 
day  before,  and  the  whole  aneurism  appeared  to  be  definitely  larger.  The  patient  insisted 
upon  leaving  the  hospital  at  once  to  return  to  his  home  in  South  Carolina. 

Aneurism  of  the  First  Part  of  the  Transverse  Arch  of  the  Aorta. 

J.  D.,  an  unmarried  sailor,  aged  37,  entered  the  Johns  Hopkins  Hospital  on  Jan.  5, 
1909,  complaining  of  pain  in  the  chest  and  inability  to  sleep.  He  had  had  no  infectious 
diseases  except  gonorrhoea,  denied  spyhilis,  and  gave  no  history  of  secondaries.  Except  for 
occasional  sprees,  he  uses  alcohol  in  moderation.    As  a  sailor  he  has  always  done  heavy  work 

He  was  well  until  about  four  months  before  admission,  when  he  had  an  attack  of 
"  heavy  pressure  "  and  tightness  across  his  chest  at  night,  and  some  weeks  later  stinging 
pains  in  his  chest  3-4  cm.  above  the  xiphoid  process,  which  seemed  to  radiate  to  both 
sides  of  the  chest  and  to  pass  through  to  the  back.    The  pressure  kept  him  from  sleeping. 

Upon  examination  the  veins  upon  the  left  side  of  the  neck  were  found  to  be  dilated, 
and  the  veins  were  much  more  prominent  than  on  the  right.  There  was  no  tracheal  tug. 
There  was  an  area  of  dulness  behind  the  medial  end  of  the  right  clavicle,  the  manubrium, 
and  the  medial  half  of  the  left  clavicle,  which  was  continuous  with  the  upper  border  of 
cardiac  dulness.  The  left  radial  pulse  was  somewhat  smaller  than  the  right  and  seemed 
to  be  a  trifle  retarded.  Maximal  pressure  in  the  right  radial  ranged  from  115  to  130  mm. 
Hg,  in  the  left  from  85  to  110  mm.  Hg. 

Fluoroscopic  examination  by  Dr.  Baetjer  showed  a  pulsating  tumor  about  the  size 
of  a  hen's  egg  projecting  almost  entirely  to  the  left  of  the  sternum  opposite  the  first  and 
second  interspaces  (transverse  portion  of  the  arch  of  the  aorta). 

The  patient  was  discharged  somewhat  improved  after  a  short  sojourn  in  the  hospital. 

Aneurism  of  the  Left  Side  of  the  Transverse  Arch. 

H.  D.  K.,  brush-maker,  aged  49,  admitted  to  the  surgical  service  of  the  Johns  Hopkins 
Hospital  on  March  14, 1908,  complaining  of  aneurism.  Family  history  was  negative.  He  had 
been  perfectly  healthy  all  his  life  except  for  an  attack  of  pleurisy  six  years  before  admis- 
sion, an  attack  of  gonorrhoea  at  19,  and  a  chancroid,  not  followed  by  secondaries,  at  25. 

Two  weeks  before  admission  he  felt  a  burning  pain  in  the  left  chest  and 
had  some  shortness  of  breath,  both  of  which  have  become  worse  since  then.  He  sometimes 
is  awakened  with  shortness  of  breath  and  precordial  pain.  For  the  past  year  his  voice  has 
been  husky,  a  condition  which  set  in  suddenly  after  violent  exertion  while  splitting  wood. 

He  is  a  well-nourished  man  of  rather  anxious  expression.  The  pupils  are  equal  and 
react  to  light  and  accommodation.  There  is  a  well-marked  tracheal  tug.  Chest  expansion 
is  slight  on  respiration.  There  is  a  definite  pulsation  over  the  first  left  interspace  and 
sternoclavicular  junction,  in  which  area  the  shocks  accompanying  the  two  sounds  are 
readily  palpable. 

Note  by  Dr.  Boggs. — H  e  a  r  t  :  Maximal  impulse  in  fifth  left  interspace  11  cm.  from 
midsternal  line;  dulness  extends  to  this  point  on  left,  reaches  above  to  middle  of  third 
rib,  and  on  right  2.5  cm.  in  third  left  interspace.  Cardiohepatic  angle  is  normal.  There 
is  dulness   behind   the   manubriu n^ extending  to  left,  as  per  diagram,  8.5  cm. 


652  DISEASES   OF   THE    HEART   AND    AORTA. 

in  first  interspace  and  below  to  second  interspace,  on  the  right  to  just  beyond  the  sternal 
margin.  On  palpation  over  the  dull  area  there  is  a  strong  lifting  pulsation, 
maximal  at  a  point  5.5  cm.  to  left  and  definitely  expansile.  No  thrill  felt.  Diastolic  shock 
well  marked.  At  apex  and  inward  toward  the  base  there  is  a  very  short  systolic  murmur, 
which  is  not  transmitted  beyond  the  border  of  the  heart.  First  sound  is  rather  tapping 
at  apex.  Along  the  left  sternal  border  this  murmur  increases  in  intensity  and  is  maximal 
over  the  mass  above  the  heart  at  the  point  of  greatest  pulsation,  where  there  is  a  well- 
marked  systolic  bruit  followed  by  a  ringing  second  sound.  A  very  faint  systolic  murmur 
is  heard  at  the  aortic  ring,  and  the  second  sound  is  clear.  No  diastolic  murmur.  The 
second  pulmonic  is  louder  than  the  second  aortic.  The  pulse  is  of  good  volume,  regular, 
rather  high  tension,  and  not  collapsing.  Vessel  wall  definitely  thickened.  Some  cyanosis 
of  finger-tips  and  lips.  The  volume  of  the  pulse  on  the  right  side  is 
decidedly  larger  than  on  the  left.  There  is  a  circumscribed  area  of 
dulness  in  the  left  interscapular  region  in  which  percussion  note  has 
a  peculiar  wooden  tympany  like  that  over  consolidated  lung.  Over  this  area  the  breath 
sounds  are  rather  more  intense  than  over  the  rest  of  the  lung  but  they  are  not  tubular 
in  character. 

On  January  20  the  aneurism  was  wired,  under  Schleich  solution  anaesthesia,  by  Dr. 
Finney,  with  twelve  feet  of  silver-copper  wire,  through  which  a  10-MA  current  was  passed 
(Moore  Corradi  method).  Clotting  took  place  promptly.  The  patient  stood  the  opera- 
tion well.  The  patient  Was  considerably  relieved  as  regards  pain,  but  the  pulsation  soon 
returned. 

Aneurism  of  the  Descending  Aorta. 

Notes  of  the  following  case  are  taken  from  the  records  of  the  Johns  Hopkins  Hospital: 

Ch.  L.,  colored  laborer,  aged  48,  was  first  admitted  to  the  Johns  Hopkins  Hospital 
on  October  14,  1898,  complaining  of  pain  in  the  back,  left  side,  and  abdomen. 

His  family  history  was  negative.  He  had  always  been  healthy,  but  had  measles, 
whooping-cough,  tertian  malaria,  and  at  17  had  syphilis  which  was  not  adequately 
treated.  He  has  done  a  great  deal  of  hard  work  on  a  farm,  has  drunk  a  great  deal  of  whiskey, 
and  smoked  heavily. 

His  present  trouble  began  suddenly  about  four  years  ago,  when  he  was  seized  with 
a  severe  pain  in  the  lower  left  abdomen.  This  lasted  a  couple  of  weeks.  It  was 
always  relieved  when  his  thighs  were  flexed  upon  the  abdomen,  and  was  always  increased 
after  exposure  to  bad  weather.  Four  years  after  this  a  pain  in  the  left  side  of  the 
back  appeared,  which  has  gradually  increased.  This  also  is  relieved  by  flexing  the  thighs. 
For  the  past  six  years  he  has  passed  blood  in  the  stools  during  periods  when  the  pain  in 
the  left  flank  was  worse. 

A  note  by  Dr.  Futcher  at  that  time  states,  that  "  the  patient  was  found  lying  in  bed 
on  the  left  side  with  the  knees  flexed.  Pupils  are  of  normal  size,  equal,  and  react  to  light 
and  accommodation.  The  lung  expansion  and  vocal  fremitus  are  diminished  over  the 
entire  left  lung,  and  the  breath  sounds  were  exaggerated  in  front  and  in  the  axilla.  There 
were  a  few  moist  rales  in  the  third  and  fourth  left  interspaces.  Behind,  the  breath  sounds 
are  very  indistinct  below  the  angle  of  the  scapula.  The  percussion  note  was  found  to  be 
impaired  over  the  entire  left  front  as  far  down  as  the  fifth  rib  and  over  the  entire  left 
back,  being  flat  below  the  angle  of  the  scapula. 

Heart. — The  maximal  impulse  was  seen  in  the  fifth  interspace  7.5  cm.  from  the  mid- 
line, but  dulness  extended  3  cm.  to  the  left  of  this  point.  Both  the  first  and  second  sounds 
were  reduplicated. 

The  liver  was  slightly  enlarged;  the  spleen  just  palpable.  There  were  no  masses  nor 
areas  of  tenderness  in  the  left  flank  to  account  for  the  pain. 

On  Oct.  21  Dr.  Futcher  noted  a  definite  heaving  of  the  entire  body  of  the  sternum 
and  a  well-marked  systolic  retraction  in  the  eighth,  ninth,  and  tenth  left  interspaces  be- 
hind. A  tracheal  tug  was  present,  but  the  vocal  cords  were  not  paralyzed.  The  pulse  was 
equal  on  the  two  sides. 

In  spite  of  rest,  restricted  diet,  and  potassium  iodide  and  repeated  gelatin  injections, 
his  pain  in  the  back  gradually  became  worse,  compelling  him  to  seek  relief  by  lean- 
ing over  tbe  back  of  the  chair.  It  became  so  severe  that  it  was  not  relieved 
by  30  mg.  (gr.  ss)  of  morphine.  However,  later  in  his  stay  his  condition  gradually  became 
better  and  the  pain  became  a  little  less  frequent  and  less  intense. 


ANEURISM. 


653 


There  was  very  little  change  in  his  condition  between  that  time  and  March,  1902, 
when  for  the  first  time  there  was  noted  a  definite  systolic  pulsation  in  the  left 
interscapular  region  which  gradually  increased  until  it  involved  three  ribs  and  interspaces. 
His  condition  gradually  became  worse.  Respiratory  movement  almost  entirely  disappeared 
upon  the  left  side  and  a  scoliosis  developed  with  concavity  toward  the  right.  The  area 
of  cardiac  dulness  increased  to  the  right,  where  pulsation  was  particularly  well  marked 
and  a  superficial  scratchy  systolic  murmur  was  heard  over  the  precordium.  His  pain 
became  so  intense  that  he  could  but  rarely  lie  down.  An  area  of  absolute  analgesia  devel- 
oped in  the  sixth  and  seventh  left  interspaces,  impaired  sensibility  to  heat,  cold,  and  pain 
being  found  in  the  fifth  interspace  as  well.  About  this  time  he  began  to  feel  pain  on  swal- 
lowing, referred  to  the  middle  of  the  sternum. 

During  the  night  of  Oct.  25  he  complained  of  pain  and  intense  shortness  of  breath, 
and  suddenly  vomited  about  50  c.c.  of  bright  red  blood.  Ten  minutes  later  he 
vomited  25  c.c.  more  blood.  He  was  quieted  with  morphine  during  the  night,  but  in  the 
early  afternoon  of  the  twenty-fifth  he  vomited  about  500  c.c.  of  blood  within  three  minutes, 
became  pulseless,  and  died. 

At  autopsy  the  heart  was  found  to  be  displaced  to  the  right  (extending  8  cm.  to 
the  right  of  the  midline)  by  a  tremendous  aneurismal  sac  18X14X9  cm.  This  sac  was 
fusiform  with  sacculations  at  its  upper  and  lower  ends.  It  arose  from  the  descending 
part  of  the  arch  and  the  descending  aorta  itself  and  pointed  backward, 
eroding  the  bodies  of  all  the  thoracic  vertebrae  from  the  fifth  to  the  tenth  as 
well  as  the  seventh,  eighth,  and  ninth  ribs.  The  erosion  of  the  intervertebral  disks  was 
much  less  marked.  The  aneurismal  sac  also  compressed  the  oesophagus  at  the  level  of  the 
bronchial  bifurcation,  where  it  eroded  through  the  oesophageal  wall,  making 
an  opening  2.5  cm.  in  diameter.  "The  edges  of  this  aperture  were  ragged  and  necrotic; 
the  tissue  about  it  dark  gray-green  in  color." 

The  aneurismal  sac  was  partly  filled  by  a  large  lamellated  clot. 

The  ascending  aorta  was  dilated  and  atheromatous;  the  descending  aorta  below  the 
aneurism  likewise. 

The  heart  was  much  enlarged;  the  walls  hypertrophic;  the  valves  normal. 

There,  were  many  pericardial  adhesions,  especially  firm  over  the  left  auricle  and  the 
coronary  veins,  and  there  were  tortuous 
patches  over  both  ventricles. 

The  stomach  contained  a  litre  of 
clotted  blood.     Other  organs  normal. 


Simple  Dilatation  of  the  Arch. 

L.  D.,  gardener,  aged  55,  native 
of  Ireland,  came  to  the  Johns  Hopkins 
Hospital  Dispensary  on  July  13,  1909, 
complaining  of  pain  on  swallowing  and 
trouble  in  passing  water. 

The  family  history  was  negative. 
The  patient  had  smallpox  at  18,  gon- 
orrhoea at  35  and  again  at  48,  and 
a  chancre  at  35  followed  by  definite 
secondary  manifestations,  for  which 
he  had  been  given  medicine  by  mouth. 
He  has  drunk  whiskey  in  excess  and 
has  done  a  good  deal  of  heavy  work. 

He  was  perfectly  healthy  until  the  past  ten  days,  since  when  he  feels  food  passing 
down  his  oesophagus  and  has  a  little  pain  which  is  referred  to  the  level  of  the  cardia.  He 
vomits  immediately  after  eating,  but  can  swallow  liquids  without  difficulty. 

Examination  reveals  a  fairly  nourished  man  of  ruddy  complexion  with  some  dilated 
venules.  The  left  pupil  is  somewhat  larger  than  the  right,  though  both  react  to  light  and 
accommodation.  There  is  a  slight  but  definite  tracheal  tug;  no  tracheal  percussion  shock. 
There  is  no  glandular  enlargement.  The  lungs  are  clear  except  for  a  few  widely  scattered 
piping  rales. 

41 


Fig.  311. 


Area  of  cardiac  dulness  in  a  patient  (L.  D.) 
with  dilated  arch  of  the  aorta. 


654  DISEASES   OF  THE   HEART   AND    AORTA. 

The  heart  is  not  enlarged;  apex  in  fifth  left  interspace  10  cm.  from  the  midline.  Dul- 
ness  extends  4.5  cm.  to  the  right.  The  relative  dulness  is  continuous  above  with  a  strip 
3.5  cm.  upon  either  side  of  the  sternum,  over  which  the  percussion  note  is  very  slightly 
impaired.  This  area  extends  up  as  far  as  the  upper  border  of  the  second  rib,  and  is  shown 
by  the  fluoroscope  to  correspond  with  a  uniform  shadow  of  the  dilated  aortic  arch.  The 
heart  sounds  are  clear;  the  second  aortic  distinct;  no  diastolic  murmur  present.  Pulse 
is  of  good  volume,  not  collapsing. 

Abdomen  shows  no  masses;  no  visible  peristalsis.  There  are  no  tenderness  and  no  ab- 
normalities palpable.  The  stomach  tube  is  passed  into  the  stomach  without  difficulty, 
and  a  very  small  amount  of  clear  fluid,  free  from  HC1,  obtained;  lavage  fluid  clear.  Des- 
moid test  negative.  He  was  given  alkaline  gentian  tincture  +  strychnine  (1  mg.  =  -go  gr.) 
before  meals,  under  which  treatment  his  symptoms  rapidly  diminished. 

Diagnosis  :  Chronic  alcoholic  gastritis,  anacidity,  dilatation  of  the  aortic  arch. 

Aneurism  of  the  Abdominal  Aorta. 

M.  P.,  machine  agent,  aged  30,  was  first  admitted  to  the  Johns  Hopkins  Hospital 
on  Oct.  31,  1899,  complaining  of  kidney  and  stomach  trouble.  The  family  his- 
tory was  negative. 

The  patient  had  had  measles,  chicken-pox,  mumps,  and  whooping-cough,  typhoid 
fever  at  23,  followed  by  pain  in  the  ankles  and  knees.  He  had  gonorrhoea  two  years  before 
admission  (about  one  year  before  the  onset  of  the  present  trouble),  but  denies  lues.  He 
worked  on  a  farm  until  his  attack  of  typhoid  fever,  since  when  he  has  not  been  strong. 
He  does  not  drink  nor  smoke  and  is  a  hearty  eater. 

The  present  illness  began  six  months  before  admission,  with  some  soreness  and  pain 
in  the  abdomen,  which  had  no  relation  to  the  taking  of  food  except  that  it  was 
more  intense  after  a  large  meal.  He  vomited  occasionally  but  rarely.  The  pain  was  at 
first  a  sharp  throbbing  pain  in  the  left  side.  It  was  so  severe  as  to 
cause  him  to  remain  in  bed  for  a  period  of  three  months,  during  which  he 
had  to  be  given  morphine.  After  the  three  months'  sojourn  in  bed  the  pain  became  less, 
and  he  was  almost  free  from  symptoms  for  about  six  weeks,  when  he  was  taken  with  a 
sudden  sharp  cutting  pain  in  the  right  side  just  under  the  ribs,  running 
around  toward  the  right  and  down  toward  the  testicle. 

On  examination  he  was  found  to  be  a  well-nourished  man  of  rather  sallow  color. 
There  was  no  glandular  enlargement.  The  lungs  were  clear  on  auscultation  and  percussion. 
The  heart  was  not  enlarged;  the  heart  sounds  clear. 

In  the  abdomen  there  was  a  very  well-marked  pulsation  visible  in  the  epi- 
gastrium. There  was  dull  tympany  over  this  area,  and  inflation  of  the  stomach  showed 
that  the  pulsating  mass  was  covered  by  the  latter.  There  was  considerable  tenderness 
over  the  pulsating  area;  Dr.  Osier  was  able  to  make  out  a  definite  soft  systolic  mur- 
mur, and  on  Nov.  5  with  the  deepest  possible  palpation  could  make  out  a  definite  mass 
with  expansile  pulsation.  The  case  was  diagnosed  as  abdominal  aneurism 
and  wiring  was  advised.    This  was  performed  by  Dr.  Finney  two  months  later. 

Note  by  Dr.  Finney. — An  incision  was  made  2.5  cm.  befow  the  xiphoid.  The  stomach 
was  retracted  downward ;  the  lesser  peritoneum  was  opened.  The  pancreas 
covered  the  lower  surface  of  the  tumor.  Attempt  was  made  to  dissect  the  pan- 
creas. This  was  abandoned  on  account  of  profuse  and  persistent  hemorrhage. 
The  incision  was  then  enlarged  upward,  the  edge  of  the  liver  elevated,  and  the  tumor 
exposed  above  and  to  the  right  of  the  pancreas.  A  needle  was  inserted  at  this  point  to  a 
depth  of  3-4  cm.  and  8-9  feet  of  silver  and  copper  alloy  wire  introduced.  Ten  milliamperes 
of  current  were  passed  for  one  hour.  The  needle  was  withdrawn,  the  wire  cut  close  to  the 
aneurismal  sac  and  turned  in  with  a  clamp.  No  bleeding.  One  or  two  bleeding  points 
about  the  pancreas  were  tied  with  fine  silk.  The  incision  was  closed.  The  patient  made 
an  uneventful  recovery  and  experienced  considerable  relief  from  pain,  so  that  nine 
months  later  it  gave  him  little  trouble,  though  the  aneurismal  pulsation  was  still 
expansile.     There  was  now  aloud  systolic  murmur  over  the  mass. 

The  pain,  however,  gradually  returned  and  never  left  him.  It  was  so  severe  that  he 
was  a  frequent  visitor  at  the  hospital  and  was  compelled  to  use  a  good  deal  of  morphine. 
He  was  admitted  to  the  writer's  ward  in  Jan.,  1904,  somewhat  worse  than  at  any  time 
previously.     The  aneurismal  mass  now  extended  from  the  ensiform  to   within   3 


ANEURISM.  655 

centimetres  of  the  umbilicus.  Its  surface  was  smooth  and  no  areas  of  bulg- 
ing could  be  made  out. 

On  Jan.  7  the  leucocytes  were  5000;  the  haemoglobin  90  per  cent.  He  was  quite  well 
(when  given  morphine)  until  the  night  of  Jan.  21,  when  he  had  a  s  u  d  d  e  n  a  t  t  a  c  k  of 
most  intense  pain  in  the  lower  back  and  abdomen,  "causing  him  to  cry  out  and  toss 
about,  arching  his  back  and  stiffening  all  his  muscles  in  his  attempts  to  bear  the  pain  in 
silence."  There  was  no  objective  change  in  the  abdomen,  but  the  tenderness  over  the 
aneurism  was  more  marked  than  before. 

The  next  day  he  had  several  attacks  of  pain  and  vomiting.  At  4.00  p.m.  the  vomit- 
ing was  very  severe  and  was  accompanied  by  intense  pain  and  sudden  collapso. 
His  color  became  a  ghastly  pallor.  He  became  almost  pulseless  before  any  one  could 
reach  him.  He  was  still  conscious  and  complained  of  great  pain  in  the  back  and 
right  side  of  the  abdomen,  to  relieve 
which  .15  Gm.  (gr.  iiss)  of  morphine 
were  necessary,  given  within  an  hour. 
At  5.45  p.  m.  a  small  saline  infusion 
was  given  and  caused  the  pulse  to 
improve  slightly.  Strychnine,  2  mg. 
(aV  gr.),  +  digitalin  (German),  .15  mg. 
(io  gr.),  had  no  effect.  The  maximal 
blood-pressure  before  the  collapse  was 
130  mm.  Hg,  after  it  was  70  mm.  Hg. 

The  next  day  there  was  dulness 
throughout  the  right  flank  extending 
up  to  liver  dulness  (due  to  outpouring 
of  blood  into  the  peritoneal  cavity). 
The  systolic  murmur  over  the  tumor 
disappeared,  but  the  aneurismal  mass 
still  pulsated.  The  haemoglobin  was 
found  to  have  fallen  to  55  per  cent.; 
the  leucocytes  rose  to  17,500. 

During  the   next   few  days   the 

patient's  condition  seemed  to  improve.  Fig-  3}?;~Tum°T  and  Pnlsa}^  >n  a  case  of  patient 
Pr,,  ,       ,  ,,  .  (M.  r.)  with  aneurism  of  the  abdominal  aorta. 

Ihe  pulse  became  stronger;  the  maxi- 
mal blood-pressure  rose  to    120   mm. 

Hg.  However,  his  kidneys  absolutely  ceased  secreting.  He  did  not  void  at  all  spon- 
taneously, and  50  c.c.  of  clear  reddish  liquid,  of  neutral  reaction  and  with  a  specific 
gravity  of  1030,  was  all  that  could  be  obtained  on  catheterization  on  the  evening  of 
Jan.  24.  It  contained  a  large  amount  of  albumen,  no  sugar,  no  casts,  a  few  red  blood- 
corpuscles,  and  a  large  number  of  pus-cells.  This  was  the  last  urine  obtainable,  even  by 
catheter. 

From  this  time  on  the  patient's  condition  became  worse.  He  complained  of 
sudden  shocks  like  electric  shocks  through  his  nervous  system,  to  which  he  responded 
by  sudden  single  twitches.  He  had  no  general  convulsions.  His  mind  remained 
perfectly  clear,  his  pulse  good  until  the  morning  of  Jan.  26  (five  days  after  the  rupture), 
when  his  pulse  gradually  became  weaker,  he  lapsed  into  unconsciousness,  and  died  at 
10.30  p.  m. 

Autopsy  confirmed  the  clinical  diagnosis,  showing  a  large  saccular 
aneurism  of  the  abdominal  aorta  which  had  ruptured  into  the  retroperi- 
toneal tissue  and  lesser  peritoneal  cavity,  causing  infarction  of  the  left  kidney  and  oblitera- 
tion of  the  vessels  to  the  right.  There  was  thrombosis  of  all  renal  vessels  and  a  tremendous 
hemorrhage  into  the  greater  peritoneal  cavity  as  well.  This  rupture  had  evidently  occurred 
at  the  time  of  the  collapse  on  Jan.  22.  There  was  an  island  of  clot  within  the  coil 
of  silver  wire  within  the  sac,  but  a  wide  free  blood  channel  between  this  clot 
and  the  aneurismal  wall,  so  that  the  clot  had  not  strengthened  the  latter 
in   the   least. 

It  is  probable  that  during  the  months  following  the  wiring,  while  he  was  free  from 
pain,  the  clot  filled  the  entire  aneurismal  sac,  and  that  the  eddy  currents  dissected  it  free 
from  the  aneurismal  wall  about  the  time  that  the  pains  returned. 


656 


DISEASES    OF   THE   HEART   AND    AORTA. 


Fig.  313. —  Tortuous  subclavian  artery,  simu- 
lating a  small  aneurism.  The  tumor  which  it 
formed  above  the  clavicle  is  indicated  by  the 
shading. 


DIAGNOSIS. 

The  diagnosis  of  thoracic  aneurism  is,  as  a  rule,  easy,  especially  with 
the  aid  of  the  X-ray.  Most  of  the  conditions  with  which  it  can  be  confused 
have  been  mentioned  above.  The  most  important  of  these  are  simple 
dilatation  of  the  aorta,  mediastinal  tumors,  pulsating  empyema  or  encapsu- 
lated pericarditis,  and  enlarged  mediastinal  or  branchial  glands.  Any  of 
these  may  cause  the  dulness,  the  tracheal  tug,  the  inequality  of  pupils 
and  pulse.  The  systolic  thrill  and  murmur  may  also  be  communicated  by 
a  very  solid  tumor  or  may  arise  in  a  very  vascular  sarcoma,  aberrant  thy- 
roid with  stroma,  or  metastasis  from 
a  medullary  carcinoma  or  hyperne- 
phroma. A  diastolic  shock  is  scarcely 
ever  felt  over  even  the  most  vascu- 
lar tumors,  but  is,  of  course,  well 
marked  over  a  dilated  aorta.  The 
presence  of  a  forcible  expansile 
pulsation  in  the  interspaces  is  suffi- 
cient to  exclude  tumors;  but  in  the 
first  and  second  interspaces  when 
there  is  no  actual  bulging  it  may 
be  due  to  a  simple  dilatation  of  the 
aorta.  The  tracheal  tug  may  further 
be  due  simply  to  displacement  of  the  heart  or  aortic  arch  or  to  enterop- 
tosis,  while  the  inequality  of  the  pulse  may  arise  from  the  presence  of  adhe- 
sions or  arteriosclerotic  plaques  about  the  origin  of  the  subclavian  arteries. 
The  absolute  diagnosis  can  almost  always  be  made  by  X-ray  exam- 
ination, but  even  then  a  tumor  may  be  encountered  whose  shadow  shows 
no  expansile  pulsation  and  whose  nature  remains  in  doubt.  The  homogene- 
ous shadow,  with  its  regular  spherical  or  oval  form  and  its  connection 
with  the  aorta,  is  usually  evidence  of  aneurismal  nature. 

In  doubtful  cases  the  greatest  care  is  necessary,  for  the  physician  should 
always  bear  in  mind  that  the  earlier  the  aneurism  can  be  treated  the  greater 
the  chance  of  cure,  and  this  stage  of  hope  is  usually  the  stage  in  which  the 
physical  signs  are  still  far  from  definite. 

Occasionally  a  tortuous  carotid  or  subclavian  artery  presenting  its 
convexity  in  the  supraclavicular  fossa  may  simulate  an  aneurism,  so  that, 
as  in  the  case  seen  in  Fig.  313,  it  is  necessary  to  outline  the  supposed  aneu- 
rism with  the  tip  of  the  little  finger.  In  this  case,  which  had  once  been 
diagnosed  aneurism,  it  was  possible  to  reach  below  the  convexity  and  to 
feel  the  outline  of  a  narrow  but  tortuous  subclavian  artery.  Of  course, 
the  X-ray  examination  in  such  a  case  would  at  once  clear  up  the  diagnosis, 
even  if  the  outline  of  the  artery  could  not  be  felt. 

Another  condition  which  may  simulate  aneurism  of  the  subclavian 
artery  is  a  dilated  jugular  bulb,  which  appears  as  a  pulsating  sac  above  the 
clavicle.  This  is  especially  marked  when  tricuspid  insufficiency  is  present. 
In  such  cases  the  arterial  blood-pressure  may  be  low  and  the  arterial  pulses 
weak;  nevertheless,  the  pulsation  is  so  feeble  and  the  connection  with  the 
dilated  veins  so  evident  that  it  should  never  be  mistaken  for  an  aneurism. 


ANEURISM. 


657 


DISSECTING  ANEURISM. 

Shakelton  in  1822  gave  the  first  descriptions  of  dissecting  aneurisms, 
which  were  soon  confirmed  by  Hope  (1833)  and  Henderson  (1843).  In 
this  condition  the  coats  of  the  aorta  are  split  longitudinally  into  two  sleeves, 
— an  outer,  originally  formed  by  the  adventitia,  and  later  lined  by  new- 
formed  intimal  endothelium;  and  an  inner  sleeve  representing  the  original 
tube  of  the  aorta,  compo.sed  of  the  original  intima  and  media,  and  later 
also  covered  with  new-formed  endothelium. 

PATHOLOGY. 

The  condition  is  not  an  extremely  rare  one,  so  that  Bostroem  in  1887 
was  able  to  collect  reports  of  177  cases.  It  usually  arises  in  the  aorta, 
especially  at  the  beginning  of  the  descending  arch,  and  not  infrequently 
is  formed  as  the  continuation  of  a  simple  aneurism  of  the  arch.  From 
this  region  it  commonly  extends  along  the  whole  length  of  the  aorta  to 


Fig.  314. — Dissecting  aneurisms.  A.  Specimen  of  a  dissecting  aneurism  (partial  clot  formation) 
in  a  man  with  only  two  aortic  cusps.  (From  the  Army  Medical  Museum,  Washington,  D.  C.)  B.  Dis- 
secting aneurism  of  L.  R.,  involving  the  arch  and  the  descending  aorta.  (After  MacCallum;  kindness 
of  the  Johns  Hopkins  Hospital  Bulletin.) 


the  bifurcation,  the  arteries  sometimes  arising  from  the  inner,  sometimes 
from  the  outer  tube.  Occasionally  the  split  occurs  between  the  layers  of 
the  media,  so  that  both  sleeves  have  a  wall  of  media.  Very  infrequently 
the  outer  tube  ruptures  into  the  inner  tube  near  its  lower  end,  so  that  the 
blood  passes  back  into  the  latter. 

The  most  satisfactory  explanation  for  this  remarkable  lesion  seems 
to  be  the  following  (v.  Moller,  Flockemann,  Schede) :    As  long  as  the  lumen 
of  the  artery  is  uniform,  the  blood  exerts  only  a  lateral  pressure  upon  the 
42 


658  DISEASES   OF   THE   HEART    AND    AORTA. 

arterial  walls,  which  acts  "  across  the  grain  "  of  the  arterial  coats.  However, 
when  calcified  plaques  project  into  the  lumen,  these  tend  to  impede  the 
blood-current  so  that  the  longitudinal  pressure  of  the  latter  acts  as  well. 
As  Bostroem  has  shown,  the  resultant  force  acts  in  a  parabola  pointing 
outward  and  downward.  When  this  is  acting  upon  an  area  where  the  media 
is  thinned  or  absent,  it  tends  not  only  to  split  the  coats  "with  the  grain" 
but  also  to  push  the  adventitia  outward.  The  wall  gives  way,  the  split 
lengthens,  and  the  outer  sleeve  is  formed.  Whether  or  not  the  aorta  then 
ruptures  depends  upon  the  ability  of  the  adventitia  alone  to  withstand 
the  blood-pressure. 

The  coagulation  of  the  blood  within  the  sac  depends  upon  the  formation 
of  fibrin  ferment  in  the  tissues  of  the  adventitia  and  the  rapidity  of  the 
blood-flow  within  the  new-formed  sac.  It  is  quite  frequent  for  extensive 
and  even  total  coagulation  of  the  contents  to  take  palce. 

SYMPTOMS    AND    SIGNS. 

A  considerable  proportion  of  the  cases  of  dissecting  aneurisms  give 
no  outward  manifestation  during  life  and  are  accidental  findings  at  autopsy. 
A  large  number  give  the  usual  signs  of  ordinary  aneurism,  especially  when 
they  arise  as  a  continuation  of  the  latter.  This  is  well  exemplified  by  the 
following  case,  which  was  under  the  writer's  observation  during  his  last 
admission  to  the  hospital.  (The  pathological  findings  and  clinical  notes 
are  taken  from  the  report  of  Professor  MacCallum.) 

L.  R.,  negro,  aged  30,  had  been  treated  in  the  Johns  Hopkins  Hospital  one  year 
previous  to  his  final  admission,  at  which  time  the  diagnosis  of  aneurism  of  the  aorta 
had  been  made.  At  the  final  admission  the  patient  was  found  to  be  suffering  from  an 
arthritis  with  symptoms  of  general  fever,  sweating,  etc.  The  heart  was  enlarged,  dulness 
extending  13.5  cm.  to  left  and  3  cm.  to  right  of  midline.  There  was  visible  impulse  and 
heaving  in  second,  third,  fourth,  fifth,  and  sixth  interspaces,  far  out  in  first  and  second 
left  interspaces.  Heart  sounds  were  clear,  dull,  and  ringing;  second  sound  followed  by 
soft  diastolic  murmur  in  third  left  interspace,  not  heard  in  neck. 
Patient  died  in  delirium  with  high  fever. 

Autopsy  showed  general  streptococcus  septicaemia,  hemorrhagic  nephritis,  acute 
purulent  arthritis,  obliterative  pericarditis,  aneurism  of  ascending  aorta,  dissecting  aneu- 
rism of  the  descending  aorta.  The  aortic  orifice  is  not  dilated  (8  cm.  in  circumference).  A 
large  aneurismal  sac  (7  cm.  in  diameter)  lies  behind  the  pulmonary  artery;  it  extends 
upward  in  the  aorta  to  the  arch,  beyond  which  the  tube  becomes  double,  the  inner  tube 
(the  original  lumen  of  the  aorta)  having  for  its  walls  the  original  intima  plus  media, 
the  outer  tube  media  plus  new-formed  endothelium.  Numerous  trabecule  jut  out 
transversely  into  its  lumen.  Some  of  the  intercostal  vessels  arise  from  the  new,  some  from 
theoloiumen.  The  left  renal  artery  arises  from  the  old  lumen;  the  right  has  been  torn 
and  arises  from  the  outer.  At  the  lower  end  above  the  bifurcation  the  outer  tube  has 
ruptured  back  into  the  original  lumen. 

Another  type  is  exemplified  by  a  case  under  the  care  of  Professor 
Halsted;  also  reported  by  MacCallum. 

Patient,  aged  60,  subject  to  mental  disturbance  and  epileptiform  attacks,  complained 
on  May  28  of  intense  pain  over  the  whole  body,  which  he  could  not  locate.  On  May  28  his 
abdomen  was  much  distended  and  he  was  jaundiced.  There  was  pain  in  the  region  of 
the  appendix.  His  temperature  was  100°.  Leucocytes  20,000.  Exploratory  laparotomy 
showed  an  extremely  distended  colon  which  was  relieved  by  colostomy.  Patient  died 
the  next  day. 


ANEURISM.  659 

Autopsy  showed  a  dissecting  aneurism  along  the  whole  aorta,  splitting 
the  media.  The  outer  sleeve  of  the  descending  arch  perforated  into  the  posterior  mediasti- 
num, giving  rise  to  a  tremenduous  hsematoma  which  distended  that  space  down  to  the 
diaphragm.  The  rupture  had  evidently  given  rise  to  the  pain;  the  disintegration  of  red 
corpuscles  in  the  clot  had  caused  the  hematogenous  jaundice.  Both  these  phenomena 
are  common  in  cases  of  this  type. 

ANEURISM  OF  THE  PULMONARY  ARTERY. 

Aneurisms  of  the  pulmonary  artery  are  very  rare  as  compared  with 
those  of  the  aorta.  Henschen  (1906)  has  recently  summed  up  the  reported 
cases.  In  contrast  to  aortic  aneurism,  he  finds  that  there  is  no  close  rela- 
tionship to  hard  work;  18  out  of  34  cases  (50  per  cent.)  were  in  men,  16  (47 
per  cent.)  in  women;  39  per  cent,  occurred  under  the  age  of  30  (as  com- 
pared with  18  per  cent,  of  aortic  aneurisms).  Acute  infectious  diseases 
and  lues  seem  to  be  the  main  etiological  factors.  The  ductus  arteriosus 
Botalli  was  frequently  found  open  (17.5  per  cent.),  which  would  indicate 
that  some  disturbance  during  fetal  life  or  soon  after  birth  had  been  a  pre- 
disposing factor.  Frequently  there  is  a  certain  degree  of  narrowing  of  the 
pulmonary  artery  (32  per  cent.).  In  8  cases  (20  per  cent.)  there  were  also 
marked  arteriosclerotic  changes  in  the  pulmonary  artery. 

Among  40  cases  there  were  the  following  complications:  pulmonary 
stenosis  2;  relative  pulmonary  insufficiency  5;  organic  pulmonary  insuffi- 
ciency; other  valvular  lesions  3. 

The  subjective  symptoms  are  not  pathognomonic  and  are  very  similar 
to  those  of  congenital  heart  disease;  palpitation,  dyspnoea  and  cardiac 
asthma,  constriction  of  the  chest,  cough,  often  oedema  of  the  lungs  and 
blood-tinged  expectoration,  intense  cyanosis,  oedema,  anasarca,  ascites, 
hydrothorax.  Death  sometimes  results  suddenly  from  rupture,  sometimes 
from  intercurrent  pericarditis  and  endocarolitis,  sometimes  from  diseases 
of  the  respiratory  tract. 

DIAGNOSIS. 

According  to  Henschen,  the  diagnosis  is  justified  when  the  following 
signs  are  all  present  simultaneously: 

1.  Intense  cyanosis  and  other  signs  of  stasis,  constriction,  and  bloody 

expectoration,  sometimes  sternal  pain. 

2.  Prominence  of  second  and  third  left  costal  cartilages  or  second  left 

interspace  and  well-defined  dulness  or  X-ray  shadow  in  this  area. 

3.  Pulsation  and  well-defined  thrill  anol  murmur  in  second  left  inter- 

space. 

4.  Loud  superficial  rasping  systolic  murmur. 

5.  Hypertrophy  of  the  right  heart. 

6.  Absence  of  dilatation  or  hypertrophy  of  left  heart  (apex  dulness 

not  outside  the  mammillary  line) . 

7.  Absence  of  other  signs  of  aortic  aneurism. 

The  X-ray  shadow  furnishes  the  most  important  aid  in  diagnosis. 
However,  the  correct  diagnosis  was  made  intra  vitam  only  once  or 
twice   in   his   40   cases. 


660  DISEASES   OF  THE   HEART   AND    AORTA. 


ANEURISM  OF  THE  ABDOMINAL  AORTA. 

Owing  to  its  frequency  (10-14  per  cent,  of  aneurisms)  and  its  surgical 
accessibility,  aneurism  of  the  abdominal  aorta  is  of  great  importance.  Owing 
to  its  exposed  situation,  trauma  is  a  more  frequent  cause  than  in  thoracic 
aneurism.  As  Sibson  has  shown,  it  is  usually  (133  out  of  171  cases)  situated 
just  below  the  diaphragm  and  above  the  cceliac  axis,  in  the  place  where  it 
gives  the  greatest  number  of  symptoms  and  is  most  inaccessible  to  operation. 

The  most  important  symptom  of  aneurism  of  the  abdominal  aorta 
is  abdominal  pain,  — epigastric  or  in  the  regions  of  kidney  and  gall- 
bladder, sometimes  in  the  flanks,  sides,  and  back.  The  pain  is  usually 
more  marked  on  one  side  than  the  other,  but  may  be  bilateral.  Until  the 
appearance  of  a  palpable  tumor  the  condition  may  be  readily  mistaken 
for  renal  calculus,  gastric  ulcer,  or  other  abdominal  disease,  or  for  psoas 
abscess.  The  pain  may  be  so  intense  as  to  require  morphine,  even  in  large 
doses,  though  acetanilid,  antipyrin,  aspirin,  etc.,  may  be  of  use  at  first. 
Palpitation  is  also  commonly  felt  in  the  aneurism. 

All  these  symptoms  are  common  in  neurasthenic  women  who  have 
vigorously  pulsating  abdominal  aortas,  especially  associated  with  enterop- 
tosis.  It  is  probable  that  in  this  condition  the  peritoneal  moorings  of  the 
aorta  are  rather  loose.  When  the  arterial  pressure  rises  at  systole,  the  angle 
curves  of  the  abdomnal  aorta  and  common  iliac  arteries  tend  to  straighten 
themselves  and  thus  throw  the  aorta  forward  toward  the  abdominal  wall, 
at  the  same  time  giving  a  painful  tug  upon  the  abdominal  nerves  as  they 
emerge  from  the  vertebral  column.  The  looser  the  moorings  of  the  aorta 
the  greater  its  excursion  and  the  greater  the  pull  upon  structures  other 
than  those  which  normally  hold  it.  Arteriosclerosis  of  the  abdominal 
vessels  may  also  give  rise  to  similar  symptoms. 

Mere  pulsation  of  the  aorta  in  the  epigastrium  and  elsewhere,  even 
when  associated  with  quite  intense  pain,  is  therefore  not  necessarily  a  sign 
of  abdominal  aneurism.  In  doubtful  cases  it  is  most  important 
to  outline  the  whole  course  of  the  aorta  by  pressing  the 
fingers  of  the  two  hands  down  on  either  side  of  the  vessel  so  as  to  include 
the  abdominal  aorta  between  them.  The  expansile  nature  of  the  pulsation 
can  be  felt  by  pressing  downward  and  inward.  Any  irregularity  or  bulging 
along  its  course  may  be  felt  readily  in  this  way.  For  the  diagnosis 
of  an  aneurism  it  is  necessary  to  outline  a  tumor  with 
expansile  pulsation  arising  from  the  abdominal  aorta,  limited  in 
extent  above  and  below,  and  spherical  or  oval  in  shape.  There  is  usually 
a  well-marked  thrill  over  an  aneurism.  The  pulse-wave  in  the  femorals  is 
usually  much  retarded  in  aneurism  (apex  beat— femoral  pulse  interval  = 
0.24+  sec.)  but  not  in  simple  aortic  pulsation.  The  early  diagnosis  may 
sometimes  be  made  with  the  fluoroscope,  care  being  taken  to  empty  the 
bowels  by  a  day  or  two  free  purgation  and  preliminary  milk  diet,  and  then 
to  examine  the  abdomen  with  a  "compression  diaphragm"  (Kompres- 
sionsblende)  so  as  to  push  the  other  structures  aside.  Oblique  illumina- 
tions and  inflation  of  stomach  and  colon  with  air  may  be  helpful. 

As  the  aneurism  grows  it  may  press  upon  the  renal  arteries  and  veins 
and  may  cause  albuminuria,  cylindruria,  hematuria,  or  even  anuria 


ANEURISM.  661 

and  death  from  this  cause.  It  may  press  upon  the  intestines  and  cause 
intestinal  paralysis,  with  death  from  obstruction,  or  may  give 
rise  to  many  symptoms  from  pressure.  Erosion  of  the  vertebrae 
and  pressure  on  the  cord  or  cauda  equina  may  lead  to  paraplegia 
(flaccid)  and  may  cause  most  intense  pain. 

Abdominal  aneurisms  may  rupture  the  retroperitoneal  tissue  into 
the  peritoneum,  especially  the  lesser  peritoneal  sac  into  the  stomach, 
intestines,  or  vena  cava.  They  rupture  externally  in  the  epigastrium.  The 
rupture  is  attended  with  excruciating  pain  and  often  collapse,  but  death 
may  not  ensue  for  some  time  thereafter,  as  the  clotting  of  blood  in  a  small 
space  may  prevent  further  outflow  from  the  vessels.  Thus,  in  the  case 
cited  below,  the  aneurism  ruptured  into  the  retroperitoneal  tissue,  com- 
pressing the  renal  vessels.  The  pain  accompanying  and  following  rupture 
was  excruciating,  probably  owing  to  stretching  of  the  solar  plexus. 

PROGNOSIS  AND  TREATMENT  OF  ANEURISM. 

In  spite  of  the  fact  that  aneurisms  occasionally  cease  to  develop  or 
even  undergo  spontaneous  cure  by  thrombosis,  this  procedure  is  to  be  re- 
garded as  a  rarity,  and  it  is  not,  under  any  circumstances,  to  be  expected. 
By  far  the  greater  number  of  aneurisms  cause  the  death  of  the  patient 
within  from  one  to  five  years,  though  occasionally  they  remain  stationary 
for  twTenty-five  or  thirty.  It  is,  therefore,  necessary  to  attempt  to  modify 
the  course  by  treatment.  As  the  intrathoracic  aneurisms  were  not  well 
known  to  the  ancients,  their  therapy  for  aneurism  was  confined  to  ligature 
of  the  peripheral  arteries. 

Valsalva  (1666-1723)  recommended  lessening  the  force  of  the  heart- 
beat by  absolute  rest  in  the  recumbent  posture,  "starvation  diet."  and 
frequent  removal  of  small  quantities  of  blood  by  venesection.  The  two 
former  procedures  were  revived  by  Tufnell  in  1874.  Tufnell  reported  a 
number  of  cases,  especially  of  aneurism  of  the  abdominal  aorta,  cured  by 
restriction  of  the  daily  intake  to  ten  ounces  of  solids  and  ten  ounces  of 
liquids  for  several  weeks. 

-p.      ,  f    ,  f  Bread  and  butter 60  Gm.  (Bii) 

15reaktast I  Milk 60  c.c.  (Bii) 

n.  f  Meat 60-100  Gm.  (Bii-iii) 

inner I  Milk 75-125  c.c.  (giii-ir) 

f  Bread 60  Gm.  (Bii) 


Supper . 


I  Milk 60  c.c.  (Bii) 


The  patient  is  given  no  water,  and  is  not  allowed  to  rise  from  the  horizontal  position 
even  for  an  instant.  As  a  result  of  this  the  blood-pressure  falls  and  the  pulse-rate  also. 
In  his  first  case  the  pulse-rate  fell  from  104  to  69  per  minute,  equalling  a  diminution 
of  50,400  beats  in  twenty-four  hours.  The  wall  of  the  aneurism  is  spared  just  this  amount 
of  strain,  the  volume  of  blood  diminishes,  and  the  aneurismal  sac  may  gradually  contract 
down,  facilitating  clotting. 

Tufnell's  results  (cure  of  two  abdominal  and  one  popliteal  aneurism) 
are  rather  striking,  but  the  treatment  imposes  the  greatest  hardship  on 
the  patient  and  few  have  the  hardihood  to  give  it  an  adequate  trial.  That 
the  restriction  of  fluid  to  ten  ounces  daily  may  be  harmful  is  suggested  by 


662  DISEASES  OF  THE  HEART  AND  AORTA. 

the  fact  that  his  first  case  developed  uraemia  at  the  end  of  the  treatment 
and  died  from  that  about  as  soon  as  he  would  probably  have  died  from  the 
natural  progress  of  the  aneurism. 

Alonzo  Taylor  has  made  very  careful  studies  of  the  blood  in  three  patients  under 
Tufnell  treatment,  who  were  also  receiving  potassium  iodide  1  Gm.  (gr.  xv)  and  calcium 
chloride  2  Gm.  (gr.  xxx)  daily,  and  who  were  being  bled  (250  c.c.)  every  eighteen  days. 
He  found  no  change  in  the  concentration  of  the  blood  or  in  calcium  in  the  blood,  and  only 
slight  fall  of  red  corpuscles.  The  coagulation  time  was  unchanged  in  one  patient,  slightly 
shortened  in  another.  The  aneurisms  became  somewhat  smaller,  but  no  cures  resulted. 
At  the  Johns  Hopkins  Hospital  the  method  was  tried  very  assiduously  for  many  years, 
supplemented  by  subcutaneous  gelatin  injections  as  suggested  by  Lancereaux.  Later  cal- 
cium lactate  has  been  used.  There  have  been  but  few  satisfactory  results  (Futcher) ,  th  ougb 
Professor  Osier  stated  that  he  had  seen  several  cases  of  cure  in  his  extensive  experience. 

Potassium  iodide  was  used  in  aneurism  by  Bouillaud  (1859) 
and  Chuckerbutty  (1862),  and  especially  by  Balfour,  who  found  that  it 
caused  great  relief  from  the  pain,  and  claimed  that  the  aneurism  also  dimin- 
ished considerably  in  size.  Subsequent  experience  demonstrates  the  cor- 
rectness of  the  claim  that  aneurismal  pains  are  often  relieved  by  potassium 
iodide,  but  few,  if  any,  cures  of  well-defined  thoracic  aneurisms  can  be  ob- 
tained by  its  use.  Its  modus  operandi  is  still  obscure,  probably  acts  pri- 
marily upon  the  spirochetes  and  causes  healing  of  the  luetic  arteritis. 
Gibson  thinks  that  "  we  may  admit  it  to  be  extremely  probable  that  under 
the  influence  of  iodide  of  potassium  the  nutrition  of  the  walls  of  the  sac,  as 
well  as  of  the  whole  of  the  arterial  system,  undergoes  improvement." 

Wiring. — The  reason  that  an  increased  coagulability  of  the  blood  and 
a  slowed  circulation  do  not  of  themselves  produce  intrasaccular  clotting 
is  that  the  latter,  like  the  vessels,  is  lined  with  endothelium  and  does  not 
furnish  fibrin  ferment.  As  stated  by  Moore  in  1864,  "  the  first  indispensable 
condition  for  the  cure  of  a  thoracic  aneurism  is  to  provide  means  of  eliciting 
fibrin  from  the  blood  "  (producing  fibrin  ferment  in  situ),  and  the  "  second 
....  to  extend  the  surface  within  it  on  which  the  fibrin  may  coagulate." 
In  order  to  supplement  these  deficiencies,  Moore  suggested  the  introduction 
of  fine  wire  into  the  aneurismal  sac.  Murchison  submitted  to  him  a  case 
of  aneurism  of  the  ascending  aorta  which  pointed  on  the  surface  of  the  chest. 
Moore  slowly  introduced  twenty-six  yards  of  fine  iron  wire  through  a  fine 
needle.  The  pulse  fell  from  116  to  92,  the  pulsation  of  the  tumor  almost 
ceased,  but  the  patient  died  in  collapse  two  days  later. 

Previously  to  Moore,  Guerad  (1821),  Petrequin  (1845),  and  Ciniselli 
(1847)  induced  clotting  by  passing  weak  electric  currents  between  the  tips 
of  two  needles  introduced  into  the  sac  (galvanopuncture).  Corradi  com- 
bined the  two  methods  by  using  the  wire  as  one  pole  of  the  battery. 

The  writer  is  indebted  to  Prof.  J.  M.  T.  Finney  for  the  following  descrip- 
tion of  his  procedure  in  wiring  aneurisms : 

The  wire  used  in  this  operation  is  an  alloy  of  80  parts  copper  to  1000 
silver,  of  about  0.33  mm.  thickness  (old  English  gauge  No.  27),  drawn  so 
as  to  be  very  springy.1    Previous  to  the  operation  it  should  be  wrapped  upon 

1Gescheider  Bros.,  Cor.   Monument   and   Gay  Sts.,  Baltimore,  prepared  this  wire 
according  to  Dr.  Finney's  directions. 


ANEURISM. 


663 


an  ordinary  spool  so  that  it  will  preserve  the  curve  even  after  insertion  into 
the  aneurismal  sac  and  curl  around  and  around  within  the  latter.  Wire  and 
spool  are  sterilized  by  boiling.  The  wire  is  introduced  into  the  aneurismal 
sac  through  an  ordinary  infusion  needle,  which  should  be  just  large  enough 
to  allow  the  wire  to  enter.  This  needle  must  be  carefully  insulated  by  dip- 
ping in  black  enamel,  after  which  it  is  dry  sterilized  by  heating  in  a  test-tube 
at  160°  (Centigrade)  for  one  hour.  (Heating  with  water  or  steam  might 
loosen  the  enamel.) 

Before  proceeding  with  the  operation  a  cathode  pad  electrode,  at  least 
8x10  cm.  in  size,  is  placed  over  the  patient's  back,  while  a  sterile  anode  wire 
of  the  medical  battery  is  connected  with  the  distal  end  of  the  sterile  silver 
wire.  The  proximal  end  of  the  wire  is  inserted  into  the  needle  before  the 
operation  is  begun. 

Just  before  the  operation  the  patient  may  be  given  a  hypodermic  injec- 
tion of  morphine  15  to  30  mg.  (gr.  \  to  \),  the  skin  over  the  aneurism  care- 


Fig.  315. — Diagram  showing  the  various  methods  for  the  operative  treatment  of  aneurism.  Arrows 
indicate  direction  of  the  blood  stream.  A.  Ligature  above  and  below  the  sac  (Antyllus).  B.  Ligature 
above  and  below  the  sac;  removal  of  the  sac  (Hueter).  C.  Ligature  above  and  at  some  distance  from 
the  sac  (Hunter).  V.  V.  represent  vasa  vasorum.  D.  Ligature  below  the  sac  (Brasdor,  Wardrop). 
E.  Metal  band  (Halsted).  F.  Obliteration  of  the  sac  (Ma tas).  a,  laying  the  sutures  in  the  sac;  b,  arterial 
tube  left  patent. after  tightening  sutures;  c,  entire  lumen  obliterated  by  sutures.  G.  Successful  wiring  of 
a  sacculated  aneurism  by  the  Moore-Corradi  method,  showing  the  electrodes  ( +  ,  — )  in  place.  H.  Wiring 
of  an  aneurism  with  wide  mouth,  showing  the  action  of  eddy  currents  in  penetrating  between  the  clot 
and  the  aneurism  wall.     (Compare  with  Fig.  316.) 


fully  sterilized,  and  a  little  sterile  1  per  cent,  cocaine  or  novocaine  solution 
injected.  In  inserting  the  needle  the  skin  should  be  drawn  aside  a  little, 
so  that  the  opening  in  the  sac  may  not  remain  exactly  beneath  the  skin 
puncture,  after  the  needle  is  removed;  the  danger  of  infection  of  any  ensuing 
haematoma  may  thus  be  lessened.  The  entrance  of  the  needle  into  the  sac 
is  marked  by  the  egress  of  a  small  amount  of  blood.  The  wire  is  then  pushed 
in  slowly,  while  an  assistant  holds  and  rotates  the  spool  in  order  to  avoid 
kinking  and  to  allow  the  wire  to  coil  up  well  within  the  sac.  After  about 
10  feet  of  wire  has  been  inserted,  the  wire  is  cut  off  about  1  foot  from  the 


664  DISEASES  OF  THE  HEART  AND  AORTA. 

skin  and  connected  by  a  clamp  with  the  anode  wire  of  the  battery.  The 
galvanic  current  is  now  very  gradually  turned  on  until  a  strength  of  10  milli- 
amperes  is  reached,  and  this  is  allowed  to  run  for  30  minutes,  after  which  it 
is  gradually  raised  to  20  milliamperes  for  10  minutes  unless  this  should  cause 
great  discomfort  to  the  patient.  The  current  is  then  turned  off,  the  needle 
removed,  and  the  excess  of  wire  cut  off.  In  cutting  off  the  wire  the  skin 
should  be  held  taut  between  two  fingers,  to  prevent  the  formation  of  a 
hsematoma,  and  the  stump  of  wire  then  cut  off  with  a  curved  scissors,  ex- 
erting as  much  pressure  as  possible  so  that  when  pressure  is  removed  the 
stump  of  wire  shall  be  buried  well  below  the  level  of  the  skin  and  the  skin 
shall  slide  smoothly  over  it.  If  necessary,  pressure  over  the  tumor  may  be 
continued  in  order  to  avoid  the  formation  of  a  hsematoma,  for  the  latter 
becomes  infected  easily  and  the  presence  of  an  area  of  inflammation  may 
vitiate  the  result  of  the  wiring. 

Even  when  the  clotting  within  the  sac  is  complete,  the  end  result  of  the 
wiring  is  still  in  doubt.  Thus,  in  14  cases  cited  by  Hunner  which  had  been 
treated  by  wiring  alone,  two  cases  of  abdominal  aneurism  (Morse  and  Langton) 
had  been  cured;  in  twenty-three  cases  (seventeen  thoracic)  there  were  three 
cures  (17.7  per  cent.).  Prof.  Finney  has  recently  reported  a  series  of  24 
cases,  all  treated  by  himself  by  the  Moore-Corradi  method,  with  three  recov- 
eries, though  in  many  of  the  cases  life  was  undoubtedly  prolonged  and  the 
patient's  comfort  greatly  increased.  Rosenstirn's  case  of  thoracic  aneurism 
was  still  living  and  well  twenty  years  after  the  operation. 

It  is  evident  that  there  is  great  variation  in  the  results  obtained  in  dif- 
ferent cases,  and  the  factors  which  determine  this  merit  some  considera- 
tion. In  fusiform  and  partially  sacculated  aneurisms  the  clot  held  in  the 
meshes  of  wire  rarely  resists  the  impact  of  the  blood  stream  and  may  be 
carried  away  in  large  emboli,  and  death  from  such  embolism  is  by  no 
means  rare,  so  that  the  treatment  may  sometimes  actually  hasten  the 
patient's  death.  In  aneurisms  of  this  form  there  is  little  to  be  hoped  from 
the  operation. 

In  well-sacculated  and  especially  in  bottle-shaped  aneurisms  with  nar- 
row necks,  better  results  may  be  obtained,  for  here  the  clot  may  completely 
fill  the  sac  (Fig.  315)  so  that  the  blood  stream  may  glide  over  its  surface 
instead  of  gradually  shattering  the  clot  by  striking  full  upon  it.  In  wide- 
mouthed  sacs,  however,  though  the  clot  may  at  first  fill  the  sac  completely, 
it  often  happens  that  the  blood  stream  gradually  pushes  in  between  the 
clot  and  the  aneurismal  wall,  so  that  the  area  of  expansile  pulsation  can 
be  felt  day  by  day  encroaching  upon  the  central  solid  area  whose  pulsa- 
tion is  only  transmitted,  until  finally  the  entire  clot  has  been  dissected  free 
by  the  blood  stream  and  remains  in  mid-channel  as  an  island  of  clot  held 
in  the  meshes  of  wire  but  no  longer  giving  support  to  the  aneurismal  wall 
(Fig.  316). 

This  loosening  of  the  clot  is  facilitated  not  only  by  the  general  stretch- 
ing of  the  aorta  walls  under  the  influence  of  a  high  maximal  blood-pressure, 
but  still  more  so  by  the  large  expansions  and  retractions  which  occur  at 
approximately  normal  pressures  where  the  elasticity  of  the  aorta  is  greatest. 
Such  large  pulsations  are  particularly  common  under  nervous  excitement. 


ANEURISM.  665 

It  is  evident,  therefore,  that  in  order  to  secure  the  best  results  the  aneu- 
rismal  sac  should  be  as  small  and  its  neck  as  narrow  as  possible  before  the 
wiring  is  undertaken.  This  is  best  secured  by  a  long  period  of  preliminary 
treatment  with  the  modified  Tufnell  method,  absolute  rest  in  bed  in  the 
horizontal  position,  with  diet  and,  especially,  fluids  very  much  restricted. 
In  aneurisms  of  the  aorta,  which  is  an  artery  of  the  elastic  type,  the  blood- 
pressure  may  be  still  further  reduced  by  sodium  nitrite,  erythrol  tetranitrate 
or  vasotonin,  though  in  aneurisms  of  arteries  with  muscular  walls  a  relax- 
ation of  the  latter  may  not  be  desirable.  Mental  quiet  should  be  insured 
in  every  way  possible,  but  it  must  be  remembered  that  isolating  the  patient 
from  the  visits  of  his  friends  and  prohibiting  him  from  reading  in  most  cases 
merely  leaves  him  a  prey  to  the  soul-racking  worry  from  the  contempla- 
tion of  his  condition,  and,  as  Cannon  and  de  la  Paz  have  shown,  this 
worry  in  itself  keeps  up  the  blood-pressure.  Sedatives  should  be  freely  used, 
bromides,  veronal,  or  trional,  as  much  as  conditions  allow,  and  should  be  sup- 
plemented by  codeine  in  15  or  30  mg.  (gr.  %  to  K)  doses,  or  even  morphine 
where  pain  or  unrest  demands.  Quiet  of  long  duration  should  be  secured  at 
any  cost. 

In  order  to  bring  the  coagulability  of  the  blood  up  to  its  maximum, 
calcium  lactate  should  be  administered  in  doses  of  1  to  2  grams  (grs.  xv 
to  xxx),  best  given  in  syrup  of  sarsaparilla,  four  times  a  day  for  a  consider- 
able period  both  before  and  after  the  operation,  and  milk  should  form  a  large 
part  of  the  diet.  This  preliminary  treatment  should  be  kept  up  for  several 
weeks  or  a  month,  so  as  to  bring  the  patient  into  the  most  favorable  possible 
condition  for  the  operation;  for  the  outlook  is  much  better  in  such  a  case 
than  in  an  aneurism  whose  walls  and  mouth  are  stretched  by  a  high  blood- 
pressure. 

The  treatment  after  the  wiring  is  no  less  important  than  the  preliminary 
treatment,  but  should  be  of  even  longer  duration.  It  is  all-important  that 
the  clot  must  be  given  a  chance  to  harden  and  it  should  have  an  opportunity 
to  become  as  firm  and  as  adherent  as  possible  to  the  walls  of  the  sac.  As  is 
shown  in  Fig.  300,  adhesions  between  sac  and  thrombus  are  relatively  slight 
and  form  but  slowly,  but  nevertheless  they  are  of  the  greatest  importance. 

Too  much  stress  cannot  be  laid  upon  the  harmful  role  of  mental  excite- 
ment mentioned  above,  for  the  large  pulse-throbs  tear  the  wall  away  from  the 
clotted  mass  that  cannot  move  with  it,  and  thus  prepare  a  channel  into  which 
the  blood  stream  pushes  its  way.  The  entrance  of  such  a  channel  between 
the  wall  and  the  margin  of  the  clot  (Fig.  315)  is  indeed  an  unfavorable  sign,  a 
sign  for  redoubled  precautions,  but  one  which  is  by  no  means  hopeless.  The 
clot  itself  is  loaded  with  fibrin  ferment,  and  if  quiet  is  resumed  secondary 
clotting  may  set  in.  The  writer  saw  this  strikingly  illustrated  in  the  case 
of  a  physician  with  an  aneurism  of  the  descending  part  of  the  arch  wired 
by  Prof.  Finney,  who  was  recently  under  his  observation  at  the  Johns  Hop- 
kins Hospital.  At  the  operation,  on  Nov.  17,  1910,  per- 
fect clotting  was  secured,  the  aneurismal  protrusion  flattened 
somewhat,  and  the  expansile  character  of  the  pulsation  disappeared.  Eight 
days  later  he  had  several  extremely  anginal  attacks,  so  severe 
that    he   writhed    in   pain,   and    then    he    "had  a  distinct 


666  DISEASES  OF  THE  HEART  AND  AORTA. 

feeling  of  something  giving  way  inside  the  aneu- 
rism.'' After  that  the  expansile  pulsation  returned 
about  the  margin  of  the  tumor.  The  patient  was  kept  at  absolute  rest  in 
bed,  but  for  several  weeks  afterwards  he  was  very  restless,  had  many 
disagreements  with  the  attendants  and  nurses,  and  gave  vent  to  frequent 
outbursts  of  temper.  During  this  period  there  was  no  im- 
provement and  the  expansile  pulsation  became  worse.  At  this  stage 
he  was  first  seen  by  the  writer,  who  was  able  to  bring  him  into  a  calmer 
frame  of  mind,  and,  as  a  result  of  frequent  visits,  much  persuasion, 
and  vigorous  doses  of  potassium  bromide,  this  mental  calm  was  tolerably 
well  maintained  until  he  left  the  hospital.  During  this  period  the 
pulsation  gradually  diminished.  On  January  10,  1911, 
he  "  felt  a  sudden  cooling  of  the  left  arm  and  then  a  lessened  pulsation  in 
the  aneurism."  There  was,  however,  still  some  expansile  pulsation  in  the 
upper  left  axilla,  and  a  systolic  murmur  over  the  entire  aneurismal  sac 
longest  in  duration  over  the  expansile  portion.  With  continued  rest,  mental 
quiet,  and  bromide,  pulsation  gradually  diminished,  and  by  January  29, 
1911,  the  mass  had  become  about  1  cm.  smaller  and  had  receded  entirely 
out  of  the  axilla.  Though  the  pulsation  was  more  marked,  it  had  entirely 
lost  its  expansile  character;  and  it  seemed  probable  that  the  apparent 
increase  in  pulsation  was  due  to  greater  freedom  in  the  movement  of  the 
sac  after  receding  from  the  axilla.  There  was  no  longer  any  murmur  audible 
over  the  tumor. 

All  these  signs  seemed  to  indicate  a  complete  clotting  throughout  the 
aneurismal  sac,  a  result  which,  but  a  few  weeks  before,  had  been  quite  unhoped 
for.  The  patient  remained  in  the  hospital  and  at  rest  for  another  month, 
making  a  period  of  three  months  after  the  operation,  and  left  the  hospital 
in  excellent  condition  with  no  sign  of  expansile  pulsation.  At  time  of  writing 
a  year  later,  he  is  still  in  excellent  condition  and  there  have  been  no  signs 
of  return  of  the  pulsation. 

In  striking  contrast  to  this  favorable  result  was  another  patient  whose 
aneurism  was  in  about  the  same  part  of  the  aorta  as  that  of  the  patient 
mentioned  above,  but  considerably  smaller  and  apparently  better  saccu- 
lated. He  was  wired  by  Dr.  Finney  a  few  months  later  than  this  patient, 
and,  as  in  the  preceding  case,  the  expansile  pulsation  completely  disappeared. 
The  patient  was  a  very  restless  man,  and  in  spite  of  advice  left  the  hospital 
within  a  couple  of  weeks  after  the  wiring,  promising  to  keep  quiet  at  home. 
The  quiet  was  only  relative.  A  few  weeks  later  he  went  to  a  baseball  game, 
at  which  he  was  carried  away  by  his  enthusiasm  and  became  much  excited. 
At  this  time  he  felt  something  giving  way,  the  pulsation  came  back,  and  he 
returned  to  the  hospital  within  forty-eight  hours.  He  was  wired  again, 
with  complete  cessation  of  expansile  pulsation,  but  again  remained  restless 
and  fretful.  The  pulsation  returned  once  more,  and  a  third  wiring  was  done 
at  his  request,  though  with  little  hope  of  recovery.  As  was  to  be  expected, 
this  failed  to  quell  the  tide,  and  he  died  within  two  months. 

This  second  patient  had  a  lesion  which  seemed  much  more  favorable 
for  wiring  than  the  first,  the  primary  result  was  better,  and  his  outlook  then 
seemed  far  more  favorable.    The  decisive  difference  lay  in  the  after-treatment. 


ANEURISM.  667 

The  first  patient  submitted  gracefully  to  a  long  stay  in  the  hospital,  allowed 
secondary  clotting  to  set  in  and  to  regain  the  ground  lost,  and  then  remained 
long  enough  to  permit  the  clot  to  become  solidly  fixed.  The  second  patient 
obtained  a  better  primary  result,  but  left  the  hospital  before  the  clot  was 
solidly  fixed,  submitted  it  to  a  strain  before  it  was  able  to  withstand  one, 
and  paid  the  penalty  with  his  life. 

The  excellent  results  which  can  sometimes  be  obtained  by  a  careful 
combination  of  both  preliminary  and  after-treatment  are  well  illustrated  by 
a  patient  treated  by  Drs.  C.  L.  Jones,  of  Jamestown,  and  C.  S.  Hamilton,  of 
Columbus,  Ohio,  to  whom  the  writer  is  indebted  for  the  following  data :  The 
patient  was  a  chef  48  years  old,  free  from  venereal  disease,  whose  aneurism 
appeared  within  a  few  days  after  he  had  been  thrown  from  a  street-car.  The 
tumor  was  most  marked  in  the  second  right  interspace  about  five  centimetres 
to  the  right  of  the  midline.  The  patient  was  put  upon  absolute  rest  and  Bal- 
four's modification  of  Tufnell's  diet  (250  c.c.  fluids  and  300  Gm.  solids  in 
twenty-four  hours),  and,  after  forty-three  days'  preliminary  treatment,  the 
aneurism  was  wired  in  the  usual  manner  by  Dr.  Hamilton.  Recovery  was 
uneventful  except  for  occasional  pains  relieved  by  morphine.  The  patient 
remained  in  the  hospital  for  three  weeks,  and  was  keep  at  rest  and  under 
continual  observation  for  four  months,  with  potassium  iodide,  light  diet, 
and  morphine  to  relieve  the  pains  which  he  occasionally  felt.  After  this 
period  he  led  an  active  life  and  died  from  some  unknown  cause  about  six 
years  later. 

The  excellent  result  obtained  in  this  case  seems  to  be  due  largely  to  the 
careful  treatment,  especially  the  preliminary  treatment.  The  after-treatment, 
though  adequate  in  this  case,  might  well  prove  too  short  in  many  others. 

As  can  be  seen  from  the  foregoing,  the  treatment  is  quite  as  important 
as  the  operation  itself.  In  justice  to  both  himself  and  the  patient,  the  sur- 
geon should  before  undertaking  the  case  insist  that  the  patient  consent  to 
remain  under  treatment  and  absolute  rest  for  from  three  to  five  months, 
at  least  a  month  of  which  should  precede  the  operation,  and  at  least  another 
month  should  elapse  after  the  last  trace  of  expansile  pulsation  has  been  felt 
in  the  tumor.  Only  threatened  rupture  of  the  aneurism  or  intolerable  symp- 
toms justify  an  operation  without  prolonged  preliminary  treatment. 

In  the  syphilitic  cases  potassium  iodide  and  inunctions  of  mercur}' 
should  be  given  freely  to  bring  about  as  far  as  possible  the  death  of  the  spiro- 
chetes in  the  arterial  wall  as  well  as  the  resolution  of  the  syphilitic  infiltra- 
tions about  the  vasa  vasorum  and  to  bring  the  walls  of  the  aneurism  and  the 
aorta  in  its  vicinity  into  the  best  possible  condition. 

Since  one  of  the  main  difficulties  encountered  in  the  operative  treatment 
of  aneurism  consists  of  the  lack  of  organization  of  the  thrombus  after  it  has 
once  formed,  it  is  possible  that  in  certain  cases  a  combination  of  MacEwan's 
method  with  the  Moore-Corradi  might  be  of  benefit;  that  is  to  say,  the  inner 
wall  of  the  aneurism  might  be  lightly  scratched  with  a  roughened  wire  before 
introducing  the  mass  of  wire  through  which  the  current  is  to  be  passed.  The 
removal  of  considerable  areas  of  intimal  endothelium  without  injuring  the 
other  layers  of  the  aneurismal  wall  would  enable  the  organization  of  the  clot 
to  go  on  at  a  much  greater  rate  than  is  possible  if  the  intima  remains  intact. 


668 


DISEASES  OF  THE  HEART  AND  AORTA. 


WIRE 


CLOT 


On  the  other  hand,  it  must  be  borne  in  mind  that  the  walls  of  many  aneurisms 
are  much  thinner  than  one  would  anticipate  from  external  examination  of 
the  tumor,  and  unless  the  greatest  care  were  taken  in  the  manipulation  great 
damage  to  the  sac  and  even  perforation  or  rupture  might  result.  Under  no 
circumstances  should  this  procedure  be  attempted  over  areas  where  second- 
ary bulgings  are  present  such  as  are  shown  in  contour  in  Fig.  302,  since  these 
indicate  a  weakening  of  the  wall  over  the  corresponding  area. 

Compression.  —  Aneurisms  of  the  peripheral  arteries,  and  especially 
of  the  abdominal  aorta,  are  sometimes  cured  by  compressing  that  vessel 
above  the  aneurism.    This  was  done  successfully  by  Murray  in  1864,  who 

obliterated  the  aneurism  and 
the  femoral  pulse  by  means  of 
a  tourniquet  wound  around 
the  body  above  the  tumor.  A 
number  of  similar  successful 
cases  have  been  reported  since 
Murray's,  especially  when  the 
aorta  is  compressed  with  the 
fingers.  The  operator  cannot 
continue  digital  compression 
longer  than  five  or  ten  min- 
utes at  a  time,  so  that  it  is 
often  the  custom  to  obtain 
the  assistance  of  a  whole 
class  of  medical  students 
working  in  relays.  In  this 
way  Shepherd  and  others  have 
been  able  to  keep  the  aorta 
occluded  for  twenty-four  hours,  and  have  brought  about  recovery. 

On  the  other  hand,  the  prolonged  pressure  may  bring  about  necrosis 
of  the  abdominal  wall,  intestine  and  pancreas,  or  secondary  peritonitis, 
and  intestinal  obstruction  may  result  (Bryant,  Lunn  and  Benham,  Moxon 
and  Durham) .  The  method  is  therefore  still  a  daring  one,  and  is  probably 
more  severe  and  less  certain  than  Halsted's  metal  band  method.  Moreover, 
Sibson  found  133  out  of  177  abdominal  aneurisms  (75  per  cent.)  above 
the  level  of  the  cceliac  axis  where  they  could  not  be  reached  by  pressure. 

Ligature  and  Partial  Occlusion. — Double  Ligature. — The  oldest  method 
of  treating  aneurisms  of  the  peripheral  arteries  is  to  ligate  them  above 
and  below  the  sac  (Antyllus)  (Fig.  315,  A),  after  opening  the  latter  to 
remove  the  blood.  A  more  modern  modification  of  this  method  is  that  of 
Hueter,  who  dissected  out  the  entire  sac  after  ligating,  thus  removing  a 
large  mass  of  tissue  which  would  otherwise  become  gangrenous. 

Proximal  Ligature. — Ambroise  Pare  (sixteenth  century)  departed  from 
the  procedure  of  Antyllus  by  merely  ligating  the  artery  close  above  the 
aneurism  (proximal  ligature — close  to  the  aneurism).  This  cut  off  the 
blood  supply  to  the  walls  of  the  latter  and  to  its  vicinity,  inducing  necrosis 
and  suppuration,  so  that  Anel  (1710),  Desault  (1785),  and  John  Hunter 
(1785)  were  led  to  adopt  the  proximal  ligature  at  a  considerable  distance 
above  the  aneurism  (ligature  of  brachial  for  aneurism  of  the  radial  artery; 


Fig.  316. —  Specimen  of  wired  abdominal  aneurism, 
showing  an  island  of  clot  within  the  coils  of  wire  sur- 
rounded by  a  free  blood-channel. 


ANEURISM.  669 

ligation  of  femoral  below  the  adductors  for  popliteal  aneurism;  ligation  of 
femoral  above  the  adductors — in  Scarpa's  triangle — for  popliteal  aneurism). 

Distal  Ligature. — In  the  eighteenth  century  Brasdor  and  later  Wardrop 
practised  ligation  of  the  artery  below  the  aneurism  (distal  ligature)  in 
cases  like  aneurism  of  the  innominate  in  which  the  proximal  ligature  was 
impossible.  As  a  result  of  the  procedure,  a  fusiform  aneurism  of  the  innomi- 
nate becomes  practically  a  sacculated  or  flask-shaped  aneurism  of  the  aorta, 
the  innominate  artery  being  converted  into  a  blind  sac  with  narrowed 
neck,  and  coagulation  is  thus  facilitated.  This  operation  is  still  the  one 
most  commonly  performed  for  aneurisms  of  the  innominate,  carotid,  and 
first  part  of  the  subclavian  artery.  Sheen  has  collected  statistics  of  36 
cases  of  innominate  and  subclavian  aneurism,  22  before  1880  with  1  recov- 
ery, 14  after  1880  with  8  recoveries,  7  after  1890  with  5  recoveries  and  5 
cures.  To  this  list  might  be  added  2  cases  of  Haltsed  and  1  of  Finney 
with  recovery  and  cure.  The  deaths  before  1880  were  usually  due  to  sepsis 
and  hemorrhage.  In  operating  upon  the  innominate  artery  it  is  most  im- 
portant that  both  the  carotid  and  subclavian  arteries  should  be  ligated, 
for  if  one  of  these  arteries  be  left  open  (as  in  the  case  of  J.  B.)  the  pressure 
in  the  sac  is  increased  without  stopping  the  blood-flow  through  it,  and  the 
growth  of  the  aneurism  is  actually  favored. 

Moore  in  his  first  paper  suggested  the  combination  of  this  form  of 
ligation  with  wiring  for  aneurisms  of  the  innominate.  This  double  proced- 
ure has  not  attracted  much  attention,  as  in  the  absence  of  sepsis  the  simple 
ligature  is  often  satisfactory,  but  it  is  no  doubt  applicable  in  a  certain 
number  of  cases  where  ligation  is  not  quite  adequate. 

The  chief  objection  to  the  simple  ligation  of  arteries 
lies  in  the  fact  that  the  permanent  results  are  often  unsatisfactory,  for 
either  the  ligature  may  be  so  tight  as  to  produce  necrosis  of  the  tissues 
under  it  and  thus  bring  on  rupture  of  the  artery,  or,  as  Halsted  has  shown, 
the  arterial  lumen  may  be  re-established  in  spite  of  the  ligature.  In  many 
of  Halsted's  experiments  upon  ligating  the  larger  arteries,  the  lumen  of  the 
artery  gradually  dilated  above  and  below  the  ligature,  so  that  the  latter 
was  left  surrounded  by  a  thin  membrane  or  septum  of  scar  tissue.  This 
septum  then  perforated  in  one  or  two  places. 

Occlusion  with  Metal  Bands.  —  To  obviate  this  and  for  other  reasons 
Halsted  has  devised  a  very  ingenious  procedure,  which  consists  in  the  occlu- 
sion of  the  vessel  by  surrounding  it  with  wide  metal  bands.  These  metal 
bands  take  the  place  of  the  ligature;  but  when  properly  applied,  do  not 
occlude  the  vasa  vasorum,  and  hence  permit  the  proper  nourishment  of  the 
arterial  wall.  Their  effect  is  more  certain  than  that  of  ligatures,  since  they 
do  not  allow  the  lumen  to  be  re-established.  The  chief  advantage,  how- 
ever, lies  in  the  ability  of  the  operator  to  obtain  a  partial  occlusion  of  the 
vessel  sufficient  to  reduce  pulsation  in  the  aneurism  to  any  desired  degree, 
without  obliterating  the  circulation  below  before  a  collateral  circulation 
has  been  established.  This  renders  it  the  operation  par  excellence  in  ab- 
dominal aneurisms  and  aneurisms  of  the  iliac  and  femoral  arteries,  in  which 
the  other  procedures  are  likely  to  be  dangerous. 

The  bands  are  made  of  No.  33  sheet  aluminum  of  a  width  varying  from  5  to  15  milli- 
metres according  to  diameter  of  the  artery  which  is  to  be  occluded.    The  strip  is  cut  a  little 


670  DISEASES   OF   THE   HEART   AND    AORTA. 

longer  than  the  circumference  of  the  artery  (as  shown  by  a  tape  passed  around  the  artery) . 
All  the  sharp  edges  must  be  carefully  filed  off  until  they  are  smooth  and  round,  lest  they 
cut  into  the  walls  of  the  artery.  The  strip  is  then  inserted  into  a  specially  devised  holder 
(Fig.  315,  E),  where  it  is  held  in  a  slot;  from  this  it  may  be  extruded  by  pressing  upon  the 
rammer  above;  and  as  it  is  extruded  below  it  is  curled  by  the  curve  at  the  foot  of  the  slot. 
The  faster  the  strip  is  extruded  the  more  tightly  it  is  curled.  The  curved  foot  of  the  holder 
is  placed  beneath  the  artery,  which  is  held  just  tightly  enough  against  the  instep  of  this 
foot  to  almost  occlude  the  lumen.  The  strip  is  extruded  by  pushing  the  rammer  just  fast 
enough  to  give  the  desired  curl.  Tension  on  the  artery  is  then  relaxed.  The  pulse  can  be 
felt  in  the  artery  below  the  band,  accompanied  by  a  well-defined  thrill.  The  band  is  then 
tightened  by  rolling  it  gently  under  the  fingers  of  one  hand  while  palpating  the  artery  below 
it  with  the  other.  The  degree  to  which  the  band  is  tightened  depends  upon  the  artery 
affected.  In  the  case  of  the  abdominal  or  descending  thoracic  aorta  it  should  be  rolled  until 
the  thrill  has  greatly  diminished  but  not  disappeared;  in  the  larger  branches  of  the  aorta 
the  pulse  may  be  made  to  disappear  absolutely.  In  a  few  minutes  a  regurgitant  pulse 
may  mark  the  appearance  of  a  collateral  circulation.  When  this  operation  is  performed 
successfully,  the  artery  becomes  gradually  occluded  at  the  point  of  constriction,  and  a 
rich  collateral  circulation  formed,  so  good  in  fact  that  in  one  case  in  which  Professor  Halsted 
had  occluded  the  descending  thoracic  aorta  Erlanger  found  the  blood-pressure  in  the  femoral 
(eight  months  afterward)  only  thirty  millimetres  below  that  in  the  brachial.  For  practical 
purposes  this  exactly  duplicates  the  conditions  in  the  adult  type  of  stenosis  of  the  isthmus 
of  the  aorta  (see  page  546).  except  that  the  anastomoses  take  place  later  and  hence  are 
not  quite  as  extensive. 

Professor  Halsted  has  now  operated  upon  a  number  of  cases  with  very- 
promising  results,  and  the  operation  gives  promise  that  in  the  hands  of  a 
surgeon  who  has  practised  the  technic,  it  may  completely  supersede  the 
methods  of  ligature  and  compression. 

Arteriorrhaphy  (Matas  Operation). — R.  Matas  in  1905  introduced  an 
entirely  new  technic  in  treating  the  aneurism  of  peripheral 
arteries  exactly  in  accordance  with  the  principles  of 
treating  inguinal  he  mi  a — by  obliteration  of  the  sac.  The  opera- 
tion is  performed  bloodlessly. 

The  limb  is  elevated,  an  Esmarch  rubber  bandage  put  on,  or  bleeding  from  the  main 
artery  prevented  by  compression  with  a  traction  loop,  adjustable  clamps  (Crile's),  padded 
forceps,  or  digital  compression.  A  free  incision  parallel  to  the  long  axis  of  the  sac  is  then 
made  down  to  the  sac  to  expose  its  whole  length.  Any  important  nerves  or  veins  should 
be  dissected  away  from  it.  The  sac  is  then  freely  opened  and  emptied. 
It  is  then  ready  for  closure.  In  most  cases  it  will  be  decided  to  obliterate  the  sac  completely, 
but  in  some  cases  of  fusiform  aneurism  it  may  be  preferable  to  leave  a  lumen  the  size  of 
the  original  artery. 

When  the  sac  is  to  be  completely  obliterated,  the  lining  of  the  sac 
is  thoroughly  scrubbed  over  its  whole  extent  with  sterile  gauze  soaked  with  salt  solution 
to  remove  the  endothelial  layer  of  the  intima,  and  thus  accelerate  union.  The  sutures 
(chromicized  gut)  are  then  applied  very  much  like  Lembert's  intestinal  sutures.  The 
most  important  point  is  to  approximate  carefully  intima  to  intima.  The  sutures 
are  laid  in  three  layers  in  such  a  way  that  the  cross-section  of  the  sac  after  suture  is  made 
to  form  a  Y;  the  first  and  deepest  layer  of  sutures  shutting  off  the  sac  from  the  artery  at 
the  Y,  and  the  third  layer  obliterating  the  cavities  in  each  arm  of  the  Y  (Fig.  315,  F). 

In  suturing  a  fusiform  aneurism  the  lumen  of  the  artery  is  preserved  by  placing  the 
first  layer  of  sutures  over  a  rubber  tube  which  is  inserted  into  the  artery.  After  the  new 
lumen  is  thus  provided  for,  the  rest  of  the  sac  is  scrubbed  and  the  sutures  laid  in  the  usual 
way.  Care  must  be  taken  to  preserve  the  blood  supply  and  nutrition  of  the  sac,  and  all 
portions  of  it  which  have  been  dissected  away  from  their  vascular  surroundings  should  be 
excised. 

In  1908  Matas  reported  the  results  of  86  such  operations,  including 
aneurisms  of  the  femoral,  the  iliofemoral,  tibial,  gluteal,  external  carotid, 


ANEURISM.  671 

axillary,  brachial,  and  subclavian  arteries,  as  well  as  the  abdominal  aorta 
(the  latter  both  fatal):  78  recoveries;  8  deaths;  4  cases  of  gangrene;  4  re- 
lapses, all  in  operations  where  the  lumen  was  restored.  In  view  of  the  fact 
that  these  86  operations  were  performed  by  fifty-two  different  operators 
the  excellent  results  obtained  are  a  striking  argument  in  favor  of  the  feasi- 
bility of  the  operation. 

Experimental  Surgery  of  the  Aorta. — Although  not  yet  available  for  practical  surgery, 
the  experiments  of  Alexis  Carrel  (Jour.  Exper.  Med.,  1912,  xv,  389;  1912,  xvi,  17)  upon  the 
permanent  intubation  of  the  aorta  are  extremely  promising  for  the  surgery  of  the  future. 
Carrel  has  been  able  actually  to  open  the  dog's  aorta,  insert  a  tube  of  glass  4.5  centimetres 
long,  suture  it  in  place  and  then  close  up  the  thorax  without  impairing  the  circulation  of 
the  animal.  Meltzer's  method  of  intratracheal  insufflation  was  used  upon  opening  the 
thorax  and  the  greatest  care  was  employed  to  prevent  bleeding  into  the  pleural  cavities, 
which  were  walled  off  from  the  surrounding  structures  by  pads  of  silk  soaked  in  petrolatum. 
An  ordinary  glass  tube  with  slightly  everted  edges  was  used,  and  tied  into  the  aorta  with 
heavy  silk  ligatures.  The  nine  animals  upon  which  he  has  performed  this  operation  lived 
for  periods  varying  from  several  days  to  more  than  three  months;  death  occurring  from 
ulceration  of  the  tube  through  the  wall  of  the  aorta  or  from  the  formation  of  a  thrombus 
at  the  site  pressed  upon  by  the  end  of  the  tube.  As  Carrel  states,  however,  "  It  is  probable 
that  the  use  of  a  tube  of  the  proper  calibre,  form  and  composition  would  be  followed  by 
better  results,"  and  it  is  far  from  impossible  that  with  such  improvements  in  technique, 
after  extensive  trials  upon  animals  with  diseased  as  well  as  with  healthy  aortas,  the  pro- 
cedure may  come  to  be  applicable  to  the  treatment  of  aneurisms  in  human  beings. 

BIBLIOGRAPHY. 

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More  complete  historical  accounts  are  given  by 

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1894,  i,  560;  and  Osier,  W.:  Aneurism,  Mod.  Med.,  Phila.  and  N.  Y.,  1908,  iv,  448;  also 

Gibson,  G.  A.:  Diseases  of  the  Heart  and  Aorta,  Edinb.  and  Lond.,  1898;  to  which  the 

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Fabris,  A. :  Experimented  Untersuchungen  ueber  die  Pathogenese  der  Aneurysmen,  Arch. 

f.  path.  Anat.,  u.  s.  w.,  Berl.,  1901,  clxv,  439. 
Ophiils,  W. :  Some  Notes  on  Arteriosclerosis  of  the  Aorta,  Am.  J.  M.  Sc,  Phila.  and  N.  York, 

1906,  cxxxi,  978. 


672  DISEASES  OF  THE  HEART  AND  AORTA. 

Hirsch,  J.  L.,  and  Robins,  M.  C:  A  Case  of  Aneurism  of  the  Aorta  of  Twenty-five  Years' 

Duration,  Maryland  M.  J.,  Baltimore,  1903,  xlvi,  93. 
Weinberger,  M. :  Ueber  die  Diagnostik  und  klinischen  Verlauf  der  mycotisch-embolischen 

Aneurysmen  und  Gefassrupturen,  sowie  der  Influenzaendokarditis,  Ztschr.  f.  klin. 

Med.,  Berl.,  1907,  xlii,  457. 
Libman,  E.:  Cases  of  Mycotic  Aneurisms,  Trans.  N.  Y.  Path.  Soc,  April,  1905;  and  Mt. 

Sinai  Hosp.  Rep.,  N.  Y.,  1905,  481.     A  Case  of  Embolic  Aneurisms,  Mt.  Sinai  Hosp. 

Rep.,  N.  Y,  1905,  488. 
McCrae,  J.:  A  Case  of  Multiple  Mycotic  Aneurysms  of  the  First  Part  of  the  Aorta,  J.  Path. 

and  Bacter.,  Edinb.  and  Lond.,  1905,  x,  373. 
Clarke,  T.  W.:  Repeated   Copious    Hsemoptoysis  from   an  Aortic  Aneurism  Extending 

into  the  Right  Lung  and  finally  Rupturing,  Bull.  Johns  Hopkins  Hosp.,  Bait.,  1905, 

xvi,  98. 
Arnold,  H.  D.:  Cause  of  Death  in  Aneurisms  of  the  Thoracic  Aorta  which  do  not  rupture; 

Report  of  five  cases,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y,  1902,  cxxiii,  72. 
Hare,  H.  A.,  and  Holder,  C.  A.:  Some  Facts  in  regard  to  Aneurism  of  the  Aorta,  ibid.,  1899, 

cxviii,  399. 
Broadbent,  W.  H.  and  J.  H.  F. :  Heart  Disease  and  Aneurysm  of  the  Aorta,  4th  edition, 

N.  Y.,  1906. 
Oliver,  W.  S.:  Physical  Diagnosis  of  Thoracic  Aneurism,  Lancet,  Lond.,  1878,  ii,  406. 
Sewall,  H.:  Some  Considerations  other  than  Aortic  Aneurism  which  determine  the  Occur- 
rence of  the  Tracheal  Tug,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1901,  cxxii,  150. 
Wenckebach,  K.  F.:  Ueber  pathologische  Beziehungen  zwischen  Athmung  und  Kreislauf 

beim  Menschen,  Samml.  klin.  Vortrage  begr.  v.  R.  Volkmann,  Leipz.,  1907,  N.  F.  Inn. 

Med.,  140-141. 
Smith,  H.  L.:  A  New  Sign  in  Thoracic  Aneurysm,  Am.  Med.,  Phila.,  1902,  hi,  814. 
Francois-Franck:  Recherches  cliniques  et  experimentales  sur   la   valeur  comparee  des 

signes  fournis  par  l'examen  du  pouls  radial  dans  les  aneurysmes  du  tronc  brachio- 

cephalique  de  l'aorta  et  de  l'artere  sous  claviere.     Importance  du  retard  du  pouls, 

J.  de  l'anatomie  et  de  la  physiol.  norm,  et  path,  de  l'homme  at  des  anim.,  Par.,  1878, 

xiv,  113.    Recherches  sur  la  diagnostic  du  siege  des  aneurismes  de  l'aorta,  ibid.,  1879, 

xv,  97. 
Marey,  E.  J. :  La  circulation  du  sang  a  l'etat  physiologique  et  dans  les  maladies,  Paris,  1881. 
V.  Ziemmsen,  A. :  Ueber  den  Pulsus  differens  und  seine  Bedeutung  bei  Erkrankungen  des 

Aortenbogens,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1890,  xlvi,  288. 
Baetjer,  F.  H. :  The  X-ray  Diagnosis  of  Thoracic  Aneurysms,  Bull.  Johns  Hopkins  Hosp., 

Bait.,  1906,  xvii,  24. 
Holzknecht,  G.:  Die  Rontgenologische  Diagnostik  der  Erkrankungen  der  Brusteingeweide, 

Fortschr.  a.  d.  Geb.  d.  Rontgenstr.,  Hamb.,  1901,  Erganzungsheft,  6. 
Milanoff :  Etude  de  la  douleur  et  de  quelques  autres  symptomes  des  aneurismes  de  l'aorte 

thoracique  descendente,  These,  Par.,  1900. 
Andreef :  Contribution  a  l'6tude  des  aneurismes  de  l'aorte  descendente,  These,  Toulouse,  1904. 
Osier,  W.:     Aneurism  of  the  Descending  Thoracic  Aorta,  Internat.  Clin.,  Phila.,  1903, 

xiii  ser.,  i,  1. 
Hewlett,  A.  W.,  and  Clark,  W.  R.  P.:  The  Symptoms  of  Descending  Thoracic  Aneurism, 

Am.  J.  M.  Sc,  Phila.  and  N.  Y.,  1909,  cxxxvii,  792. 
Bostroem:  Das  geheilte  Aneurysma  dissecans,  Deutsch.  Arch.  f.  klin.  Med.,  Leipz.,  1887, 

xlii,  1. 
Schede,  Fr.:  Zur  Aetiologie,  Verlauf,  und  Heilung  der  Aneurysma  dissecans  der  Aorta. 

Arch.  f.  path.  Anat.  u.  s.  w.,  Berl.,  1906,  cxcii,  52. 
MacCallum,  W.  G.:  Dissecting  Aneurism,  Bull.  Johns  Hopkins  Hosp.,  Bait.,  1909,  xx,  9. 
Henschen,  S.  E. :  Das  Aneurysma  Arteriae  pulmonalis,  Volkmann's  Samml.  klin.  Vortrage, 

Leipz.,  1906.  No.  422-423. 
Albertini  and  Valsalva.     Quoted  from  Gibson. 
Tufnell,  J.:  The  Successful  Treatment  of  Aneurism  by  Consolidation  of  the  Contents  of 

the  Sac,  Lond.,  1875.     The  Successful  Treatment  of  Aneurism  by  Position  and  Re- 
stricted Diet,  Trans.  Med.  Chir.  Soc.  Lond.,  1874,  lvii,  83. 
Taylor,  A.  E. :  The  Effects  upon  the  Blood  of  the  Tufnell  Method  and  the  Calcium  Salts 

in  the  Treatment  of  Aortic  Aneurism,  J.  Exp.  Med.,  N.  Y.,  iii. 


ANEURISM.  673 

Lancereaux  and  Paulesco:  Du  traitement  des  anevrismes  en  g6ne>al  et  de  1'anevrisme  de 
l'aorte  en  particulier  par  injections  sous-cutanees  d'une  solution  gelatineuse,  Bull, 
de  l'Acad.  de  MeU,  Par.,  1897. 

Futcher,  T.  B.:  The  Treatment  of  Aneurisms  by  Subcutaneous  Gelatin  Injections,  J.  Am. 
M.  Asso.,  Chicago,  1900,  204. 

Bouillaud:  Gaz.  des  hop.,  Par.,  1859,  61. 

Chuckerbutty:  Brit.  M.  J.,  Lond.,  1862,  ii,  61,  85.    Quoted  from  Balfour. 

Balfour,  G.  W.:  On  the  Treatment  of  Aneurism  by  Iodide  of  Potassium,  Edinb.  M.  J.,  1869, 
xiv,  33.  Further  Observations  on  the  Treatment  of  Aneurism  with  Iodide  of  Potas- 
sium, ibid.,  1870,  xv,  47. 

Moore,  C.  H.:  On  a  New  Method  of  Procuring  the  Consolidation  of  Fibrin  in  Certain  Incur- 
able Aneurisms,  Trans.  Med.  Chir.  Soc,  Lond.,  1864,  xlvii,  129. 

Murchison,  C:  Report  of  a  Case  of  Saccular  Aneurism  of  the  Ascending  Aorta  projecting 
through  the  Anterior  Wall  of  the  Left  Side  of  the  Chest,  ibid.,  136. 

P^trequin:  Suite  et  fin  du  memoire  concernant  une  nouvelle  m^thode  pour  gu£rir  certains 
aneurismes  sans  operation  a  l'aide  du  galvanopuncture,  Rec.  d.  trav.  Soc.  med.  d. 
Indre-et-Loire,  Tours,  1845,  117;  also  Compt.  rend,  de  l'Acad.  d.  Sc,  Paris,  1845, 
xxi,  992. 

Ciniselli,  L.:  Osservazione  di  aneurismi  dell'  aorta  trattati  coll  elettropuntura,  Gior.  d.  r. 
Accad.  di  med.  di  Torino,  1872,  35,  xii,  418;    Gazz.  Med.  di  Milano,  1847,  vi,  9. 

Hunner,  G.  L.:  Aneurism  of  the  Aorta  treated  by  Insertion  of  a  Permanent  Wire  and 
Galvanism  (Moore-Corradi  Method),  Bull.  Johns  Hopkins  Hosp.,  Bait.,  1900,  xi,  263. 

Rosenstirn,  J.:  The  Surgical  Treatment  of  a  Case  of  Aneurism  of  the  Arcus  Aortse,  with  a 
Case  cured  by  the  Loreta-Barwell  Method,  Am.  J.  M.  Sci.,  Phila.  and  N.  Y.,  1891,  ci,  55. 

Murray,  W. :  An  Account  of  a  Case  of  Aneurism  of  the  Abdominal  Aorta  which  was  cured 
by  Compression  of  that  Artery  immediately  above  the  Tumor,  Trans.  Med.  Chir.  Soc. 
Lond.,  1864,  xlvii,  187. 

Shepherd,  F.  J.:  Digital  Compression  for  Aneurism,  Montreal  M.  J.,  1903,  xxxii,  70. 

Bryant,  Lunn  and  Berham,  Skerritt,  Paget.  Quoted  from  Pringle,  J.  J. :  A  Case  of  Aneu- 
rism of  the  Abdominal  Aorta  treated  by  Laparotomy  and  the  Introduction  of  Steel 
Wire  into  the  Sac,  Trans.  Med.  Chir.  Soc.  Lond.,  1887,  lxx,  261. 

For  details  of  the  various  ligatures  see 

Lobker:  Aneurisma,  Eulenberg's  Realencycl.  d.  ges.  Heilk.,  Wien  und  Leipz.,  3d  ed.,  1894, 

i,  560,  or  Ref.  Handb.  Med.  Sc,  or  various  text-books  of  surgery. 
Sheen,  W. :  Results  of  Ligature  of  the  Innominate  Artery,  Ann.  Surg.,  Phila.,  1905,  xlii,  1. 
Halsted,  W.  S.:  Partial,  Progressive  and  Complete  Occlusion  of  the  Aorta  and  other  Large 

Arteries  in  the  Dog  by  Means  of  the  Metal  Band,  J.  Exp.  Med.,  N.  York,  1909,  xi,  373. 

The  Partial  Occlusion  of  Blood-vessels,   especially  of  the  Abdominal  Aorta,   Bull. 

Johns  Hopkins  Hosp.,  Bait.,  1905,  xvi,  346. 
Matas,  R.:  An  Operation  for  the  Radical  Cure  of  Aneurism  based  upon  Arteriorrhaphy, 

Ann.  Surg.,  Phila..  1903,  xxxvii,  1903.    J.  Am.  M.  Asso.,  Chicago,  1906.    Statistics 

of  Endoaneurismorrhaphy,  or  the  Radical  Cure  of  Aneurism  by  Intrasaccular  Suture, 

ibid.,  1908,  li,  1667. 


43 


PART  IV. 

i. 

THYROID  HEART. 

The  cardiac  disturbances  associated  with  thyroid  disease  were  the 
most  striking  features  observed  by  Parry  in  1815  in  the  first  described  cases 
of  exophthalmic  goitre.  His  first  case  died  of  heart  failure.  Graves  (1835), 
Basedow  (1848),  Stokes  (1854),  and  Trousseau  (1856)  were  also  impressed 
by  the  cardiac  features  of  this  disease.  Trousseau  found  them  especially 
important  in  the  "formes  frustes  "  or  "  atypical "  forms  to  which  he  called 
attention,  likening  such  cases  to  a  defaced  ("  fruste  ")  coin. 

The  important  role  which  these  "formes  frustes"  of  Basedow's1 
disease  play  in  many  cases  of  so-called  cardiac  neurasthenia  and  hysteria 
has,  since  Trousseau,  been  recognized  with  increasing  frequency,  and  espe- 
cially since  Friedrich  Kraus  in  1899  called  attention  to  them  by  introducing 
the  term  "Kropfherz"  ("goitre  heart"  or  thyroid  heart),  which  is  now 
widely  used  in  Germany. 

FORMS    OF    CARDIAC    DISTURBANCE    DUE    TO    THYROID    DISEASE. 

Strictly  speaking,  as  shown  by  Rose,  Schranz,  and  Minnich,  there  is 
some  cardiac  disturbance  with  all  forms  of  goitre.  Four  main  forms  of 
cardiac  disturbance  may  thus  be  distinguished,  due  to: 

I.  Pressure  of  the  goitre  upon  the  trachea,  bronchi,  veins,  chest, 
and  sympathetic  ganglia  (in  simple  goitre) ,  pneumo-mechanical 
goitre  heart  (Rose) . 
II.  Hypothyroidism  (in  myxcedema,  cretinism,  and  achondroplasia) . 

III.  Hyperthyroidism  (exophthalmic  goitre  and  formes  frustes). 

IV.  Goitre  secondary  to  the  cardiac  disease  (goitre  cardiaque,  "  car- 

diac goitre"). 

CARDIAC   DISTURBANCES   FROM   PRESSURE   OF   THE   THYROID. 

Potain  in  1863  and  Rose  in  1878  reported  cases  of  heart  failure  and 
more  or  less  sudden  death  in  cases  in  which  large  colloid  goitres  pressed 
upon  the  veins  and  trachea.    Such  a  goitre  has  several  mechanical  effects: 

1.  It  may  prevent  adequate  filling  of  the  lungs  and  thus 
produce  emphysema,  deficient  aeration  of  the  blood,  and  later  asphyxia. 
The  chronically  deficient  aeration  of  the  blood  may  lead  to  secondary  car- 
diac overstrain  and  finally  to  myocardial  weakness.  This  will  be  enhanced 
by  all  pulmonary  infections. 

1  Basedow  ("Bas-e-do").    Dock  after  a  careful  study  of  priorities  advises  the  accept- 
ance of  this  name,  which  was  the  first  unobjectionable  term  given  and  is  the  one  most  widely 
accepted. 
674 


THYROID   HEART.  675 

2.  The  goitre  often  presses  on  the  sympathetic  ganglia  on 
one  or  both  sides  of  the  neck,  thus  stimulating  the  accelerators  and  bringing 
on  a  chronic  tachycardia  just  as  is  produced  in  Basedow's  disease.  Muller's 
muscle  in  the  orbit  may  also  be  stimulated  and  exophthalmos  produced. 
This  exophthalmos  is  often  unilateral.  The  condition  of  exoph- 
thalmos and  tachycardia  from  the  pressure  of  a  simple 
goitre   is  known  as  pseud  o-Basedow's   disease.1 

Case  of  Simple  Goitre  Resembling  Basedow's  Disease. 

Such  a  case  is  represented  by  that  reported  by  Potain  in  1863 :2  M.  K.,  servant  girl, 
aged  50.  Complains  of  palpitation,  feeling  of  pressure  in  chest,  attacks  of  suffocation, 
irregular  menstruation.  She  has  had  goitre  all  her  life,  unaffected  by  iodine  treatment. 
For  some  years  her  eyes  have  been  larger  than  before.  She  has  lost  weight,  has  suffered 
from  dyspnoea  especially  on  exertion,  she  has  throbbing  of  the  goitre,  and  her  legs  are 
swollen.  Her  pulse  is  152,  irregular.  Apex  is  in  the  sixth  interspace  13  cm.  from  midline. 
There  is  heaving  of  the  entire  precordium.  At  the  apex  and  over  the  precordium  there  is 
a  meso-systolic  murmur.  The  veins  of  the  neck  are  dilated.  There  is  a  large  goitre  which 
does  not  pulsate  and  no  murmur  is  heard  over  it.  Digitalis  is  without  effect, 
and  the  patient  died  from  pulmonary  oedema  1 1  days  after  admission. 

Autopsy  showed  colloid  cystic  goitre  with  some  hemorrhages  from  stasis,  slight 
infarction  of  the  lungs,  and  a  somewhat  enlarged,  very  flabby  heart. 

The  livor,  orthopnoea,  asphyxia,  and  sudden  death,  as  in  Rose's  case, 
are  due  to  pressure  upon  the  air-passages,  and  are  to  be  regarded  as  cardiac 
symptoms.  The  respiratory  origin  of  this  suffocation  is  seen  in  the  very 
marked  inspiratory  (not  systolic)  retraction  of  all  the  thoracic  interspaces. 


CARDIAC   AFFECTIONS    OF    HYPOTHYROIDISM    (CARDIOPATHIA 
THYREOPRIVEA)    (KRAUS). 

In  all  the  conditions  in  which  there  is  atrophy  of  the  glandular  tissue 
of  the  thyroid  and  diminution  in  the  internal  secretion  of  the  gland,  there 
are  symptoms  of  cardiac  weakness.  The  patients  get  out  of  breath  on  very- 
slight  exertion.  The  pulse  is  small  and  weak,  but  may  be  either  slow  or 
slightly  accelerated  (Kraus).  This  is  due  to  the  fact  that  the  physiological 
vagus  tone  is  largely  due  to  the  thyroid  secretion  (v.  Cyon),  and  when  it 
is  deficient  there  is  an  overstimulation  of  the  accelerators.  However,  as 
Kraus  points  out,  the  cardiac  features  in  cachexia  thyreoprivea  are  not 
prominent  features  of  the  disease,  and  hence  are  of  little  importance  in 
connection  with  diseases  of  the  heart. 

Revilliod  has,  however,  called  attention  to  another  effect  of  hypo- 
thyroidism upon  the  circulation,  namely,  early  arteriosclerosis  with  cal- 
careous deposits.  This  effect  has  also  been  produced  by  v.  Eiselsberg  in 
new-born  lambs  from  which  he  removed  the  thyroid  glands.  In  contrast 
to  other  experimental  arteriosclerosis,  the  arterial  changes  affected  the 
intima  and  not  the  media. 

1  In  some  cases,  however,  this  is  not  due  to  pressure  on  the  sympathetic  but  to  the 
activation  of  thyreoglobulin  by  the  iodine  treatment.  Occasionally,  moreover,  a  goitre 
shows  in  one  part  colloid  degeneration,  in  another  hyperplasia  like  that  of  Basedow's  disease. 

2  Bull,  de  la  Soc.  d'Anat.  de  Paris,  1863,  p.  87,  quoted  from  Minnich. 


676 


DISEASES  OF  THE  HEART  AND  AORTA. 


DISTURBANCES  DUE  TO  HYPERTHYROIDISM. 

Basedow's  Disease   (also  "Formes  frustes,"  and  Accidental  Hyperthyroidism 
in  the  Treatment  of  Obesity). 

As  stated  above,  these  conditions  present  the  most  important  cardiac 
features  which  are  due  to  disturbed  thyroid  metabolism. 

PATHOLOGY,    PATHOGENESIS,    AND    PATHOLOGICAL   PHYSIOLOGY. 

The  veil  of  mystery  has  been  lifted  from  diseases  of  the  thyroid  by  the 
hands  of  the  physiological  chemists.  The  surgeons  Astley  Cooper,  Reverdin,  and 
Kocher  had  found  that  extirpation  of  the  thyroid  for  goitre  led  to  myxoedema, 
and  Pisenti  Gley  and  Vassale  had  demonstrated  that  these  symptoms  could  be 
prevented  by  feeding  the  dried  thyroid  substance.  But  the  accurate  knowledge 
dates  from  the  studies  of  Baumann  and  his  pupils,  Roos  and  Oswald. 

But    the    real    understanding    of 
pathological    thyroid   function    dates 
from  the  chemical  studies  of  Baumann 
and  his  pupils,  Roos  and  Oswald,  and 
from  the  recent  studies  of  E.  C.  Kendall. 
Baumann  showed  that  the  active 
principle  of  the  gland  was  an  iodine- 
containing  substance  from  which  he 
was   able   to   split  off  by  hydrolysis 
with  H2SO4  a  substance  of  relatively 
simple  molecular  structure  containing 
the  iodin,  which  he  termed  iodothyrin. 
His  pupil  Oswald   believed  that  the 
physiologically  active  substance  was 
an   iodine-containing   globulin    (iodo- 
thyroglobulin).    He  thought  that  the 
colloid  of  the  thyroid  represented  the 
uniodized  form  of  the  same  protein 
(thyroglobulin),  and  that  this  thyro- 
globulin  could  not  be  absorbed  into 
the  blood  until  it  took  up  iodin,  where- 
upon it  would  be  absorbed  and  amide  from  the  lumen  of  the  acini  would  betaken 
up  by  the  blood  and  would  exert  all  the  physiological  activity  of  the  thyroid. 
Kendall,  however,  has  recently  isolated  what  is  undoubtedly  the  physi- 
o'ogically  active  principle  of  the  thyroid  in  pure  crystalline  form. 

He  obtains  this  substance  by  hydrolyzing  the  thyroid  proteins  in  ethyl 
alcohol  containing  one  per  cent,  sodium  hydroxide.  The  substance  forms 
sheaves  of  needle-like  crystals  which  melt  at  about  220°  C,  and  are  soluble  in 
strong  alkalies  and  ammonia  but  insoluble  in  acids,  water,  alcohol,  ether  and 
sodium  carbonate.  It  contains  60  per  cent,  of  iodin  and  analysis  shows  that 
each  molecule  contains  one  indol  nucleus,  iodin  groups  and  one  amino  nitro- 
gen (di-iodo  indol?).  The  reactions  with  carbonic  acid  suggest  a  combination 
yielding  also  a  more  or  less  unstable  COOH  group  entering  into  the  molecule. 
Kendall  has  tested  this  substance  both  experimentally  and  chemically, 
and  has  found  that  prolonged  injections  into  animals  cause  tachycardia, 
changes  in  the  electrocardiogram  and  signs  of  overaction  of  the  heart  as  well 
as  tremor,  emaciation  and  diarrhoea. 


Fig.  317. — Photograph  of  a  patient  with 
Basedow's  disease.  (Kindness  of  Prof.  Blood- 
good.) 


THYROID  HEART.  677 

On  the  other  hand,  injections  into  myxcedematous  children  caused  dis- 
appearance of  the  myxcedema  and  other  signs  of  thyroid  deficiency  and  led 
to  return  of  the  child  to  take  on  a  normal  growth,  appearance,  and  mentality. 
The  skin  and  hair  also  return  to  normal.  This  substance,  therefore,  possesses 
all  the  characteristics  of  the  thyroid  extract  itself.  Other  fractions  derived 
from  thyroid  substance  are  devoid  of  these  activities.  He  finds  the  substance 
present  and  possessed  of  the  same  characteristics  when  extracted  from  por- 
tions of  glands  removed  from  patients  with  Basedow's  disease,  and  therefore 
fails  to  find  evidence  of  any  alteration  of  the  thyroid  secretion  (dysthyreosis) 
in  this  condition,  as  some  investigators  have  claimed. 


Fig.  318. — Photograph  of  a  portion  of  the  thyroid  gland  removed  from  the  patient  shown  in  Fig.  317. 

(Kindness  of  Prof.  Bloodgood.) 

Pathological  Anatomy. — The  typical  thyroid  of  advanced  Basedow's 
disease  is  characterized  by  hyperplasia  of  the  epithelial  cells  lining  the  acini, 
so  that  the  cells  of  the  single  layer  of  epithelial  cells  multiply  into  irregular 
papillary  masses  several  layers  thick  and  protrude  into  the  lumen,  which  they 
may  completely  fill  or  may  leave  it  partially  filled  with  colloid. 

A  similar  hyperplasia  may  take  place  when  part  of  the  gland  has  been 
removed  (Halsted,  Marine),  though  this  may  be  produced  by  a  response  to 
slight  infection  or  to  the  stimuli  of  abnormal  cellular  environment. 

Marine  and  Williams  and  L.  B.  Wilson  have  noted  that  in  the  cases  with 
the  most  severe  symptoms  the  hyperplasia  of  the  gland  is  most  intense  and 
the  acini  filled  with  colloid  have  been  replaced  by  acini  filled  with  hyper- 
plastic cellular  masses.  For  purposes  of  correlation  with  the  clinical  findings 
Wilson  has  adopted  a  classification  of  thyroid  gland  obtained  at  operation 
based  upon  the  amount  of  hyperplasia  and  upon  the  ratios  between  hyper- 
plastic and  colloid  containing  acini. 

Wilson's  classification  is  based  upon  the  following  characteristics: 

(1)  Degree  of  intra-alveolar  proliferation  (intra-alveolar  prohyper- 
plasia)  leading  to  the  formation  of  several  layers  of  cells. 

(2)  Presence  of  a  varying  amount  of  non-staining  secretion.  (This  is 
one  of  the  principal  concomitants  of  intoxication  from  thyroid  secretion.) 

(3)  Exfoliation  of  cells.  (This  corresponds  to  a  chronic  process  with 
retrogression  of  symptoms.)  The  stainable  secretion  plays  little  role  in  the 
genesis  of  symptoms. 

(4)  Increase  in  the  number  of  the  alveoli,  and  formation  of  young  alveoli 


678  DISEASES  OF  THE  HEART  AND  AORTA. 

(adenoma  formation).  (The  clinical  condition  of  adenoma  patients  is  parallel 
to  that  of  other  goitres  and  depends  largely  upon  the  amount  of  non-stain- 
ing secretion  that  is  present.) 

Wilson  divides  his  cases  into  several  groups: 

I.  Increased  intra-alveolar  tissue. 

A.  Hard  nodular  gland,  dry  surface,  alveoli  small  (0.06  to  0.2  mm.)  but 
contains  some  proliferation  into  certain  alveoli  with  the  formation  of  several 
layers  of  cells  within  the  alveoli.  Small  amount  of  thin,  non-staining  secre- 
tion in  the  alveoli;  symptoms  mild. 

B.  Hard  granular  cut  surface  with  glairy  secretion;  large  amount  of  thin 
non-staining  secretion  in  alveoli ;  large  amount  of  intra-alveolar  epithelial  pro- 
liferation.   Severe  nervous  symptoms  and  circulatory  weakness. 

C.  Granular  glairy  surface  with  some  gelatinous  areas.  Numerous  pap- 
illary projections  into  the  lumina  of  the  acini,  but  some  exfoliation  of  cells. 
Large  amount  of  non-staining  secretion  and  some  stainable  secretion  within 
the  acini.    Severe  clinical  symptoms  regressing. 

D.  Large  hard  nodular  gland  cut  surface  gelatinous,  very  large  alveoli 
(0.6  to  1.0  mm.).  Numerous  intra-alveolar  papillae  but  much  exfoliation. 
Symptoms  of  hyperthyroidism  which  are  not  as  severe  as  they  have  been. 

II .  Increase  in  number  of  alveoli  with  presence  of  young  alveoli  (adenoma) . 

E.  Hard  nodular  gland  with  small  cysts.  Small  alveoli  recently  formed 
(adenoma),. with  small  amount  of  thin  non-staining  secretion.  Symptoms  mild. 

F.  Soft  collapsing  gland,  increased  number  of  alveoli,  containing  a  large 
amount  of  thin,  non-staining  secretion.  Nervous  and  circulatory  symptoms 
severe. 

G.  Gelatinous  surface  with  large  alveoli  containing  stainable  secretion, 
some  exfoliation  of  the  parenchymal  cells.    Mild  symptoms  continuous. 

H.  Cut  surface  of  gland  gelatinous  and  filled  with  cysts.  Alveoli  large 
(0.2  to  0.5  mm.)  and  of  adenomatous  type.  Marked  exfoliation.  Large 
amount  of  well-stained  secretion.     Symptoms  mild  or  of  moderate  grade. 

In  accordance  with  Wilson's  classification  Henry  Plummer  has  found 
that  of  the  patients  who  come  to  operation  for  symptoms  of  hyperthyroidism 
("thyrotoxicosis")  approximately  32  per  cent,  have  hyperplastic  glands  and 
68  per  cent,  non-hyperplastic.  Of  the  patients  having  hyperplastic  goitre 
99.2  per  cent,  have  toxic  symptoms;  of  those  having  non-hyperplastic  goitre 
from  20  to  32  per  cent,  are  toxic.  In  the  hyperplastic  cases  the  symptoms 
develop  rapidly  and  more  than  half  the  cases  of  this  type  seen  at  the  Mayo 
Clinic  come  for  operative  relief  within  the  first  year  after  the  onset  of  symp- 
toms in  which  the  nervous  system  is  chiefly  involved.  On  the  other  hand,  in 
non-hyperplastic  cases,  the  toxic  symptoms  develop  usually  after  an  average 
lapse  of  fourteen  years,  and  cardiac  damage  dominates  the  clinical  picture. 

Plummer  has  found  that  in  the  cases  of  hyperplastic  goitre  which  are 
characterized  by  severe  symptoms  the  maximal  blood-pressure  is  decidedly 
elevated,  rising  progressively  from  an  average  of  138  to  139  mm.  Hg  in  pa- 
tients from  10  to  25  years  to  155  mm.  in  patients  from  35  to  40;  whereas  in 
the  patients  with  non-hyperplastic  goitre,  the  blood-pressure  ranges  from  118 
to  124  mm.  between  10  and  25,  135  mm.  from  35  to  45.  After  40  to  45  it 
ranges  from  145  to  155  and  is  about  the  same  in  both  classes  of  cases.  The 
minimal  (diastolic)  pressure  averages  75  to  85  in  the  non-hyperplastic  cases, 


THYROID  HEART. 


679 


70  to  78  in  the  hyperplastic  so  that  in  the  latter  the  pulse  pressure  is  always 
definitely  increased.  Plummer  believes  that  the  height  of  the  systolic  pres- 
sure is  somewhat  indicative  of  the  degree  of  intoxication. 

PHYSIOLOGICAL    EFFECTS    OF   THYROID   SECRETION. 

The  effects  of  excess  of  thyroid  secretion  in  the  blood  are : 
1.  An    increase   in    metabolism,    especially  in  the  oxidation 
processes  and  the  breaking  down  of  proteids  in  the  tissues  and  bone,  giving 


Fig.  319. — Drawing  of  a  histological  specimen  from  the  same  thyroid.  The  histological  picture 
of  advanced  thyroid  hypertrophy  observed  in  cases  of  Graves's  disease  in  which  the  symptoms  are  most 
marked.  (Bloodgood,  Surg.,  Gyn.  aad  Obstcs.,  August,  1905,  vol.  i,  p.  113.)  This  drawing  was  made  in 
June,  1903. 

rise  to  an  increase  in  N  and  P2O5  (Fr.  Miiller)  excreted  and  in  the  gas  metab- 
olism (Magnus-Levy).  In  man  this  finds  its  concrete  expression  in  the  loss 
of  weight,  due  especially  to  loss  of  muscle  substance  (Baumann  and  Roos). 
2.  There  is  a  general  stimulation  of  the  peripheral 
nerves  both  medullated  and  sympathetic.  V.  Cyon,  Roos,  Oswald  and 
Kraus,  and  Friedenthal  have  shown  that  these  substances  have  several 
distinct  actions  on  the  circulation. 

A.  They  stimulate  the  depressor  or  afferent  nerves  from  the  heart,  giving  rise  on  the 
one  hand  to  the  cardiac  sensations,  palpitation,  and  anginal  pains,  and  on  the  other  hand 
to  the  vasodilation  and  low  diastolic  blood-pressure  which  are  often  observed  in  these  cases. 

B.  They  stimulate  both  the  vagi  and  the  accelerator  nerves.1  The  action  upon  the 
accelerators  predominates,  however,  and  tachycardia  is  thus  produced.  The  vagus  still 
remains  irritable,  however,  and  the  heart  can  be  slowed  by  pressure  on  it.     The  same 

1  In  most  of  these  effects  this  sympathicotonic  predominates,  as  shown  by  Eppinger, 
Falta,  and  their  collaborators  (see  page  19). 


680  DISEASES  OF  THE  HEART  AND  AORTA. 

stimulation  of  the  other  fibres  of  the  cervical  sympathetic  gives  rise  to  the  peculiar  ocular 
signs  of  Basedow's  disease. 

C.  Cleghorn  has  shown  that  thyroid  extract  has  a  direct  action  on  the  cardiac  muscle, 
increasing  the  size  and  force  of  the  contraction,  which  manifests  itself  in  the  increased 
pulse-pressure,  increased  maximal  pressure,  and  cardiac  hypertrophy. 

Biochemical  Evidences  of  Hyperthyroidism. — Falta  and  Zuelzer,  Kraus,  and  Frieden- 
thal  have  shown  that  thyroid  extract  directly  antagonizes  adrenalin  in  its  pupillo-dilator 
action  on  the  frog's  eye,  and  that  this  can  be  used  as  a  test  for  hyper- 
thyroidism  in    clinical    cases. 

Another  important  biochemical  blood  test  for  hyperthyroidism  is  that  of  Reid  Hunt, 
who  has  shown  that  the  blood  of  such  patients  increases  the  resistance  of  mice  to  poisoning 
with  acetonitrile  and  morphine,  so  that  the  lethal  dose  is  thus  doubled. 

All  these  investigations  have  proved  without  doubt  that  in  Basedow's  disease  there 
is  an  excess  of  thyroid  secretion  into  the  blood  (as  claimed  by 
Mobius),  and  that  the  secretion  is  indistinguishable  from  that  of  the  normal  thyroid, 
representing  a  condition  of  hyperthyreosis  (increased  secretion)  rather  than  of 
dysthyreosis  (altered  secretion).  Whether  they  will  be  of  practical  value  in  the 
diagnosis  of  the  puzzling  "formes  frustes"  remains  still  to  be  determined,  since  the  excess 
of  thyreoglobin  in  the  blood  of  these  cases  may  be  too  small  for  chemical  recognition. 

It  is  possible  that  this  anti-adrenalin  action  may  be  responsible  for  the 
brownish  pigmentation  (Jellinek's  sign)  which  occurs  in  many  cases  of  hyper- 
thyroidism, especially  about  the  eyelids.  This  pigmentation  somewhat  resem- 
bles the  pigmentation  of  Addison's  disease  (lack  of  adrenalin  secretion).  Kraus 
and  Friedenthal  have  also  found  that  this  antagonistic  action  upon  the  frog's 
pupil  is  valuable  in  diagnosis,  since  it  is  given  by  the  blood  of  patients  with  Base- 
dow's disease,  but  not  by  the  blood  of  neurasthenics  and  hysterical  patients.1 

V.  Cyon  has  shown  the  very  important  fact  that  injection  of 
thyroid  extract  or  iodothyrin  causes  an  increased  blood 
flow  through  the  thyroid  gland,  probably  thus  acting  as  a 
hormone  to  increase  its  own  secretion  and  to  introduce  a  vicious  circle: 

Hyperthyroidism 

(Basedow's  disease) 

t  I 

Increased  thyroid  Increased  blood  flow 

secretion  •*—  through  thyroid 

It  is  this  increased  dilatation  of  the  arteries  which  gives  rise  to  the 
murmurs  over  the  thyroid  in  Basedow's  disease  (Guttmann). 

ETIOLOGICAL   FACTORS. 

Basedow's  disease  is  more  common  in  women  than  in  men  (805  women, 
175  men  in  Buschan's  980  cases) ;  60  per  cent,  occur  in  the  fourth  decade  of 
life  (Buschan).  In  Passler's  58  cases  there  were  4  under  15  years,  29  at  from 
15  to  25  years,  18  at  25  to  45  years,  7  over  45  years. 

Basedow's  disease  is  very  widespread,  but  is  somewhat  more  rare  in 
regions  where  simple  goitre  is  common  than  elsewhere, 
perhaps  owing  to  the  lesser  intake  of  iodine.  Heredity  plays  some  role;  mental 
and  nervous  disease,  diabetes,  and  tuberculosis  are  often  found  in  the  same 
family.  In  one  famous  family  reported  by  Osterreicher  eight  out  of  ten 
children  of  a  hysterical  woman  had  Basedow's  disease,  and  one  of  these 
daughters  had  three  children  with  the  same  illness. 

1  It  seems  doubtful  whether  the  blood  of  cases  with  mild  formes  frustes  contains 
enough  excess  of  thyreoglobulin  to  give  this  test  a  hard-and-fast  diagnostic  significance. 


THYROID  HEART.  681 

The  following  list  gives  the  predisposing  factors  in  the  series  of  A.  Kocher 
and  of  Landstrom:  „ 

Cases 

Gradual  onset  with  etiological  factors  unknown 28 

Pregnancy 10 

Chlorosis 7 

At  first  menstruation 6 

After  fright,  shock,  or  grief 5 

After  fatigue 8 

Infectious  diseases  (influenza  alone,  7) 13 

Old  simple  goitre 5 

Sojourn  at  high  altitude 2 

Heredity 1 

Appendicitis 1 

Total W 

It  will  be  seen  that  infectious  diseases  and  especially  influenza  constitute 
the  most  common  cause.    De  Quervain  has  found  a  subacute  thyroiditis  quite 
common  in  these  conditions,  especially  in  influenza,  typhoid  fever,  rheumatism 
(as-  in  Parry's  first  case) ,  and  diphtheria,  and  this  thyroiditis  was  followed  by 
Basedow's  disease  within  a  few  months  in  about  20  per  cent,  of  the  cases. 
Boggs  and  Sladen  have  found  mild  thyroiditis  present  in  most  of  the  cases  of 
typhoid  fever  in  which  the  pulse  is  over  120  at  the  height  of  the  fever.    Tonsil- 
litis may  also  be  a  forerunner;  and  Engel-Reimers  has  found  acute  thyroiditis 
in  secondary  lues  leading  to  Basedow's  disease.    After  pregnancy  the  hyper- 
thyroidism which  is  normally  present  in  that  condition  may  increase  and  lead 
directly  into  Basedow's  disease.    The  coexistence  of  puerperal  infec- 
tion,   mastitis,    fright,    grief,    or    shock  undoubtedly  pre- 
disposes to  the  disease,  as  in  the  case  of  a  girl  under  Friedrich  Miiller's  care, 
whose  symptoms  began  when  she  was  suddenly  deserted  by  her  lover  just  after 
the  birth  of  an  illegitimate  child.  In  one  of  v.  Graefe's  cases  the  symptoms  set 
in  within  a  few  days  following  a  night  of   sexual    excesses.     These 
factors  may  act  by  producing  a  reflex  dilatation  of  the  vessels  in  the  thyroid. 
Thus,  Trousseau  writes  of  a  woman  of  53  who  suffered  deep  grief  from  the 
death  of  her  father.    ''One  night,  after  she  had  been  crying  for  a  long  time,  she 
suddenly  felt  her  eyes  swell  and  lift  up  her  lids,  her  thyroid  gland  increase 
notably  in  size  and  throb  in  an  unusual  manner;  she  had  at  the  same  time 
violent  palpitation  of  the  heart.  "  The  writer  on  one  occasion  had  the  oppor- 
tunity to  observe  a  case  of  acute  enlargement  of  the  thyroid  in  a  man  of  thirty, 
associated  with  tremor,  tachycardia,  palpitation,  slight  v.  Stellweg's  but  no 
other  ocular  sign.     The  disturbance  followed  the  ingestion  of  two  cups  of 
strong  coffee  at  a  time  of  great  worry  and  was  complicated  by  a  mild  attack 
of  "grippe."    The  enlargement  of  the  thyroid  was  sufficient  to  prevent  button- 
ing the  collar.    It  subsided  entirely  after  24  hours,  and  with  it  the  symptoms 
of  hyperthyroidism.    It  is  probable  that  the  grippe  (influenza  or  streptococcus 
infection)  rendered  the  thyroid  particularly  sensitive. 

SYMPTOMS. 

The  classical  pathognomonic  symptoms  of  exophthalmos  are  the  well- 
known  triad  of  struma,  tachycardia,  and  exophthalmos,  or 
the  tetrad  of  struma,  tachycardia,  exophthalmos, 
and  tremor. 

These  are  well  described  by  Parry  (1815)  in  his  first  case,  a  married  woman,  aged  37, 
who  had  ' '  caught  cold  in  lying  in,  and  for  a  month  suffered  under  a  very  acute  rheumatic 
fever.    Subsequently  she  became  subject  to  more  or  less  palpitation  of  the  heart 


682  DISEASES  OF  THE  HEART  AND  AORTA. 

very  much  augmented  by  bodily  exercise,  and  gradually  increasing  in  force  and  frequency 
till  my  attendance,  when  it  was  so  violent  that  each  systole  shook  the  whole  thorax.  Her 
pulse  was  196  in  a  minute,  very  full  and  hard,  alike  in  both  wrists,  irregular 
as  to  strength,  and  intermitting  at  least  once  in  six  beats.  .  .  .  Twice  or  thrice  she  had 
been  seized  in  the  night  with  asense  of  constriction  and  difficulty  in  breathing, 
which  was  attended  with  spitting  of  a  small  quantity  of  blood.  She  described  herself  also 
as  having  frequent  and  violent  stitches  of  pain  about  the  lower  part  of  the 
sternum.  .  .  .  About  three  months  after  lying  in,  while  she  was  suckling  her  child,  a 
lump  about  the  size  of  a  walnut  was  perceived  on  the  right  side  of  her  neck.  This 
continued  to  enlarge  till  the  period  of  my  attendance,  when  it  occupied  both  sides  of  her 
neck  so  as  to  have  reached  an  uncommon  size,  projecting  forward  before  the  lower  angle 
of  the  jaw.  The  part  swelled  was  the  thyroid  gland.  The  carotid  arteries  on 
both  sides  were  greatly  distended,  the  eyes  were  protruded  from 
their  sockets,  and  the  countenance  exhibited  an  expression  of  agitation 
and  distress,  especially  on  any  muscular  exertion,  which  I  have  rarely  seen  equalled.  .  .  . 
Bowels  were  usually  lax.  .  .  .  For  a  week  she  has  had  cedematous  swelling  of 
her  legs  and  thighs."     (The  patient  died  with  symptoms  of  heart  failure.) 

Besides  the  pathognomonic  triad,  increased  nervous  excitability,  tremor, 
loss  of  weight,  and  pigmentation  of  the  skin,  especially  about  the  eyelids,  are 
important  accessory  symptoms. 

The  chief  symptoms  of  Basedow's  disease  may  be  grouped  in  the  following 
categories,  and  arrangedinwhatisapproximatelytheorderof  increasing  severity. 

Cardiac  Phenomena. — Palpitation,  continuous  slight  elevation  of  pulse- 
rate,  with  occasional  attacks  of  intense  tachycardia  brought  on  by 
emotion,  excitement,  or  exercise,  or  occasionally  on  awakening;  vis- 
ible pulsation  and  dilatation  of  carotid  arteries;  pulse  collapsing; 
angina  pectoris;  hypertrophy  of  the  heart;  precordial  heaving  and 
intense  pulsation;  irregularity  of  pulse;  dilatation  of  heart;  heart 
failure;  ascending  oedema,  etc. 

Psychic  Symplons. — General  nervousness,  insomnia,  restlessness,  mental 
exuberance  alternating  with  depression  and  melancholia,  delusions 
and  hallucinations. 

Ocular. — Staring  gaze  without  winking  for  considerable  periods.  Widen- 
ing of  palpebral  slit  (Dalrymple,  v.  Stellweg's  sign),  lids  do  not  follow 
eyeballs  perfectly,  a  white  streak  of  sclera  is  seen  between  lid  and 
cornea,  especially  on  glancing  downward  or  upward  (v.  Graefe's  sign), 
inability  to  converge  in  looking  at  near  objects  (Mobius'  sign), 
exophthalmos,  overflow  of  tears,  pain  and  feeling  of  tension  in  the 
eyeballs,  corneal  ulceration. 

Peripheral  Nerve  Symptoms. — Fine  tremor  (from  8  to  10  per  second), 
especially  of  the  finger  tips,  nystagmus,  superficial  and  cog-wheel 
breathing,  astasia-abasia,  hyperesthesias  and  paresthesias  occasion- 
ally, inability  to  frown  or  wrinkle  forehead  (Joffroy's  sign). 

Cutaneous  (from  vasodilation  and  anti-adrenalin  action). — Feeling  of  heat, 
continuous  and  intense;  lowered  electrical  resistance;  sweating;  color 
usually  pale  brownish — Addison-like  pigmentation,  especially  about 
eyelids  (Jellinek);  flushes;  localized  transitory  oedema,  especially 
about  eyelids;  scleroderma. 

Nutritional  (increased  rapidity  of  metabolic  processes — loss  of  N  and 
P2O5). — Loss  in  weight;  sometimes  absolute  anorexia,  sometimes 
excellent  appetite;  attacks  of  diarrhoea,  often  with  slimy  stools; 
polyuria;  glycosuria.    Fever  (varying  from  99°  to  104°). 


THYROID  HEART.  683 

Blood. — Slight  leucocytosis  without  change  in  red  blood-corpuscles  or 
secondary  anaemia;  polymorphonuclears  50-55  per  cent., lymphocytes 
20-25  per  cent.,  largemononuclears  8-16  per  cent,  (large 
mononuclear  leucocytosis  present  in  formes  frustes).    (Barker,  Caro.) 

Psychic  Manifestations. — The  psychic  symptoms  in  hyperthyroidism 
have  been  very  aptly  compared  to  the  well-known  effects  of  over-indulgence  in 
coffee — increased  activity  of  thought,  restlessness,  irritability,  insomnia,  and 
in  the  more  severe  cases  garrulity  and  delusions.  As  mentioned  above,  over- 
indulgence in  coffee  may  sometimes  be  followed  by  enlargement  of  the  thyroid. 
There  can  be  little  doubt  that  many  cases  of  so-called  neurasthenia  and  hys- 
teria are  due  to  a  more  or  less  transitory  state  of  over-secretion  of  the  thyroid. 
This  is  particularly  true  when  the  symptoms  are  accentuated  at  the  menstrual 
periods,  for  then  the  thyroid  secretion  is  increased.  It  is  possible  that,  as  sug- 
gested by  Graves,  the  "globus  hystericus"  may  be  due  to  an  acute  swelling 
(erectile  expansion)  of  the  thyroid.  Neurasthenic  symptoms  may,  however, 
have  a  basis  in  hyperthyroidism  in  cases  when  this  would  be  least  expected. 
For  example,  a  young  physician  in  robust  health  recently  complained  to  the 
writer  of  having  suffered  from  insomnia  and  palpitation  for  several  months, 
during  which  time  he  had  been  compelled  to  forego  his  accustomed  daily 
exercise.  On  closer  observation,  however,  he  observed  that  at  about  the  time 
his  symptoms  had  begun  he  noticed  a  slight  swelling  of  his  thyroid  which  had 
persisted  ever  since,  although  he  had  no  tremor. 

Cardiac  Signs  and  Symptoms. — The  cardiac  symptoms  also  have 
some  similarity  to  those  of  an  overdose  of  coffee,  especially  the  palpitation. 
This  symptom  is  probably  due  to  the  direct  stimulation  of  the  afferent  nerves 
of  the  heart  (depressor),  which  has  been  shown  by  v.  Cyon  to  result  from 
injection  of  thyroid  extracts,  iodothyroin  and  thyreoglobulin.  Palpitation  is 
the  earliest  and  often  the  most  severe  symptom. 

The  tachycardia,  like  most  of  the  signs  of  Basedow's  disease,  results 
from  the  stimulation  of  the  accelerator  nerves  and  from  the  degree  to  which 
this  outweighs  the  effect  upon  the  vagus.  The  pulse-rate  maybe  continuously 
elevated  (over  120) ,  or  the  tachycardia  may  be  latent  and  attacks  of  rapid  pulse 
may  be  brought  out  only  by  slight  disturbance  of  the  equilibrium  or  by  the  admin- 
istration of  very  minute  doses  of  thyroid  extract  (Emerson,  quoted  by  Barker). 
In  these  attacks  the  pulse-rate  rises  gradually  during  a  few  minutes 
and  falls  gradually  (in  contrast  to  idiopathic  paroxysmal  tachycardia), 
but  in  one  case  v.  Hoe&slin  has  seen  sudden  doubling  and  sudden  halving  of 
the  rate.  Strubing  has  found  that  pressure  upon  the  vagus  slows  the  rapid 
heart  of  Basedow's  disease,  showing  that  there  is  no  paralysis  of  that  nerve. 

Although,  as  Cleghorn  has  shown,  thyroid  extract  increases 
the  force  and  size  of  cardiac  contraction  (the  increased  pulse- 
pressure  shows  increased  cardiac  output),  the  persistent  over-stimulation  of 
this  organ  draws  so  much  upon  its  reserve  force  that  it  may  readily  suffer  from 
overstrain  and  undergo  acute  dilatation.  Afferent  impulses  through  the 
depressor  nerves,  which  are  already  in  a  state  of  increased  irritability,  may 
give  rise  to  symptoms  of  typical  angina  pectoris,  with  referred  pain  down  the 
arms  and  precordial  hyperajsthesia.  This  thyroid  type  of  angina  pectoris  has 
been  described  on  page  391.  Prolonged  overstrain  may  result  in  failure  of 
either  the  left  or  the  right  heart,  and  symptoms  of  pulmonary  or  systemic 
decompensation  (oedema,  ascites,  etc.)  set  in. 


684  DISEASES  OF  THE  HEART  AND  AORTA. 

The  irregularity  is  probably  due  to  occasional  extrasystoles, 
though  careful  analyses  of  its  nature  are  lacking.  In  one  case  reported  by 
v.  Hoesslin  there  was  definite  paroxysmal  tachycardia  with  sudden  onset 
and  sudden  cessation — approximate  halving  and  doubling  of  rate,  but 
Hirschfelder  finds  that  this  condition  is  a  rare  one  in  Basedow's  disease. 
The  attacks  of  tachycardia  and  palpitation  most  commonly  begin  and  end 
by  a  gradual,  though  rapid,  change  of  rate,  and  indicate  a  simple  exaggera- 
tion of  physiological  variations. 

The  maximal  blood-pressure  is  usually  high,  the  minimal 
normal;  the  pulse-pressure  increased;  this  shows  that  there  is  an  increased 
systolic  output  with  low  peripheral  resistance,  and  corresponds  well  with 
the  experimental  results  from  injection  of  thyroid  tissue  juice  (Pressaft). 
In  10  cases  of  Basedow's  disease  Krause  and  Friedenthal  found: 

Lowest.  Average.  Highest. 

Cm.  H2O.    Mm.  Hg.        Cm.  H2O.    Mm.  Hg.       Cm.  H2O.     Mm.  Hg. 

Maximal  blood-pressure .. .     145  106  182  134  215  158 

Minimal  blood-pressure.  ..      85  62  89.5        65.8  90  66 

This  accords  with  the  writer's  experience,  but  in  the  early  cases  and 
"formes  frustes"  the  maximal  pressure  may  not  be  elevated  even  when 
there  is  tachycardia. 

The  heart  is  usually  enlarged  and  hypertrophied,  the  apex  impulse 
forcible,  and  the  large  systolic  excursions  impart  a  heaving  to  the  whole 
chest.  In  periods  of  overstrain  from  exertion  or  excitement  there  may  be 
transitory  dilatation  of  the  heart,  and  this  uniformly  occurs  during  the 
chronic  heart  failure.  There  is  often  a  blowing  systolic  murmur  heard 
over  both  ventricles  and  at  the  apex,  perhaps  due  to  functional  insuffi- 
ciencies of  the  auriculoventricular  valves. 

Heart  failure  is  the  immediate  cause  of  death  in  most  cases  of  Base- 
dow's disease. 

Ocular  Manifestations. — The  ocular  manifestations  are  peculiar  and 
very  characteristic.  V.  Graefe  (1857)  called  attention  to  the  fact 
that  when  the  eyes  moved  upward  and  downward  the  lids 
did  not  follow  them  perfectly,  but  a  streak  of  white  sclera  could 
be  seen  between  lids  and  cornea  (Graefe's  sign).  Dalrymple  and  in 
1867  v.  Stellwag  noted  the  widening  of  the  palpebral 
slits,  the  staring  expression,  the  absence  of  winking.  V.  Stellwag's 
sign  is  in  most  cases  the  earliest  characteristic  sign  of  Basedow's  disease. 
Mobius'  sign  is  the  inability  to  converge  the  two  eyes  when 
looking  at  a  very  near  object. 

The  origin  of  these  signs  is  very  simple.  Claude  Bernard,  when  he  first 
stimulated  the  cervical  sympat  he  tic  ,  demons  t  rat  e  d  that  widen- 
ing of  the  palpebral  slit  and  dilatation  of  the  pupil  resulted 
and  that  the  eyeball  was  pushed  forward.  Aran  and  Kaufmann  (1860) 
demonstrated  that  this  exophthalmos  resulted  from  stimulation  of  Muller's 
non-striated  muscle  in  the  eyelid,  which  is  innervated  by  the  cervical  sympathetic. 
These  experiments  were  confirmed  by  a  number  of  writers,  especially  MacCallum  and  Cor- 
nell (1904).  The  exact  course  of  the  fibres  of  Muller's  muscle  and  their  mode  of  operation 
has  been  described  by  Landstrom.  Landstrom  finds  that  the  fibres  of  smooth  muscle 
form  a  narrow  cuff,  or  truncated  cone,  encircling  the  anterior  portion  of  the  orbit.  The 
fibres  at  the  posterior  border  of  the  cuff  pass  backward  and  are  inserted  into  the  sclerotic 
coat  of  the  eyeball.    The  fibres  forming  the  anterior  margin  of  the  cuff  are  inserted  into  the 


THYROID   HEART. 


685 


upper  or  lower  lids,  in  which  they  run  obliquely  toward  the  palpebral  slit.  The  middle 
portion  of  the  cuff  constitutes  the  fixed  point  from  which  the  muscle  acts,  and  is  attached 
by  short  fibrous  bands  to  the  bony  wall  of  the  orbit.  Contraction  of  this  muscle 
therefore  tends  to  draw  the  eye  forward  (exophthalmos)  as  well 
as  to  pull  the  lids  apart  (Dairy  m  pie  and  v.  Stellwag's  sign). 
The  delicate  coordination  of  lid  movement  and  eye  movement 
is  disturbed  by  this  added  traction  upon  the  lid  (v.  Graefe's 
sign).  Moreover,  the  contraction  of  these  fibres  tends  to  keep 
the  axes  of  the  eyes  divergent,  and  thus  antagonizes  conver- 
gence   (Mobius'    sign). 


Fig.  320. — Diagram  showing  the  relation  of  the  various  anatomical  structures  concerned  in  the 
production  of  the  ocular  and  cardiac  manifestations  of  Basedow's  disease.  A.  Distribution  of  the  branches 
of  the  cervical  sympathetic  to  the  heart,  thyroid  gland,  and  eyelids.  The  arrows  indicate  the  direction  in 
which  stimulation  of  the  cervical  sympathetic  moves  the  eyelids  and  eyeball.  SYMP  N,  sympathetic  nerve 
plexus;  SUP.  C.  GANG,  MID.  C.  GANG,  INF.  C.  GANG,  superior,  middle,  and  inferior  cervical  ganglia. 
B.  Relation  of  Miiller's  muscle  to  the  eyeball  and  structures  within  the  orbit  (schematic).  Miiller's  muscle 
(MULL)  is  shown  in  black.  The  arrows  indicate  the  direction  of  its  pull.  TEND,  tendinous  attach- 
ment of  Miiller's  muscle  to  the  orbit,  septum  orbitale  (SEPT.  ORB).  C.  Section  through  the  lateral 
portion  of  the  orbit  (semi-schematic,  modified  from  Landstrom).  ORB,  orbitalis;  LEV,  levator  palpe- 
brarum;   CO NJ,  conjunctiva;    SCLER,  sclera;    RECT  MED,  rectus  medius. 


Muscular  Changes. — A  fine  tremor  beginning  in  the  fingers,  with  8-10 
contractions  per  second,  has  been  shown  by  Marie  to  be  almost  common 
enough  to  be  included  among  the  cardinal  symptoms.  It  is  probably  due 
to  the  overstimulation  of  the  peripheral  nerves,  and  finds  its  analogue  in 
the  tremor  from  coffee  and  tobacco.  Tremor  of  the  tongue  and  sudden 
movements  of  the  tongue  and  lips  are  not  as  common  as  in  alcoholism.  It 
is  probable  that  the  muscular  weakness  consequent  upon  the  katabolism 
of  muscle  proteid  aids  in  the  tremor. 

Astasia  abasia  (giving  way  of  the  legs  in  standing  and  walking)  is  rare, 
but  has  been  reported.   It  represents  an  extreme  grade  of  nervous  disturbance. 

The  increased  metabolism  of  N  and  P205,  with  destruction  of  muscle 
tissue,  fat,  and  to  a  lesser  extent  of  the  bones,  is  important  and  finds  its 
expression  in  the  general  loss  of  weight  (often  25  to  50  pounds) .  It  is  the 
direct  result  of  iodothyrin  intoxication. 


686  DISEASES  OF  THE  HEART  AND  AORTA. 

Diarrhoea  is  common.  There  is  often  a  good  deal  of  mucus  in  the  stools, 
suggesting  some  relation  to  the  so-called  mucous  colitis. 

Changes  in  the  Thyroid  itself. — As  regards  the  size  and  appearance  of 
the  thyroid  gland  there  is  great  variation.  In  spite  of  the  common  term 
of  "exophthalmic  goitre,"  the  thyroid  may  not  be  prominent  nor  even 
palpable.  Since  there  is  great  variation  in  the  average  size  and  weight  of 
the  thyroid  in  different  regions, — 25  to  33  Gm.  in  certain  regions,  60  Gm. 
in  others,  100  Gm.  in  Switzerland  (Oswald), — a  merely  palpable  thyroid 
need  be  of  no  diagnostic  importance.  Increase  in  the  size  of  the  thyroid 
is  equally  difficult  to  interpret.  The  size  of  the  thyroid  bears  a  definite 
relation  to  sexual  activity,  and  increases  regularly  during  menstruation 
and  pregnancy,  often  to  a  considerable  degree.  Indeed,  in  some  cases  of 
formes  frustes  it  is  not  unlikely  that  we  are  dealing  with  slight  hyperthy- 
roidism whose  intensity  is  determined  by  these  physiological  factors. 
Increased  vascularity  is  of  great  importance  in  differentiating  between 
transitory  and  persistent  hyperthyroidism.  It  can  be  demonstrated  by 
eliciting  a  murmur  and  thrill  over  the  thyroid  when  the  gland  is  pressed 
upon  (Guttmann).  This  cannot  be  produced  in  simple  goitres  or  normal 
glands. 

SECONDARY    HYPERTHYROIDISM. 

Moreover,  it  is  probable  that  in  many  neurotic,  toxic,  and  organic 
diseases  the  actions  of  nerves  or  of  hormones  arouse  the  thyroid  to  a  second- 
ary activity,  which  may,  nevertheless,  be  of  great  importance  in  determining 
the  features  of  the  case.  For  example,  Holz  has  reported  two  cases  of  exoph- 
thalmic goitre  in  children  in  whom  the  disease  subsided  on  removal  of  the 
adenoids  ;  one  case  recurred  and  again  subsided  with  the  recurrence 
and  removal  of  the  adenoids.  Accordingly  it  is  advisable  not  only  to  treat 
the  Basedow's  disease  but  also  to  look  for  and  treat  the  other  foci  of  excita- 
tion. 

DIAGNOSIS. 

It  is  evident  that,  though  there  can  be  little  doubt  as  to  the  nature 
of  well-developed  thyroidism,  there  may  be  room  for  much  debate  regarding 
cases  of  formes  frustes,  for  these  cases  must  be  differentiated  from  simple 
physiological  hypoactivity  of  the  thyroid.  Patients  should  be  carefully 
watched  for  the  development  of  ocular  signs,  especially  at  menstruation, 
since  these  are  practically  never  present  in  persons  whose  thyroid  activity 
is  normal. 

In  cases  in  which  symptoms  are  so  mild,  however,  it  is  still  important 
to  bear  in  mind  the  possibility  of  a  thyroid  origin  for  the  condition,  at 
least  in  so  far  as  an  increased  thyroid  secretion  may  arise 
reflexly  and  perpetuate  itself  through  the  vicious 
circle  mentioned  on  page  683.  It  is  probable  that  on  this  basis  the 
origin  of  many  an  obscure  "cardiac  neurosis"  will  be  cleared  up.  Hyper- 
thyroidism and  hysteria,  sexual  neurasthenias,  epilepsy,  tobacco  poisoning, 
alcoholism,  myocardial  disease,  and  valvular  diseases  are  frequently  asso- 
ciated, and  when  one  of  these  conditions  is  present  it  still  remains  important 
to  look  out  for  contributing   roles  on  the  part  of  the  thyroid. 


THYROID    HEART.  687 

Each  case  of  morbus  Basedowii  may  be  considered  as  an  autointoxi- 
cation due  to  the  passage  of  more  or  less  iodized  thyreoglobulin  from  the 
thyroid  gland  into  the  blood.  When  this  is  secreted  in  large  quantities, 
the  condition  is  outspoken  and  presents  many  of  the  symptoms,  among 
them  some  of  severe  grade.  When  but  little  excess  of  thyreoglobulin 
circulates  in  the  blood,  it  may  give  rise  to  the  "  formes  frustes"  with  but 
few  symptoms  and  those  of  the  milder  type  predominating. 

However,  even  in  the  most  atypical  cases  of  "forme  fruste"  o  n  e  o  r 
more  of  these  symptoms  may  reach  excessive  sever- 
ity, and  the  disease  may  persist  in  the  form  of  a  cardiac  neurosis,  a  psycho- 
sis, a  chronic  enteritis,  a  progressive  inanition,  a  diabetes,  or  even  a  mild 
relapsing  fever,  for  long  periods.  The  cardinal  suggestive  signs  may  be 
so  slight  in  intensity  as  to  be  noticed  only  when  the  suspicion  of  Basedow's 
disease  has  once  been  aroused  in  the  mind  of  the  examiner,  and  then  the 
coexistence  of  several  unobstrusive  features  may  make  the  condition  defi- 
nite; as,  for  example,  a  slight  staring,  anxious  expression  in  a  thin,  nervous 
woman  who  suffers  from  attacks  of  palpitation  and  precordial  pain  and 
who  manifests  a  slight  fine  tremor  of  the  fingers  and  a  tendency  to  diar- 
rhoea. On  closer  examination  it  may  be  found  that  the  lids  do  not  follow 
the  eyeballs  perfectly  and  there  is  slight  fulness  of  the  neck,  but  none  of 
these  symptoms  are  striking. 

Case  of  Basedow's  Disease  with  Anginal  Attacks. 

Mrs.  K.  M.,  housewife,  aged  23.  seen  under  treatment  at  the  Johns  Hopkins  Medical 
Dispensary  on  Dec.  29,  1906,  when  she  complained  of  palpitation  of  the  heart  and 
pain  in  the  right  chest  going  down  the  arm.  She  is  quite  nervous  and  sometimes  has 
crying  spells. 

She  is  a  rather  pale  woman,  fairly  nourished.  The  gums  and  mucous  membranes  are 
a  trifle  pale.  The  palpebral  slit  is  wider  than  normal,  but  lids  follow  eyes.  Convergence 
is,  however,  not  perfect.  The  outlines  of  the  thyroid  gland  can  be  seen;  the  gland  is  readily 
palpable,  but  not  much  enlarged.  The  lungs  were  clear  on  auscultation  and 
percussion. 

The  heart  was  not  enlarged;  sounds  clear.  Pulse  of  good  volume,  regular  in  force 
and  rhythm;  blood-pressure  apparently  low. 

She  was  given  Blaud's  pills  and  also  tincture  of  aconite  0.3  c.c.  (^iv)  and  potassium 
bromide,  without  relief.  She  was  seen  a  number  of  times  during  the  course  of  the  next 
year,  during  which  she  passed  through  a  normal  pregnancy  and  labor.  Palpitation 
continued.  A  well-marked  exophthalmos  developed  and  palpebral  slits 
became  a  little  wider  than  normal. 

During  April,  1907,  she  had  attacks  of  pain  over  the  left  side  of  the  chest 
and  down  the  front  (extensor  surface)  of  the  left  arm,  sometimes  radiating  to  the  shoulder. 
During  attacks  there  is  often  tenderness  in  the  fourth  left  interspace,  sometimes  also  in 
the  fifth,  about  the  mammillary  line.  It  never  radiates  to  the  right  of  the  midline.  These 
attacks  are  accompanied  by  palpitation  and  the  heart-rate  is  rapid.  She  also  has  a  peculiar 
fluttering  sensation,  and  occasionally  an  irregular  beat.  Tracings  at  this  period  showed 
normal  venous  and  carotid  pulse.  She  was  given  small  doses  of  ergotin  without  relief.  A 
week  later  she  was  given  calcium  lactate  0.6  Gm.  (gr.  x)  after  meals,  after  which 
she  began  to  feel  better  at  once,  though  never  relieved  by  any  other  medicine.  The  remedy 
was,  however,  far  from  specific,  and  the  old  symptoms  returned  in  spite  of  the  calcium 
lactate.  During  the  course  of  the  next  six  months  various  remedies  were  given,  none  of 
them  with  marked  effect.  It  seemed  to  both  patient  and  physicians,  however,  that  she 
experienced  a  distinct  improvement  in  symptoms  whenever  calcium 
lactate  was  given  and  distinct  retrogression  when  other  drugs  were  substituted. 
Operation  was  advised  but  not  consented  to,  and  the  patient  was  lost  sight  of. 


688  DISEASES  OF  THE  HEART  AND  AORTA. 

acute  Basedow's  disease  simulating  malignant  endocarditis. 

One  group  of  cases  to  which  attention  should  be  especially  directed 
are  those  of  very  acute  Basedow's  disease  with  fever,  prostration,  tachy- 
cardia, profuse  sweats,  sometimes  chills  and  slight  jaundice — a  clinical 
picture  very  closely  simulating  acute  endocarditis  (W.  G.  Thompson). 
These  cases  are  rather  rare,  but  very  grave.  The  diagnosis  depends  upon 
the  cardinal  symptoms  aided  by  a  negative  blood  culture. 

PROGNOSIS  AND  TREATMENT. 

Statistics  regarding  the  mortality  of  Basedow's  disease  vary  considera- 
bly, as  shown  by  the  following  list. 

V.  Dusch 12 . 5  per  cent. 

V.  Graefe    12      per  cent. 

Mackenzie  12 . 5-25  per  cent. 

Cheadle 9 . 6  per  cent. 

Billingham , 18 . 1  per  cent. 

Gaill 21 . 3  per  cent. 

Charcot 25      per  cent. 

Buschan  (900  cases) 12.5  per  cent. 

Thompson 10      per  cent. 

Williamson 25      per  cent. 

These  figures  err,  on  the  one  hand,  because  only  the  serious  cases  reach 
the  literature,  and,  on  the  other,  because  most  of  the  cases  have  been  fol- 
lowed for  only  short  periods.  Williamson,  who  followed  his  cases  for  some 
years  and  found  a  25  per  cent  mortality,  probably  approximates  the  truth. 
J.  Berry  gives  the  following  statistics  of  56  cases  treated  without 
operation : 

Complete  recovery 10 

Considerable  improvement 24 

Little  or  no  change  . . . .  „ 8 

Fatal. 14 

Even  after  recovery  recurrence  is  the  rule,  so  that  as  ex- 
cellent an  observer  as  August  Hoffmann  states  that  in  23  outspoken  cases 
he  has  not  seen  a  single  permanent  recovery! 

It  is  evident,  therefore,  that  at  the  onset  of  undoubted  Graves's 
disease  therapeutic  interference  is  necessary.  The  best  principles  in  inau- 
gurating treatment  are  those  which  may  be  deduced  from  the  findings  of 
v.  Cyon's  experiments, — i.e.,  that  the  clinical  manifestations  are  due  to 
hypersecretion  of  thyreoglobulin,  that  this  is  proportional  to  the  blood  flow 
through  the  thyroid,  and  that  the  thyroid  secretion  in  the  blood  tends 
itself  to  increase  this  flow  and  to  produce  a  vicious  circle. 

The  first  essential  of  any  palliative  treatment,  therefore,  is  to  reduce 
the  thyroid  secretion  to  its  lower  ebb  by  the  removal  of  the  two  stimulating 
causes — exercise  and  excitement.  In  the  mild  cases  a  simple  isolation  cure, 
with  absolute  rest  in  the  horizontal  position,  can  sometimes  so  lessen 
the  flow  through  the  thyroid  and  the  secretion  of  this  gland  by  diminishing 
the  size  and  number  of  heart-beats  that  the  thyreoglobulin  content  of  the 
blood  falls  to  normal  and  symptoms  subside.    If  the  rest  cure  be  prolonged, 


THYROID    HEART.  689 

the  slight  glandular  hyperplasia  of  early  cases  may  subside  and  a  permanent 
cure  may  result. 

Various  measures  assist  this  process,  especially  those  which  act  as 
psychic  sedatives.  Psychotherapy  and  suggestion,  in  so  far  as 
they  tend  to  lessen  the  elements  of  worry,  quiet  the  patient's  mind,  and 
thus  quiet  his  heart's  action,  may  aid  in  tiding  over  a  period  of  not  too 
intense  excitement.  Similarly  Mobius,  the  apostle  of  serum  therapy, 
reports  the  cure  of  one  case  by  hypnotism!  These  are,  however,  exceptional. 
Psychotherapy  in  Basedow's  disease  is  to  be  classed  among  the  valuable 
sedative  measures,  but  not  among  those  of  fundamental  therapeutics. 
Cold  wet  packs,  especially  before  retiring,  may  be  of  considerable 
assistance  (Eichhorst),  as  also  the  bromides  and  the  soporifics  (veronal, 
trional,  etc.),  though  to  a  less  degree.  Calcium  salts  are  often  very 
satisfactory  as  sedatives.  The  iodobromide  of  calcium  was  used  by  Guptill 
(1874).  In  one  case  (K.  M.)  under  the  writer's  care  calcium  lactate  was 
the  only  drug  which  caused  any  symptomatic  relief,  but  even  this  was 
not  marked.  Muller  and  others  have  used  quinine,  especially  as  the 
hydrobromate,  but  in  many  cases  it  is  without  effect. 

Iodine  as  used  by  the  earlier  observers  may  sometimes  exert 
a  positively  harmful  influence  by  activating  (iodizing)  still 
more  of  the  thyreoglobulin,  and  it  may  thus  bring  on  an  exacerbation  of 
the  condition.  The  effect  of  potassium  iodide  is  less  certainly  harmful 
and  is  sometimes  beneficial,  but  its  action  is  uncertain. 

Galvanization.  —  One  of  the  oldest  and  best  forms  of  treatment  is 
galvanization  of  the  cervical  sympathetic,  with  the 
anode  over  the  carotid  artery  and  the  cathode  at  the  nape  of  the  neck. 
With  currents  of  2-3  milliamperes,  as  used  by  Chvostek,  Benedikt,  Car- 
dew,  and  others,  it  uniformly  gives  a  certain  degree  of  improvement, 
without  effecting  a  cure.  In  early  cases  J.  O.  Hirschfelder  has  obtained 
complete  subsidence  of  symptoms  in  a  considerable  number  of  patients  by 
the  use  of  strong  currents  (20-30  milliamperes),  the  negative  pole  being 
applied  over  the  sympathetic  at  the  neck,  the  positive  over  the  thyroid  for 
two  or  three  minutes.  After  this  it  is  applied  over  the  heart.  This  vigorous 
treatment  seems  to  be  the  best  method  of  applying  electricity,  but  must 
be  continued  for  several  months. 

X=Rays. — E xposure  of  the  thyroid  to  the  Rontgen 
rays  was  introduced  by  Pusey,  Boggs,  and  Beck  in  America,  and  some- 
times shows  favorable  results.  Schwartz;  (1908)  collected  reports  of  40 
cases,  showing  gain  in  26,  improvement  in  nervous  symptoms  in  40, 
exophthalmos  better  in  15,  but  struma  lessened  in  only  8. 

Specific  Sera. — Two  forms  of  so-called  specific  sera  are  also  in  use: 
(1)  anti-thyreoidin  (thyroidectin) ,  the  serum  of  thyroidectomized  sheep 
(Mobius),  has  been  in  use  for  some  years,  and  in  spite  of  numerous  favorable 
reports  has  been  found  absolutely  without  effect  by  Ewald,  Mackenzie, 
and  Strumpell.  (2)  Beebe  has  prepared  an  antiserum  for  the  nucleo- 
proteid  of  the  thyroid  gland  from  animals  into  which  the  purified  nucleo- 
proteid  thyreoglobulin  had  been  injected,  in  the  hope  of  bringing  about 
retrogressive  changes  in  this  gland.  This  serum  has  been  used  therapeu- 
tically by  Rogers  and  by  W.  G.  Thompson,  who  report  distinctly  favorable 

44 


690  DISEASES  OF  THE  HEART  AND  AORTA. 

results,  especially  in  the  very  acute  cases  (90  cases:  23  cured,  54  improved, 
11  failed,  4  died);  but  other  observers  state  that  the  results  are  no  better 
than  those  in  ordinary  hospital  practice,  and  further  confirmation  is  needed. 
Operative  Treatment. — Thyroidectomy. — The  physiological  indication 
for  therapy  in  Basedow's  disease  is  to  lessen  the  amount  of  thyreoglob- 
ulin secreted  into  the  blood.  If  the  various  methods  intended  to  affect 
the  gland  as  a  whole  are  unsuccessful,  the  secretion  may  be  diminished  by 
removing  a  large  portion  of  the  gland  (thyroidectomy).  This  operation 
was  first  successful  in  the  hands  of  L.  Rehn  (1884),  and  has  now  come 
into  quite  general  use,  especially  through  the  work  of  Mickulicz  and  the 
Kochers  in  Europe,  and  Halsted  and  the  Mayos  in  America. 

The  operation  should  be  done  under  local  cocaine  anaesthesia.  It  may  vary  from 
ligature  of  the  arteries  to  one-half  of  the  gland,  or  this  may  be  combined  with  excision  of 
the  latter;  or,  on  the  other  hand,  one-half  of  the  gland  may  be  excised  and  the  arteries 
supplying  a  portion  of  the  other  may  be  ligated.  The  technic  and  results  in  large  series 
of  cases  have  been  reported  by  A.  Kocher,  Landstrom,  and  C.  H.  Mayo,  and  many  of  the 
important  details  by  Halsted  and  Evans. 

Kocher  (1907)  especially  calls  attention  to  the  necessity  of  suiting 
the  extent  of  the  operation  to  the  condition  of  the  patient,  especially  the 
cardiovascular  condition.  "A  systolic  blood-pressure,  even  of  195  mm. 
Hg,  does  not  forbid  operation;  .  .  .  but  if  we  find  the  blood-pressure 
below  normal  and  the  disease  highly  developed,  we  must  study  the  condi- 
tion and  especially  note  the  action  of  the  heart  after  exercise  or  excite- 
ment. Under  these  circumstances  we  might  find  a  sudden,  very  marked 
dilatation  of  the  heart,  irregularity  of  pulse,  and  a  blood-pressure  which 
cannot  be  measured  by  our  ordinary  methods." 

The  patient  should  be  given  a  preparatory  period  of  rest  and  pallia- N 
tive  treatment  to  prepare  her  for  the  operation,  and  two  or  more  opera- 
tions should  be  done  on  the  same  patient  rather  than  too  extensive  an  opera- 
tion at  one  sitting.  Kocher  never  ligates  more  than  two  arteries  nor  re- 
moves more  than  one-half  the  gland  at  one  sitting,  but  these  measures 
suffice  in  cases  that  are  not  too  far  advanced.  Halsted  has  called  particular 
attention  to  the  need  of  preserving  the  parathyroid  gland 
in  order  to  avoid  tetany.  Hence  he  advocates  tracing  out  the 
branches  to  these  small  bodies  and  then  ligating  the  main  artery  beyond 
them.  Both  Kocher  and  Halsted  insist  upon  the  greatest  care  in 
the  ligation  of  all  bleeding  points  during  the  opera- 
tion and  in  draining  off  any  small  collection  of  ser um 
which  may  collect  during  the  healing  of  the  wound.  This  greatly  diminishes 
or  obviates  the  intensification  of  Basedow  symptoms  which  sometimes 
result  a  few  days  after  operation  (probably  from  absorption  of  iodothyreo- 
globulin  upon  the  raw  surface  of  the  gland)  and  which  may  be  dangerous. 
Halsted  also  found  that  the  continuous  use  of  an  ice-bag  upon  the  neck 
during  a  few  days  after  the  operation  retards  the  absorption  from  the  gland 
and  lessens  the  frequency  of  these  symptoms. 

As  a  result  of  this  procedure  in  254  patients  (2  operations  in  71  cases), 
A.  Kocher  has  obtained  great  improvement  in  every  case,  with  abso- 
lute and  permanent  cure  in  83  per  cent.,  and  3.5  per 
cent,  of  deaths.     In  the  last  91  operations,  since  the  above  precautions 


THYROID    HEART  691 

had  been  observed,  he  has  not  had  a  single  death!  C.  H.  Mayo  had  9 
deaths  in  176  cases,  but  only  one  in  his  last  75;  and  Professor  Halsted's 
results  at  Johns  Hopkins  are  equally  favorable. 

In  cases  of  long  standing  the  exophthalmos  never  disappears,  for  the 
depths  of  the  orbit  have  become  filled  with  fat  which  continues  to  push 
the  eye  forward  after  the  contraction  of  Miiller's  muscle  has  subsided. 

Hypertrophy  of  the  heart  and  secondary  myocardial  changes  also 
remain,  perhaps  some  cardiac  weakness,  but  these  are  greatly  diminished 
when  the  continuous  cardiac  excitation  is  removed. 

It  must  be  admitted  also  that,  as  Tinker  states,  the  operation  requires 
more  skill  and  practice  than  most  surgical  procedures,  and  the  prognosis 
is  therefore  far  better  done  by  a  man  whose  experience  in  this  line  is  con- 
siderable than  by  a  surgeon  of  even  excellent  local  reputation. 

As  regards  the  indication  for  operation,  Kocher  believes  that  ''dis- 
tinct vascular  symptoms  (other  than  mere  palpita- 
tion and  tachycardia)  should  at  once  induce  surgical 
treatment."  Before  these  have  set  in,  the  palliative  method  may  be 
used  for  a  while,  and  many  cases  may  be  relieved  thereby  or  subject  only 
to  occasional  recurrences.  Should  the  mental  symptoms  and  tachycardia 
persist  or  become  more  severe,  the  physician  should  recommend  operation 
while  the  patient's  general  condition  is  still  good,  and  should  not  wait 
until  she  is  a  complete  physical  wreck  before  turning  over  the  responsibility 
to  the  surgeon.  The  surgeon  should  be  allowed  to  operate  upon  the  early 
but  chronic  cases  which  do  not  improve  under  palliative  treatment. 

These  rules  apply  as  well  to  the  cases  of  "formes  frustes"  as  to  the 
outspoken  Basedow's  disease.  The  persistence  of  psycho-  and  cardio- 
neuroses  gives  the  indications,  whether  all  the  cardinal  features  are  pro- 
nounced or  not,  and  spontaneous  recovery  is  no  more  likely  to  occur  after 
the  "  forme  fruste "  has  persisted  than  in  cases  where  all  the  signs  are  well 
marked. 

Sympathectomy  (Jonnesco's  Operation).  —  Another  operation,  which 
has  been  performed  by  Jonnesco,  is  the  removal  of  the  sympathetic  ganglia 
on  both  sides  of  the  neck.  The  result  of  this  is  usually  an  immediate  slow- 
ing of  the  pulse,  and  often  a  cessation  of  other  symptoms.  Jonnesco  reports 
several  cases  of  permanent  cure,  but  in  the  hands  of  a  considerable  number- 
of  later  observers,  among  them  Kocher,  good  results  have  been  lacking  or 
transitory,  and  this  method  should  therefore  be  cast  aside. 

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Kraus,  Fr.:  Ueber   das    Kropfherz,  Wien.  med.  Wchnschr.,  1899,  416.     Ueber   Kropf- 

herz,  Deutsch.  med.  Wchnschr.,  Leipz.,  1906,  xxii,  1889;  and  Berl.  klin.  Wchnschr., 

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1896,  xxi,  19. 
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of  the  Thyroid-Parathyroid  Apparatus,  ibid.,  1916,  lxvi,  811. 
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f.  d.  ges.  Physiol.,  Bonn,  lvi. 
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sideration of  the  Hypertrophy  of  this  Gland,  Johns  Hopkins  Hosp.  Rept.,  Bait.,  1896, 

i,  373. 
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1907,  xlix,  1158. 
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Gland,  Arch.  Int.  M.,  Chicago,  1907,  i,  378. 
Wilson,  L.  B. :  The  Pathological  Changes  in  the  Thyroid  Gland  as  Related  to  the  Varying 

Symptoms  in  Graves's  Disease,  Am.  J.  M.  Sc,  1908,  cxxxiv,  857.    (Excellent  figures.) 
Plummer,  H.  S.:  Blood  Pressure  and  Thyrotoxicosis,  Trans.  Assoc.  Am.  Phys.,  Phila.,  1915, 

xxx,  450. 
Muller,  Fr.:  Beitrage  zur  Kenntniss  der  Basedow'schen  Krankheit,  Deutsch.  Arch.  f.  klin. 

Med.,  Leipz.,  1893,  li,  335. 
Magnus-Levy,  A.:  Gaswechsel  und  Fettumsatz  bei  Myxoedemen,  Wiesb.,  1896. 
V.  Cyon,  E.:  Beitrage  zur  Physiologie  der  Schilddruse  und  des  Herzens,  Arch.  f.  d.  ges. 

Physiol.,  Bonn,  1898,  lxx,  126;  also  ibid.,  lxxi,  lxxiii,  lxxvii. 
Kraus,  Fr.,  and  Friedenthal,  H.:  Ueber  die  Wirkung  der  Schilddrusenstoffe,  Berl.  klin. 

Wchnschr.,  1908,  xlv,  1709. 
Cleghorn,  A. :  The  Action  of  Animal  Extracts,  Bacterial  Cultures  and  Culture  Filtrates  on 

the  Mammalian  Heart  Muscle,  Am.  J.  Physiol.,  Bost.,  1899,  ii,  273. 
Eppinger,  H.,  Falta,  W.,  and  Rudinger,  C:  Ueber  die  Wechselwirkungen  der  Driisen  mit 

innerer  Sekretion,  Ztschr.  f.  klin.  Med.,  Berl.,  1908,  lxvi,  1. 
Hunt,  Reid:  The  Influence  of  Thyroid  Feeding  upon  Poisoning  by  Acetonitrile,  J.  Biol. 

Chem.,  N.  Y.,  1905,  i,  43.    The  Probable  Demonstration  of  Thyroid  Secretion  in  the 

Blood  in  Exophthalmic  Goitre,  J.  Am.  M.  Asso.,  Chicago,  1907,  xlix,  240.    The  Rela- 
tion of  Iodine  to  the  Thyroid  Gland,  ibid.,  1907,  xlix,  1323. 
Jellinek:  Ein  bisher  nicht  betrachtetes  Symptom  der  Basedow'schen  Krankheit,  Wien. 

klin.  Wchnschr.,  1904. 
Guttmann,  P.:  Das  arterielle  Strumagerausch  und  seine  diagnostische  Bedeutimg,  Deutsch. 

med.  Wchnschr.,  Leipz.,  1893,  xix. 
Parry.    Quoted  from  Dock  (1.  c). 

Buschan:  Die  Basedow'sche  Krankheit,  Wien  u.  Leipz.,  1894.     Quoted  from  Hoffmann. 
Passler,  H.:  Erfahrungen  ueber  die  Basedow'sche  Krankheit,  Deutsch.  Ztschr.  f.  Nerven- 

heilk,  1895,  vi,  210. 
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Landstrom,  J. :  Ueber  Morbus  Basedowii,  Stockholm,  1907. 
Mobius,  P.  J.:  Die  Basedow'sche  Krankheit,  Nothnagel's  Handb.  der  spec.  Path.  u.  Therap., 

Wien,  1896,  xxii. 
Kocher,  A.:  Ueber  Morbus  Basedowii,  Mitth.  a.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  Jena,  1902 

ix,  1. 


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De  Quervain,  F. :  Die  Akute  nicht  eitrige  Thyroiditis,  Mitth.  a.  d.  Grenzgeb.  d.  Med.  u. 

Chir.,  Jena,  1904,  ii,  Supp.,  1.    Thyroiditis  simplex  und  toxische  Reaktion  der  Schild- 

driise,  ibid.,  1906,  xv,  297. 
Boggs  and  Sladen.    Personal  communication. 
Engel-Reimers :  Jahrb.  d.  Hamb.  Krankenanstalt,  1894,  hi,  430.     Quoted  from  Schmidt's 

Jahrb.,  1895,  cclvii,  23. 
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1894,  xxxv,  1714. 
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1896,  xliii,  25. 
Hirschfelder,  A.  D. :  Contribution  to  the  Study  of  Auricular  Fibrillation,  Paroxysmal  Tachy- 
cardia, and  the  So-called  Auriculo-  (atrio-)  ventricular  Extrasystoles,  Johns  Hopkins 

Hosp.  Bull.,  Bait.,  1908,  xix,  322. 
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thalm.,  1857. 
V.  Stellweg,  Carion:  Ueber  gewisse  Innervations.    Storungen  bei  der  Basedow'schen  Krank- 

heit,  Wiener  med.  Jahrb.,  1869,  xxvii,  25. 
Mobius,  P.  J.,  1.  c. 
Bernard,  Aran  and  Kaufmann,  and  H.  Miiller  (Ztschr.  f.  wiss.  Zool.,  1858,  ix,  541).    Quoted 

from  Landstrom. 
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N.  Y.,  1904,  lxxxv,  733. 
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Basedow,  These,  Paris,  1883. 
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Sc,  Phila.  and  N.  Y.,  1906,  cxxxii,  835. 
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lauf storungen,  Wiesb.,  1901. 
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i,  212. 
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Am.  J.  M.  Sc,  Phila.,  1874,  lxvii,  125. 
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Krankheit,  Wien.  med.  Presse,  1871,  1872,  1875. 
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Lancet,  Lond.,  lS91,.ii,  6,  64. 
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1908,  xxi,  1332. 
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M.  Asso.,  Chicago,  1908,  xlvi,  484.    A  Serum  Having  Therapeutic  Value  in  the  Treat- 
ment of  Exophthalmic  Goitre,  ibid.,  1906,  xlvii,  661. 
Rogers,  J.:  The  Treatment  of  Thyroidism  by  a  Specific  Serum,  ibid.,  1906,  xlvii,  655. 
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1907,  xlix,  1240.    With  discussion  by  Halsted  and  Mayo. 
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II. 

MISCELLANEOUS    DISTURBANCES    OF    CARDIAC    FUNCTION— 

THE    SO-CALLED    "CARDIAC    NEUROSES" 

AND    "CARDIAC    NEURASTHENIA." 

GENERAL     CHARACTERISTICS. 

One  of  the  largest  groups  of  cases  seen  by  the  clinician  is  made  up 
chiefly  of  pale,  ansemic-looking  young  patients,  with  hollow  lustreless  eyes 
and  sunken  cheeks,  who  complain  of  symptoms  which  may  be  divided  into 
two  categories: 

Symptoms.  —  1.  Symptoms  referable  to  sensory  disturbances 
about  the  heart: — palpitation,  precordial  tenderness,  pain  or  constriction, 
pains  and  sensory  disturbances  down  the  arms,  and,  in  rarer  cases,  of 
attacks  resembling  angina  pectoris. 

2.  Symptoms  referable  to  motor  disturbances  of  the  circulation, 
and  especially  to  the  distribution  of  blood  in  the  body: — cardiac  arrhyth- 
mia, weakness,  lassitude  and  weariness,  vertigo,  muscae  volitantes,  fainting 
spells,  and  an  infinite  variety  of  psychasthenic  and  nervous  symptoms. 

This  same  symptom  complex  has  already  been  encountered  in  the 
attacks  of  paroxysmal  tachycardia  (Chapter  II.),  where  it  has  been  seen 
to  result  from  "  arterial  ansemia,"  or  the  relative  depletion  of  the  arteries 
through  dilatation  of  the  veins,  especially  in  the  splanchnic  region.  Y. 
Henderson  believes  that  under  these  conditions  the  viens  are  not  overfilled, 
but  that  they  too  have  become  depleted  by  transudation  of  fluid  into  the 
lymph  and  tissue  spaces.  Mr.  C.  C.  Cody,  in  the  Johns  Hopkins  medical 
clinic,  has  found  a  very  low  venous  pressure  (  —  2  to  —7  cm.  H20)  in  a 
number  of  cases  of  neurasthenia  and  post-operative  asthenia  in  which  the 
above-mentioned  symptoms  were  present.  The  arterial  pressure  in  all 
but  one  of  these  cases  was  about  normal,  ranging  from  104  to  125  mm.  Hg. 
This  same  circulatory  state  seems  to  be  present  throughout  the  groups 
of  cases  about  to  be  discussed,  although  the  mechanisms  by  which  it  is 
brought  about  are  various. 

Changes  in  Rhythm. — Alterations  of  rhythm  are  very  common  in  this 
group  of  cases  (Hoffmann,  Mackenzie,  Reissner).  They  are  usually  associ- 
ated with  respiration,  with  a  slowing  of  the  pulse  during  inspiration  and  a 
quickening  during  expiration  (Fig.  325) .  It  will  be  noted  that  this  exactly 
corresponds  to  the  normal  centripetal  action  currents  in  the  vagus  (Eint- 
hoven,  Flohil  and  Battaerd)  which  occur  with  each  inspiration,  and  it  is 
probable  that  in  the  condition  of  heightened  excitability  this  (usually  sub- 
normal) reflex  stimulation  becomes  active.  Stadler  and  Hirsch  have  been 
able  to  produce  such  irregularities  by  inflating  the  intestines  of  dogs  and 
rabbits,  but  find  them  only  accompanying  dyspnoea.  These  observers  also 
found  that  such  inflations  of  the  intestines  were  always  accompanied  by  rise 

694 


DISTURBANCES  OF  CARDIAC  FUNCTION.  695 

of  blood-pressure.  The  writer  has  been  able  to  confirm  these  observations. 
Moreover,  McCaskey  and  Russell  find  that  an  elevation  of  30  or  40  mm. 
Hg  in  blood-pressure  may  occur  in  the  course  of  gastro-intestinal  troubles, 
especially  hyperchlorhydria  and  flatulence.  Russell  suggests  that  there  is 
a  relationship  between  chronic  gastric  intestinal  disturbances  and  sclerosis 
of  mesenteric  vessels. 

In  the  cases  of  enteroptosis  and  of  bathycardia  a  true  pulsus  para- 
doxus (diminution  or  dropping  of  beats  during  inspiration)  may  occur 
from  the  tugging  upon  the  mediastinum,  aorta,  and  great  veins  when  the 
diaphragm  is  drawn  down  during  inspiration.  In  rarer  cases,  and  espe- 
cially those  of  gastro-intestinal  origin,  small,  early  beats  resembling 
extrasystoles  are  present.  In  making  the  diagnosis  of  extrasystoles, 
however,  great  care  must  be  used,  for  it  must  be  remembered  that  in  the 


RESP. 


RADIAL 


Fig.  321. — Respiratory  arrhythmia  in  a  young  cigarette  smoker. 

usual  rhythmic  variations  in  rhythm  the  last  beat  ot  a  series  with  increasing 
rapidity  may  be  followed  by  the  pause  due  to  maximal  slowing,  and  thus 
an  extrasystole  may  be  simulated.  On  the  other  hand,  it  must  be  remem- 
bered that  no  experimenters  have  as  yet  been  able  to  produce  extra- 
systoles by  stimulating  the  extrinsic  cardiac  nerves  (Hering,  Hoffmann,  the 
writer  and  others),  and  therefore  each  case  of  the  sort  should  be  carefully 
studied  with  venous  tracings  and  electrocardiograms.  True  ventricular 
extrasystoles  demonstrable  with  the  electrocardiogram  are  often  brought 
on  by  flatulence,  though  many  writers  agree  with  Friedrich  Miiller  that 
the  presence  of  definite  extrasystoles  is  indicative  of  myocardial  disease. 

Some  years  ago  the  writer  had  under  observation  a  man  forty  years  of  age  who  was 
subject  to  palpitation  and  an  arrhythmia  brought  on  whenever  he  developed  gas  in 
the  stomach  or  intestines.  He  himself  was  able  to  distinguish  "  large  and  small  "beats 
among  the  palpitations,  and  tracings  with  modified  Erlanger  apparatus  from  veins  and 
arteries  bore  out  his  impressions.  It  is,  however,  difficult  to  decide  whether  these  small 
beats  represent  auricular  extrasystoles  or  whether  there  is  simply  a  rapid  rhythm  inter- 
rupted by  long  pauses  of  vagal  origin.  He  stated  that  nevertheless  he  was  able  to  "  out- 
walk his  doctors"  at  hill  climbing  during  periods  when  he  was  suffering  from  both  palpita- 
tion and  arrhythmia.  A  moderate  dose  (^  mg.  =  gr.  j^)  of  atropine  caused  dryness  of  the 
mouth  and  some  vertigo,  but  did  not  greatly  alter  the  pulse-rate  nor  cause  the  arrhythmia 
to  disappear.  The  patient  would  not  allow  a  larger  dose  to  be  given.  If  one  could  be  certain 
that  this  dose  had  paralyzed  the  vagus  the  extrasystolic  nature  of  the  arrhythmia  would 
be  established,  but  it  is  most  probable  that  the  vagus  was  but  little  affected  and  that  this 
evidence  cannot  be  regarded  as  conclusive. 

It  has  long  been  customary  to  designate  such  cases  as  "cardiac 
neuroses,  or,  from  the  neurasthenic  symptoms  which  are  most  striking 
to  the  physician,  as  "cardiac  neurasthenia."  On  closer  exami- 
nation, however,  it  may  usually  be  found  that  both  the  cardiac 
and  the  neurasthenic    symptoms    are  not  primary,   bul 


696  DISEASES  OF  THE  HEART  AND  AORTA. 

are  secondary  to  some  visceral  displacement  or  irritation, 
to  some  intoxication,  or  in  rarer  cases  to  some  primary 
intense  emotional  disturbance.1  The  heart  itself  is  sound,  but, 
owing  to  the  distribution  of  blood,  does  not  get  a  chance  to  do  the  work  of 
which  it  would  be  capable.  The  terms  "cardiac"  and  "neurasthenia"  are 
therefore  both  misleading,  and  it  might  perhaps  be  more  satisfactory  to  desig- 
nate such  conditions  by  the  adj ective  "pseudocardiac"  (" pseudocardiac 
enteroptosis,"  "pseudocardiac  gastralgia,"  "pseudocardiac  aerophagia,"  etc.). 

CLINICAL   GROUPINGS. 

Most  if  not  all  of  these  "cardiac  neurasthenias"  are  brought  on  by  the 
following  conditions: 

Alterations  of  the  position  of  the  heart  in  the  thorax. 

a.  Kyphoscoliosis,   narrowness  or  flatness  of  chest. 

b.  Cardioptosis   or  bathycardia  (low  heart), 

(1)  due  to  enteroptosis  (low  diaphragm), 

(2)  due  to  long  thorax  with  diaphragm  normal. 

c.  High  diaphragm  from 

(1)  flatus, 

(2)  fat, 

(3)  tight  lacing. 

Although  many  cases  arise  in  which  no  site  of  origin  can  be  found  for 
the  symptoms,  the  following  represents  a  few  of  the  more  common  causes : 

1.  Abnormal  position   of  the  heart, 

a.  From  curvature  of  the  spine. 

b.  From  pleural  adhesions. 

c.  Owing  to  a  low  diaphragm. 

2.  Visceral  reflexes. 

a.  Gastric,  oesophageal  and  intestinal. 

(1)  Air  swallowing. 

(2)  Gastritis,  gastralgias. 

b.  Sexual  organs. 

(1)  Sexual  excesses  (male  or  female). 

F  e  m  a  1  e — At  onset  of  menses  and  at  menopause;  at  menstruation; 
from  myoma  and  other  lesions  of  generative  organs. 
Male  s — Gonorrhoea,  prostatitis,  masturbation. 

3.  Intoxications. 

Tobacco. 

Alcohol. 

Coffee. 

4.  Anaemia. 

5.  Intense   emotional   disturbances. 

ALTERATIONS   IN   POSITION   OF   THE   HEART. 

DISPLACEMENT  OF  THE   HEART  FROM   MALFORMATIONS. 

The  displacement  of  the  heart  which  occurs  in  kyphosis  and  scoliosis 
is  often  the  cause  of  a  true  cardiac  weakness,  i.e.,  weakness  and  dyspnoea 
on  exertion  as  well  as  from  nervous  causes — a  so-called  constitutional  heart 
weakness  as  Kraus  terms  it. 


In  many  of  these  cases  sympathicotonic  or  vagotonic  is  well  marked  (see  page  19). 


DISTURBANCES  OF  CARDIAC  FUNCTION. 


697 


^r-TTj^v 


Fig.  322. — Cross  section  of  the  thorax  of 
a  fiat-chested  individual,  showing  the  systolic 
heaving  of  the  chest  wall  (broken  lines)  and 
the  forces  bringing  it  about.  The  outlines  of 
the  chest  wall  and  heart  during  the  systolic 
heaving  are  shown  by  the  dotted  lines  and 
obliquely  shaded  areas.  The  protrusions  and 
retractions  are  shown  by  the  arrows. 


The  patients  are  usually  pale,  rather  weak,  and  readily  become  ex- 
hausted and  cyanotic,  and  manifest  all  the  cardioneurotic  symptoms. 
The  actual  cause  of  the  trouble  lies  not  so  much  in  the  heart  as  in  the  posi- 
tion in  which  it  is  placed  in  the  thorax.     Pressure  and  tractions  upon  both 

the  venae  cavse  and  the  arteries  render 
both  inflow  and  outflow  difficult,  and 
thus  bring  about  a  high  venous  and 
a  low  arterial  pressure,  with  the 
symptoms  which  follow  in  its  wake. 
Kraus  and  recently  Herz  have 
called  attention  to  the  cardioneurotic 
symptoms  which  occur  in  all  narrow- 
chested  individuals.  Herz  calls  atten- 
tion to  the  fact  that  in  such  cases 
there  is  a  tremendous  lifting  of  the 
ribs  and  precordium  with  each  sys- 
tolic erection  of  the  heart.  This  is 
due  to  the  short  anteroposterior  and 
especially  oblique  diameter  of  the 
chest,  so  that  the  heart  pivoted 
against  the  posterior  chest  wall  must 
push  out  the  left  anterior  wall  in  order  to  complete  its  systole  (cf.  Fig.  326). 
As  will  be  noted,  this  condition  is  quite  different  from  that  which  results 
from  the  low  diaphragm  or  from  cardioptosis,  for  in  those  conditions  the 
heart  either  beats  in  the  long  axis  of  the  thorax,  or  from  its  mobility  can 
adapt  itself  to  a  narrower  chest. 

LOW  HEART. 

Even  when  there  are  no  malformations  of  the  chest,  conditions  arise 
in  which  the  position  of  the  heart  within  the  thoracic  cavity  is  altered, 
and  these  give  rise  to  cardioneurotic  symptoms.     These   conditions  are: 

I.  Cardioptosis  (wandering  or  movable  heart),  in  which  the  mediastinal 
attachments  are  loose  and  the  heart  readily  moves  from  side  to  side,  as 
well  as  up  and  down. 

II.  Bathycardia  (low  or  unsupported  heart),  in  which  the  heart  lies 
low  in  the  thorax  because  the  dome  of  the  diaphragm  is  lower  than  normal. 
This  is  sometimes  due  to  hepatoptosis  and  sometimes  to  a  congenitally 
low  liver. 

III.  The  high  heart  (high  diaphragm),  from  various  causes,  especially 
flatulence,  fat,  lacing,  and  during  pregnancy. 


MOVABLE    HEART    (CARDIOPTOSIS) . 

Cardioptosis,  or  extreme  mobility  of  the  heart  as  shown  on  change 
of  position,  was  first  described  by  Glenard  (1885)  and  by  Cherchevsky 
(1887).  The  latter  observer  noted  that,  while  the  borders  of  the  normal 
heart  move  1-3  cm.  when  the  patient  turns  from  the  left  side  to  the  right 
(while  lying  down),  a  certain  number  of  cases  (2.4  per  cent,  of  all  cases, 
according  to  Einhorn)  are  encountered  in  which  it  moves  from  4-7  cm. 


698  DISEASES  OF  THE  HEART  AND  AORTA. 

without  any  other  changes  or  any  enlargement  of  the  heart.  As  a  rule, 
the  symptoms  date  from  some  time  when  the  patient  has  lost  in  weight, 
perhaps  because  the  disappearance  of  mediastinal  and  omental  fat  causes 
the  organs  to  become  looser  than  before.  Einhorn  has  found  it  much  more 
common  in  men  (18  cases)  than  in  women  (4  cases)  and  always  associated 
with  hepatoptosis;  though  in  cases  like  that  given  below  the  element  of 
hepatoptosis  may  be  absent. 

Case  of  Cakdioptosis. 

This,  as  well  as  the  other  symptoms,  is  beautifully  illustrated  by  a  case  which  the 
writer  has  recently  seen  in  consultation  with  Dr.  L.  P.  Hamburger.  The  patient,  aged  31, 
had  been  a  trained  nurse  since  18.  Her  father  had  died  of  enlarged  heart  and  her  mother 
died  suddenly.  Except  for  scarlet  fever,  whooping-cough,  and  measles  as  a  child,  she  had 
been  perfectly  healthy  until  the  age  of  19,  when  a  dermoid  cyst  of  the  left  ovary  caused 
profuse  menstrual  bleedings.  This  was  removed  and  the  wound  drained.  Adhesions 
formed,  causing  headaches  and  backaches  and  finally  a  nervous  break-down,  so  that  a 
second  operation  was  done  nine  years  later  to  relieve  the  adhesions.  At  the  time  of  this 
operation  she  lost  14  pounds  and  was  very  nervous,  and  during  her  early 
convalescence  had  a  syncopal  attack  during  which  her  hands  and  forearms  became 
completely  blanched.  One  year  later  the  patient  felt  her  first  cardiac  symp- 
toms, suffering  palpitation,  and  when  lying  down  has  a  feeling  "as  though  the  heart 
were  turning  over"  or  "like  a  rubber  bulb  or  sponge  being  squeezed  out."  She  then  feels 
sick  and  has  a  feeling  of  oppression  in  the  chest. 

Physical  examination  shows  a  fairly  nourished  young  woman  of  good 
color;  pupils  equal  and  no  signs  of  Basedow's  disease.  The  left  lobe  of  the  thyroid  is  slightly 
hard,  but  that  organ  is  rather  small. 

The  thorax  is  quite  well  formed,  not  especially  flat.  Costal  angle  normal.  Lungs 
clear.  The  heart  is  not  enlarged  and  the  sounds  are  clear.  On  turning  from  side 
to  side,  however,  the  heart  moves  8  cm.  The  pulse  is  of  good  volume 
and  shows  a  well-marked  respiratory  irregularity  of  the  type  described  above,  but  no 
extraeystoles.  The  abdominal  walls  are  soft  but  not  especially  lax;  the  liver  does  not 
descend  when  the  patient  stands,  but  the  right  kidney  is  palpable. 

Bromides,  nitroglycerin,  and  strophanthus  have  been  without  avail;  tincture 
of  belladonna  has  somewhat  quieted  her  cardiac  symptoms.  The 
intensity  of  the  symptoms  seems  to  vary  with  her  general  condition.  Upon  being 
assured  of  the  trivial  nature  of  her  complaint,  her  symptoms 
immediately   disappeared. 

Several  months  later  she  reported,  however,  that  they  reappeared  from  time  to  time 
during  periods  when  she  was  fatigued  or  nervous.  The  presence  or  absence  of  symptoms 
was  always  quite  independent  of  the  mobility  of  the  heart.  In  spite  of  her  gain  in  weight 
and  the  improved  condition  under  treatment,  the  cardiac  borders  moved  at  least  7  cm. 
during  the  periods  when  she  was  free  from  symptoms. 

Treatment.  —  The  treatment  of  cardioptosis  presents  a  number  of  dif- 
ficulties. As  seen  from  the  case  cited  above,  the  symptoms  depend  not 
only  upon  the  actual  mobility  of  the  heart  but  also  upon  the  general 
condition  of  the  patient's  nervous  system.  It  is  the  latter  which  deter- 
mines whether  or  not  the  afferent  impulses  from  the  heart  shall  reach  the 
threshold  of  consciousness.  Accordingly,  the  unpleasant  cardiac  sensa- 
tions may  be  present  only  when  the  irritability  of  the  nervous  system  is 
increased  by  fatigue,  anaemia,  or  other  affections;  so  that  relief  of  the 
latter  by  general  measures  relieves  the  cardiac  symptoms  as  well,  without 
affecting  their  underlying  cause.  The  mobility  of  the  heart  itself  cannot 
be  treated  directly;  but  it  is  sometimes  possible,  by  overfeeding,  to 
cause  a  sufficient  deposit  of   fat  in  the    mediastinum    and    pericardium 


DISTURBANCES  OF  CARDIAC  FUNCTION. 


699 


to  diminish  the  movements  a  little.  Even  when  unsuccessful  in  this 
way,  however,  overfeeding  often  aids  by  improving  the  general  condition 
and  nervous  tone. 

GENERAL    SPLANCHNOPTOSIS. 

The  mechanism  which  gives  rise  to  the  cardiac  symptoms  of  splanch- 
noptosis (enteroptosis)  has  been  investigated  anatomically  by  Keith  and 
clinically  by  Wenckebach.  The  latter  found,  by  means  of  the  X-ray 
(fluoroscope),  that  the  most  important  effect  of  enteroptosis  was  to  remove 
the  support  of  the  liver  and  stomach  from  beneath  the  diaphragm.  The 
dome  of  the  diaphragm  was  thus  usually  seen  to  be  flattened 
and  to  be  situated  a  good  deal  lower  than  normal. 


Fig.  323. — The  low,  normal  and  high  hearts.  (Semi-schematic.)  I,  first  rib;  X,  tenth  rib;  VII, 
VIII,  spines  of  seventh  and  eighth  thoracic  vertebra?.  The  horizontal  line  represents  the  "xiphisternal 
line"  passing  through  the  sterno-xiphisternal  articulation.  The  small  white  arrow  represents  traction 
upon  the  trachea.     A,  low  heart;   B,  normal  heart;   C,  high  heart. 

The  normal  summit  of  the  dome  in  quiet  expiration  is  just  above  the  level 
of  the  fifth  rib,  and  its  horizontal  shadow  just  obscures  that  of  the  tenth  rib  behind. 
Keith  finds  that  this  is  normally  about  1  cm.  above  the  ''xiphisternal  line,'* 
a  horizontal  line  representing  the  level  of  the  sternoxiphoid  articulation.  The  upper  border 
of  the  fifth  rib  at  the  junction  with  the  cartilage  is  just  at  this  level.  In  enteroptosis  Wencke- 
bach is  able  to  see  the  X-ray  shadow  of  the  origin  of  the  tenth  and  often  the  eleventh  rib 
above  the  dome  of  the  diaphragm,  and  the  latter  lies  well  below  the  xiphisternal  line. 

The  writer  finds  that  for  ordinary  purposes  the  most  convenient  landmarks  are  the 
xiphisternal  articulation  and  the  tip  of  the  spine  of  the  eighth  thoracic  vertebra,  which 
is  just  above  the  upper  border  of  the  tenth  rib.  The  xiphisternal  articula- 
tion, the  dome  of  the  diaphragm,  and  the  tip  of  the  eighth  tho- 
racic spine  are  normally  on  a  level.  In  enteroptosis  and  low  diaphragm 
the  ribs  drop  so  that  first  two  structures  are  below  the  eighth  spine,  while  with  a  high 
diaphragm  the  ribs  are  raised  so  that  they  are  above  it  (Fig.  327) . 

Effect  on  Respiration. — The  effect  of  this  low  position  of  the  diaphragm 
is  exerted  both  upon  the  respiration  and  the  heart.  The  abdominal  respira- 
tion, which  is  due  to  the  descent  of  the  liver,  is  much  diminished.  For 
when  the  dome  of  the  diaphragm  is  flattened,  shortening  of  the  diaphragm 
does  not  push  down  the  liver,  but  pulls  upon  the  lower  ribs  in  a  hori- 
zontal or  even  upward  direction.     The  effect  of  this  pull  upon  the  lower 


700  DISEASES  OF  THE  HEART  AND  AORTA. 

ribs  (Fig.  327,  A)  is  to  narrow  the  cross  section  of  the  thorax  (Duchenne) 
at  this  level  and  to  draw  the' epigastrium  inward,  and  thus 
by  diminishing  the  air  capacity  in  this  portion  of  the  lungs  to  decrease 
greatly  the  effect  of  inspiration  both  in  sucking  air  and  in  sucking  blood 
into  the  thorax.  This  is  the  so-called  ''paradoxical  type  of 
respiration.''  Naturally,  its  effect  is  to  diminish  the  intake  of  air 
and  thus  greatly  to  enhance  the  effect  of  any  cardiac  insufficiency. 

Effect  on  Circulation. — On  the  other  hand,  the  lessened  up-and-down 
movement  of  the  diaphragm,  coupled  with  the  relaxation  of  the  abdominal 
walls,  greatly  diminishes  the  force-pump  and  suction-pump  action  by 
which  the  blood  in  the  abdominal  veins  is  forced  onward  to  the  thorax. 
There  is,  therefore,  a  tendency  for 
the  blood  to  stagnate  in  the  abdomi- 
nal viscera.  The  venous  pressure 
becomes  low.  In  consequence,  as 
Henderson  and  the  writer  have  shown, 
the  filling  of  the  heart  is  less  complete 
and  the  systolic  output  is  diminished. 

Leonard  Hill  has  shown  that  if  a 
rabbit  is  supported  in  the  erect  posture 
with  feet  down  and  head  down,  the 
blood-pressure  falls  and  cerebral  anae- 
mia sets  in.  If  one  presses  on  the 
animal's  abdomen,  the  blood-pressure 

.  '  ,  -17,   i  j     tt       i  Fig.  324. — Radiograph  of  a  patient  with  drop- 

rises   at  once.    Erlanger  and   Hooker      ping  heart  (bathycardia).    (After  Brugsch  and 

found    that    when     normal     men    Were        Schittenhelm.)  The  cardiac  shadow  is  separated 
.  ,   .  .       ,  •       ,  i  from  that  of  the  diaphragm  by  a  well-defined 

supported  and  kept  motionless  in  the      space. 

vertical    posture,   the    blood-pressure 

fell  (e.g.,  maximum  fell  from  120  mm.  to  103  mm.,  minimal  from  92.5  mm. 

to  86  mm.,  pulse-pressure  from  26.7  mm.  to  17  mm.1),  and  in  one  case  there 

was  "pallor,    yawning,    a    feeling    of   warmth,    faintness,    nausea,"    and 

threatened  syncope.    These  are  the  symptoms  of  arterial  anaemia  common 

in  patients  with  enteroptosis. 

The  low  position  of  the  diaphragm  exerts  another  effect  upon  the  heart. 
The  diaphragmatic  platform  on  which  it  rests  drops  away  like  a  trap-door 
and  leaves  it  suspended  from  the  great  vessels  and  vertebral  column  by 
the  aorta,  trachea,  mediastinum,  and  fasciae.  The  heart  thus  lies  in  the 
longitudinal  axis  of  the  body;  and,  in  systole,  the  apex  can  be  seen  to  rise 
and  to  pull  down  on  the  trachea  instead  of  moving  inward.  As  Osier  and 
Wenckebach  have  shown,  a  tracheal  tug  may  often  be  felt  and  this 
may  lead  to  a  mistaken  diagnosis  of  aneurism.  However, 
this  error  may  be  obviated  when  the  enteroptosis  is  taken  into  considera- 
tion, and  especially  when  the  tug  diminishes  upon  pressing  the  liver  upward 
and  inward. 

Moreover,  when  the  low  diaphragm  descends  in  inspiration  it  exerts 
further  traction  upon  the  mediastinum  and  thus  upon  the  aorta  as  well 
as  upon  the  great  veins,  thus  bringing  about  an  inspiratory  diminution 

1  The  fall  in  pulse-pressure  denotes  diminished  systolic  output- 


DISTURBANCES  OF  CARDIAC  FUNCTION.  701 

or  dropping  of  the  pulse-beats  (pulsus  paradoxus),  exactly 
like  that  occurring  in  pericarditis,  which  the  appearance  of  the  patient 
may  suggest. 

Physical  Signs. — The  upper  border  of  cardiac  dulness  in  these  cases 
does  not  usually  extend  above  the  third  rib.  The  total  area  and  the  area 
of  the  cardiac  shadow  are  usually  diminished  and  the  area  of  flatness  com- 
pletely obliterated.  The  attachments  of  the  heart  have  reverted  to  the 
embryonic  type,  and  that  organ  is  suspended  by  the  elongated  pericardiac 
ligament.  The  a  p  e  x  is  usually  inside  the  mammillary  line.  In  extreme 
cases  the  right  ventricle  is  seen  to  beat  in  the  epigastrium;  but  this  often 
signifies  only  a  dilatation  of  that  chamber.  The  sounds  are  usually  clear, 
but  either  sound  may  be  reduplicated.  There  is  usually  a  soft  systolic 
murmur  of  accidental  type  over  the  area  of  the  right  ventricle,  or  occa- 
sionally at  the  apex. 

The  abdomen  is  often  flat,  and  usually  shows  marked  linese 
albicantes.  The  disappearance  of  subcutaneous  fat  makes  the  walls  flabby 
and  the  viscera  are  easy  to  palpate.  The  liver  can  almost  always  be  felt 
when  the  patient  is  sitting  or  standing.  The  kidneys  are  usually  palpa- 
ble and  movable.  When  the  patient  stands,  the  viscera  gravitate  to  the 
hypogastrium,  where  a  fulness  is  seen,  giving  the  abdomen  the  profile  of 
an  interrogation  point  turned  upside  down  (i). 

Pathogenesis. — Enteroptosis  is  far  more  common  in  women  than  in 
men,  owing  to  the  stretching  of  the  abdominal  muscles  and  relaxation  of 
the  perineal  floor  in  pregnancy  and  labor.  Hence  it  occurs  more  frequently 
in  women  who  have  not  remained  in  bed  long  enough  during  the  puerperium. 
Nevertheless,  it  is  also  common  in  single  women  and  in  men  whose  abdom- 
inal muscles  are  atonic  from  lack  of  exercise,  or  in  persons  who  from  any 
cause  have  rapidly  lost  weight.  The  rapid  disappearance  of  the  intra- 
abdominal fat  uncompensated  by  contraction  of  the  abdominal  muscles 
takes  away  the  support  from  the  liver  and  facilitates  the  occurrence  of 
enteroptosis.  Indeed  this  latter  factor  is  often  more  important  than  the 
muscular  element,  and  it  is  not  uncommon  to  find  most  typical  examples 
of  enteroptosis  in  thin  persons  whose  abdominal  walls  are  not  abnormally 
flaccid. 

Tight  lacing,  as  well  as  causing  atony  of  the  abdominal  walls,  causes 
the  viscera  to  tug  at  their  ligamentous  moorings  and  finally  to  stretch 
them,  and  thus  bring  on  an  enteroptosis.  However,  while  the  corset  is 
being  worn  it  pushes  the  liver  and  diaphragm  up,  the  pelvic  organs  down. 
The  typical  corset  heart  is  the  high  heart  and  not  the  low  heart  (see 
Fig.  327,  C).  It  is  only  when  the  corset  is  taken  off  that  the  heart  and 
abdominal  organs  drop. 

Treatment. — The  treatment  follows  from  the  mechanical  conditions. 
It  is  all-important  to  push  up  the  liver.  Fr.  Glenard,  who  first  described 
enteroptosis,  showed  that  symptoms  were  relieved  by  merely  pressing  up- 
ward on  the  abdomen  with  the  hand  (just  as  in  Leonard  Hill's  rabbit  experi- 
ment), and  hence  one  of  the  oldest  forms  of  treatment  is  the  tightly  fitting 
abdominal  binder.  A  specially  made  corset  arranged  so  as  to  bring  an 
upward  pressure  upon  all  the  structures  befow  the  costal  margin  gives 
excellent  results,  especially  when  supplemented  by  pads  over  the  kidneys. 


702  DISEASES  OF  THE  HEART  AND  AORTA. 

Probably  the  best  form  is  an  adjustable  air  cushion  resting  upon  an  alumi- 
num plate  that  is  strapped  to  the  abdomen  (Wenckebach).  For  a  time 
the  attention  of  physicians  had  been  directed  to  the  individual  organ, 
especially  the  kidneys,  and  these  organs  were  sutured  into  place.  But 
experience  has  shown  that  this  only  remedies  a  small  part  of  the  trouble 
and  does  not  remove  the  real  cause. 

The  only  method  of  real  physiological  therapy  is  one  which  will  at 
once  give  support  to  the  viscera  within  the  abdomen  and  also  restore  the 
tonic  contraction  of  the  abdominal  wall.  This  can  be  accomplished  by 
accumulation  of  fat  and  by  exercise.  The  former  procedure 
is  the  one  to  be  attempted  first.  If  the  patient  can  be  kept  at  absolute 
rest  in  bed  and  overfed  with  a  diet  containing  about 
3500  or  4000  calories  in  twenty-four  hours,  a  good  deal  of  fat  may 
be  accumulated  in  about  six  weeks.  The  principal  addition  to  the  diet 
should  be  olive  oil  (15  to  25  c.c.  three  times  a  day  =  about  500  calories 
per  day  or  about  60  Gm.  (2  oz.)  of  adipose  tissue).  This  can  he  taken 
between  meals,  pure  or  flavored  with  a  little  lemon,  sherry,  brandy,  etc., 
to  suit  the  palate.  It  is  most  important  that  the  patient's  digestion  should 
not  be  disturbed  by  it.  Salads  with  dressing,  thick  soups,  and  cereals 
(especially  with  cream)  should  be  given  in  as  large  quantities  as  the  patient 
will  take,  and  she  should  be  encouraged  to  drink  milk  instead  of  water. 
Butter  and  cheese  are  also  valuable  additions  to  the  diet  when  the  patient 
can  be  made  to  take  them  in  liberal  amounts.  Cakes,  sweets,  and  even 
puddings  fall  into  the  same  category,  provided  digestion  is  perfect.  She 
should  receive  milk  or  cocoa  between  meals  and  before  going  to  sleep  at 
night.  In  short,  every  means  should  be  adopted  to  overfeed  the  patient. 
On  the  other  hand,  it  must  be  remembered  that  if  her  digestion  be  spoiled 
in  the  process,  it  will  be  impossible  to  secure  a  permanent  gain  in  weight, 
so  that  the  process  must  be  begun  gradually  and  the  patient's  appetite 
should  be  stimulated  to  keep  pace  with  the  diet. 

In  order  that  the  fat  should  be  deposited  in  the  places  where  it  will 
give  the  most  support  {i.e.,  the  retroperitoneal  tissue  and  gastrohepatic 
omentum),  the  patient  should  be  made  to  lie  with  a  pillow  under  the  small 
of  the  back  for  as  many  hours  as  possible. 

The  result  of  the  rest  and  overfeeding  treatment,  supplemented  by 
careful  bandaging,  is  most  gratifying.  With  the  return  of  intra-abdom- 
inal fat  the  patients  usually  improve  in  health  and  spirits,  symptoms  sub- 
side, and  the  element  of  cardiac  weakness  may  entirely  disappear.  The 
patient's  confidence  in  herself  (or  himself)  returns  and  the  neurasthenia 
subsides. 

Case  of  Enteroptosis. 

The  following  case,  under  the  writer's  care  in  the  Johns  Hopkins  Hospital  Dispensary, 
illustrates  the  course  of  the  condition  and  the  excellent  results  obtainable  by  treatment. 

Mrs.  Agnes  L.,  aged  31,  first  seen  Feb.  19,  1909.  Complains  of  loss  of  strength, 
weakness,  and  palpitation,  especially  on  exertion.  She  is  nervous 
and   readily  exhausted.     Has  had  no  swelling  of  the  feet. 

Family  history  negative.  Patient  was  always  healthy,  but  has  had  diphtheria  and 
is  subject  to  sore  throat.  Chlorosis  at  16.  Bowels  constipated.  Menstruation  regular 
but  painful.  She  has  had  two  children  but  no  miscarriages.  Drinks  coffee  and  tea  in 
moderation. 


DISTURBANCES  OF  CARDIAC  FUNCTION. 


703 


Present  trouble  dates  from  birth  of  last  child  four  years  ago.  She  feels 
tired  all  the  time  and  is  subject  to  weakness  and  palpitation  after  exertion.  She  sleep9 
well,  however.  Her  feet  are  never  swollen.  Two  years  ago  she  was  treated  by  another 
physician  for  the  same  trouble,  which  was  then  diagnosed  neurasthenia.  She  was  overfed 
and  made  to  lie  down  every  day.  Gained  weight  and  improved  somewhat,  but  has  lost 
weight  since  then. 

Physical  examination  shows  a  fairly  nourished  woman,  tall  and  sparely 
built.  Her  eyes  and  cheeks  are  sunken,  and  expression  is  one  of  depression.  Her  color 
is  pale,  but  the  haemoglobin  is  90  per  cent.  Thyroid  is  not  enlarged.  No  glandular  enlarge- 
ment. Thorax  is  long  and  flat  and 
held  in  the  position  of  expiration.  Costal  angle 
is  very  acute.  There  are  a  few  rales  at  the 
left  apex  (which  were  not  present  on  subse- 
quent examinations).  The  upper  border  of 
cardiac  dulness  begins  at  the  third  rib  and 
extends  in  the  fifth  interspace  to  the  left 
mammillary  line  and  in  the  fourth  30  cm.  to 
the  right  of  the  midline.  Owing  to  the  form 
of  the  patient's  chest,  however,  the  fifth  left 
interspace  is  situated  at  a  lower  level  (referred 
to  the  spine)  than  is  normal.  The  cervico- 
xiphoid  distance  is  long.  Heart  sounds  are 
clear  and  pulse  is  regular. 

Abdomen  . —  The  liver  extends  below 
the  costal  margin.  There  is  marked  gastrop- 
tosis,  the  stomach  lying  below  the  umbilicus. 
Both  kidneys  palpable.    Genitalia  negative. 

Extremities.  —  Sensation  and  re- 
flexes normal. 

Patient  was  given  an  abdominal 
bandage  and  encouraged  to  full  diet, 
especially  rich  in  butter,  milk,  eggs,  and  salad. 
Besides  this  one  tablespoonful  of  olive  oil 
three  times  a  day.  She  was  made  to  rest 
and  lie  down  several  hours  a  day  with  a 
pillow  under  the  small  of  her 
back  to  favor  deposition  of  perirenal  fat. 
Within  an  hour  after  the  abdominal  binder  was  first  put  on 
her  condition  was  markedly  improved,  her  expression  was  brighter,  and 
she  felt  more  active.  The  patient,  however,  still  stood  with  stooping  shoulders,  which 
caused  the  chest  to  continue  in  the  position  of  expiration  and  allowed  the  heart  to  hang 
low.  This  position  was  improved  by  the  use  of  shoulder  braces.  The  patient's  condition 
and  strength  steadily  improved  and  her  cardiac  symptoms  had  entirely  disappeared  after  the  - 
abdominal  bandage  was  put  on.  The  gain  in  weight  during  three  months  was  only  3£  pounds. 


Fig.  325. — Photograph  of  a  patient  with  en- 
teroptosis.  The  upper  border  of  cardiac  dul- 
ness begins  at  the  third  rib  (III);  the  heart  is 
small  and  lies  vertically.  The  liver  is  low  and 
palpable. 


Case  of  Enteroptosis  Simulating  Aneurism  of  the  Descending  Aorta. 

P.  R.,  a  wool  sorter,  aged  42,  came  to  the  Johns  Hopkins  Hospital  Dispensary  on 
March  5,  1909,  complaining  of  a  drawing  pain  in  both  sides  and  in  the  epi- 
gastrium. The  family  history  and  personal  history  were  negative.  The  patient  denies 
lues,  but  has  had  to  lift  heavy  sacks  in  his  work.  His  pain  began  about  six  weeks  before 
admission  while  he  was  at  work  and  was  accompanied  by  palpitation,  and  it  has 
continued  since  then. 

The  patient  was  a  well-nourished  man  of  good  color.  The  left  pupil  was 
larger  than  the  right,  but  both  reacted  to  light  and  accommodation.  The  thorax 
was  long  and  there  was  a  slight  funnel  breast.  The  lungs  were  clear  on  percussion  and 
auscultation.  The  area  of  cardiac  dulness  was  slightly  smaller  than  normal;  dulness 
began  above  at  the  lower  border  of  the  third  rib,  extended  7.5  cm.  to  the  left  in  the  fifth 
left  interspace  and  2.5  cm.  to  the  right  of  the  midline.  The  heart  moved  6  cm.  on 
change  of  position.    The  apex  is  3  cm.  below  the  xiphisternal  line.    The  left   radial 


704  DISEASES  OF  THE  HEART  AND  AORTA. 

pulse  was  slightly  smaller  than  the  right.  There  was  well  marked  pul- 
sation in  the  epigastrium,  and  the  liver  was  well  seen  and  readily  felt 
below  the  costal  margin.  There  was  a  well-marked  tracheal  tug 
which  diminished  when  the  liver  was  pushed  upwards  with 
the    hand . 

The  fluoroscopic  examination  by  Dr.  Baetjer  showed  that  the  aorta  was  clear.  An 
abdominal  binder  was  applied.  The  abdominal  pains  and  palpitation  ceased  and  the 
tracheal  tug  diminished  markedly.  The  patient  was  able  to  continue  work  without  dis- 
comfort.   His  pains  have  been  absent  for  over  a  year. 

LOW   HEAKT    WITHOUT    ENTEROPTOSIS    (bATHYCARDLA.). 

There  is  another  type  of  long,  flat-chested  individuals  in  whom,  al- 
though there  is  no  enteroptosis,  the  diaphragm  is  low.  The  dome  of  the 
diaphragm  is  not  flat,  but  is  well  arched.  The  insertion  of  the  diaphragm 
may  be  somewhat  lower,  and  the  length  of  the  thoracic  cage,  which  is  held 
in  the  position  of  expiration,  is  considerably  greater  than  normal  (Fig. 
327,  A).  As  a  result  of  this  lengthening  of  the  thorax,  the  distance  from 
the  structures  upon  which  the  heart  hangs  (aorta,  trachea,  mediastinum) 
to  the  diaphragm,  which  supports  it,  is  lengthened,  and  just  as  in  enterop- 
tosis the  heart  hangs  free  above  the  diaphragm.  It  is  therefore  termed 
the  "hanging  heart"  or  "dropping  heart."  It  pulls  upon  the  trachea  in 
systole  and  causes  a  tracheal  tug.  It  pulls  upon  the  aorta  in  inspiration 
and  causes  a  pulsus  paradoxus.  The  interference  with  cardiac  filling  and 
with  the  abdominal  circulation  gives  rise  to  about  the  same  symptoms 
of  cardiac  weakness  as  are  encountered  in  enteroptosis,  though  often  to 
a  less  marked  degree. 

The  diagnosis  is  usually  best  made  with  the  fluoroscope;  for  the  pres- 
ence of  a  mild  brachial  impulse  and  pulsus  paradoxus  may  cause  the  con- 
dition to  be  mistaken  for  either  aneurism  or  mediastinitis.  There  may 
even  be  a  slight  tugging  on  the  low  diaphragm  (Broadbent's  sign)  at  the 
depths  of  respiration.  It  is  extremely  difficult  to  exclude  mediastino- 
pericarditis  in  many  cases  in  which  the  palpitation,  pallor,  fatigue,  short- 
ness of  breath,  paradoxical  pulse,  etc.,  are  intense.  In  some  cases  with 
reduplicated  first  sound  mitral  stenosis  may  be  thought  of.  Absence  of 
hypertrophy  of  the  left  ventricle  (cardiac  dulness  inside  mammillary  line) 
should  exclude  organic  mitral  insufficiency  even  in  the  presence  of  a  sys- 
tolic murmur.    The  diagnosis  is  made  chiefly  on  fluoroscopic  examination. 

Treatment. — As  the  condition  is  due  to  the  low  diaphragm,  just  as  in 
actual  enteroptosis,  the  chief  indication  is  to  raise  the  diaphragm.  In 
bringing  this  about  with  normal  abdominal  walls  a  bandage  is  of  some  avail, 
but  fattening  is  not  successful. 

On  the  other  hand,  the  obliquity  of  the  ribs  is  also  at  fault,  and  this 
can  be  corrected  by  training  the  patient  to  take  deep  inspirations  and  to 
stand  with  his  shoulders  and  hips  thrown  back. 

HIGH    DIAPHRAGM. 

The  exact  opposite  condition,  that  in  which  the  diaphragm  is  so  high 
that  the  heart  is  placed  in  a  position  in  which  it  works  at  a  disadvantage 
(probably  by  interference  with  venous  inflow),  is  found  in  fat  persons,  in 
many  dyspeptics  with  flatulence,  in  emphysema,  and  in  women  as  a  result 


DISTURBANCES  OF  CARDIAC  FUNCTION.  705 

of  tight  lacing.  In  the  first  three  conditions  there  is  diminished  respiratory 
movement,  especially  the  costal  movements,  since  the  ribs  in  most  cases 
are  held  in  the  position  of  expiration  and  the  possible  excursion  thus  dimin- 
ished; while  in  persons  who  lace  tightly  abdominal  respiration  is  impeded 
and  the  respiration  is  mainly  costal.  In  these  cases  the  heart  is  raised  by 
the  diaphragm,  especially  in  inspiration,  and  thus  comes  to  lie  more  trans- 
versely to  the  axis  of  the  body.  In  such  persons  the  xiphisternal  articula- 
tion lies  above  the  level  of  the  eighth  thoracic  spine,  the  diaphragm  shadow, 
according  to  Wenckebach,  obscuring  the  ninth  and  tenth  ribs.  The  apex 
lies  in  the  fourth  interspace  outside  the  mammillary  line,  often  leading 
to  the  suspicion  of  valvular  lesion  or  myocarditis. 

This  pushing  up  of  the  heart  tends  to  impede  the  heart's  action  and 
to  produce  fall  of  arterial  pressure,  as  was  first  shown  by  v.  Frey  and  Krehl 
in  1890. 

The  clinical  result  of  these  conditions  is  to  produce  a  syndrome  not 
unlike  that  of  the  exactly  opposite  conditions,  "cardioptosis"  and  "drop- 
ping heart," — i.e.,  a  diminished  cardiac  filling, — and  is  undoubtedly  in  a 
large  measure  responsible  for  many  of  the  symptoms  of  the  "heart  of 
obesity"  and  of  indigestion. 

Treatment  must  be  directed  to  the  cause, — regulation  of  diet  for  the 
fat  and  dyspeptic,  loosening  of  the  corset  for  the  woman  who  laces.  How- 
ever, the  latter  should  be  done  gradually  enough  to  give  the  abdominal 
walls  time  to  adjust  themselves,  lest  a  true  splanchnoptosis  replace  it. 


REFLEX    CARDIAC   DISTURBANCES. 

GASTROINTESTINAL. 

Patients  with  chronic  gastro-intestinal  disturbances  often  come  to 
consult  the  physician  for  the  cardiac  symptoms  which  these  bring  about, 
— namely,  palpitation,  pain  in  the  region  of  the  heart,  tachycardia,  and 
often  irregularity  of  the  pulse,— -symptoms  which  are  all  more  deeply 
impressed  on  the  patient's  mind  than  are  the  heart-burn  and  belching  from 
the  underlying  indigestion. 

As  has  been  seen  in  connection  with  angina  pectoris,  gastric  disturb- 
ances may  cause  cardiac  symptoms.  The  motor  disturbances  (arrhythmia, 
tachycardia,  etc.)  are  in  a  large  part  due  to  the  spread  of  stimuli  from 
the  gastric  branches  of  the  vagus  to  the  cardiac,  while  the  sensory  symp- 
toms are  due  in  part  to  false  reference  of  impressions,  in  part  to  a 
similar  spreading  of  stimuli,  and  in  part  to  an  associated  hypersestheria  of 
these  branches  of  the  vagus. 

The  chief  irritants  are  butyric  and  lactic  acids  (acid  fermentation), 
excess  of  hydrochloric  acid,  and  the  gases  of  fermentation, — C02  (40  per 
cent,  in  the  absence  of  HC1),  H2,  N2,  02,  H2S,  and  often  CH4  (inflammable) 
in  butyric  acid  fermentation  (Hoppe-Seyler). 

Air  Swallowing. — One  of  the  most  important  factors  in  pseudocardiac 
dyspepsia  is  air  swallowing.  As  Wyllie  has  shown,  it  is  extremely 
common  for  persons  suffering  from  slight  gastric  discomfort  to  find  them- 
selves relieved  by  belching.     As  a  result  they  seek  further  relief  by  forcing 

45 


706  DISEASES  OF  THE  HEART  AND  AORTA. 

themselves  to  belch.  The  forced  belching  gives  only  momentary  relief, 
but  aggravates  the  discomfort,  giving  rise  to  a  familiar  sensation  of  an 
object  lying  just  behind  the  larynx.  They  belch  again  to  remove  it,  and 
the  belching  is  thus  continued  indefinitely,  always  accompanied  by  a  cer- 
tain discomfort  and  often  by  a  loud  noise. 

Mechanism  of  Aerophagia. — Wyllie  and  others  have  shown  that  the  mechanism 
of  involuntary  and  voluntary  belching  is  quite  different.  In  the  former 
case  an  excess  of  the  gases  of  fermentation  is  regurgitated  from  the  stomach,  and  this 
can  occur  only  when  there  is  an  excess  of  gas.  In  the  latter  case  the  patient  first  swal- 
lows or  gulps  the  air  by  placing  the  tongue  against  the  roof  of  the  mouth  (in  the  position  of 
pronouncing  the  consonant  "T"  and  then  exerting  a  deep  inspiration.  These  movements 
force  the  air  into  the  oesophagus.  It  remains  there  an  instant,  and  may  then  be  either 
swallowed  or  expelled  by  a  forced  expiration  with  the  glottis  closed,  causing  the  loud 
noise  of  belching  as  it  forces  apart  the  vocal  cords  and  pushes  up  the  epiglottis.  Most 
often  part  of  the  air  is  swallowed  and  part  regurgitated,  and  a  few  bubbles  of  air  remain 
in  the  oesophagus  most  of  the  time,  giving  rise  not  only  to  the  feeling  of  discomfort  but 
often  to  reflex  cardiac  disturbances.  Wyllie  calls  attention  to  the  fact  that  air  gulping 
occurs  not  only  in  man  but  also  in  horses  and  cattle,  where  the  condition  is  known  as 
"  wind  colic  "  and  "  hoven,"  which  often  becomes  so  severe  that  it  may  cause  the  death 
of  the  animal.  The  symptoms  are  "  difficult  breathing,  bloodshot  eyes,  red  mucous 
membrane,  loud  tumultuous  heart-beat,  trembling  of  front  legs,  etc."  This 
can  be  brought  about  in  dogs  by  inflating  either  stomach  or  intestines  with  air  under 
pressure,  paralysis  and  heart-failure  resulting.  Wyllie  believes  that  the  condition  is  still 
more  common  in  infants  and  in  children,  and  thinks  that  it  is  responsible  not  only  for 
wind  colic  but  for  certain  cases  of  death  with  abdominal  distention. 

Palpitation  when  patients  are  quiet  may  be  more  striking  than  actual  shortness  of 
breath  on  moderate  exertion  (unless  anaemia  is  also  present) .  But  this  is  not  an  invariable 
rule,  for  on  account  of  the  high  diaphragm  of  flatulence,  the  intensity  of  the  cardiac  dis- 
comfort, or,  on  the  other  hand,  the  habitual  weakness  of  the  patient's  muscles,  there  may 
be  actual  cardiac  weakness  as  well. 

The  treatment  of  air  gulping  is  of  the  greatest  importance.  Wyllie 
states  that  this  troublesome  habit  can  be  promptly  overcome  by  keeping 
the  mouth  open.  For  persons  who  swallow  air  in  their  sleep,  a  gag  or  cork 
has  to  be  tied  in  the  mouth.  This  method  is  in  general  use  among  veterinary 
surgeons  and  is  uniformly  successful.  It  is  evident,  therefore,  that  the 
diagnosis  of  air  swallowing  must  be  carefully  made.  In  many  cases  this 
may  be  done  by  getting  the  patient  to  show  you  how  she  usually  belches, 
the  voluntary  procedure  indicating  the  nature  of  the  process.  In  doubtful 
cases  it  may  be  necessary  to  analyze  the  gas  by  Hoppe-Seyler's  method; 
but,  as  Wyllie  remarks,  the  diagnosis  is  best  made  ex  juvantibus,  by  cessa- 
tion of  the  condition  when  the  mouth  is  kept  open.  The  possibility  of 
unconscious  quiet  air  swallowing  in  other  cases  of  flatulence  must  also  be 
borne  in  mind. 

Constipation. — An  accumulation  of  fecal  matter  is  also  a  very  common 
cause  of  cardiac  symptoms.  Extrasystoles  are  usually  more  common 
when  the  patients  are  constipated.  Kuthan  has  also  seen  patients  in 
whom  attacks  of  angina  pectoris  occurred  regularly  during  periods 
of  constipation  and  disappeared  when  the  bowels  were  kept  open.  These 
symptoms  are  produced  partly  by  the  lifting  of  the  diaphragm  and  per- 
haps also  in  part  by  the  chemical  action  of  indol,  skatol  (Russell, 
Herter),  and  other  fermentation  products.  These  substances  may  act 
directly  upon  the  intestinal  nerve  endings  or  upon  the  heart  muscle  and 


DISTURBANCES  OF  CARDIAC  FUNCTION.  707 

cardiac  nerves  after  absorption  into  the  general  circulation  (as  assumed 
by  McCaskey).  It  must  be  admitted  that  the  action  of  such  products 
is  not  very  well  known. 

Apart  from  the  general  methods,  treatment  of  the  cardiac  symptoms 
is  best  accomplished  by  treating  the  gastric  condition  with  appropriate 
diet,  lavage,  galvanization  (8  to  12  milliamperes),  and  faradization  of  the 
stomach,  etc.  The  bowels  should  be  kept  open.  The  various  forms  of 
fermented  milk  containing  lactic  acid  (buttermilk,  kephyr,  etc.)  as  well 
as  the  preparations  of  lactic  acid  bacilli  are  often  of  benefit  in  the  treat- 
ment of  intestinal  fermentation. 

Treatment  of  the  constipation  which  is  often  present  should  consist 
of  free  purgation  with  Epsom  salts,  followed  by  a  course  in  cascara,  hydro- 
therapy, abdominal  exercise,  and  a  diet  rich  in  fat,  coarse  foods,  and  in 
liquids.  The  most  important  feature  is  forcing  the  patient  to  defecate  at 
regular  hours  and  at  no  other  times. 

REFLEXES  FROM  THE  SEXUAL  ORGANS. 

Practically  all  the  disturbances  of  the  sexual  organs  are  accompanied 
by  the  pseudocardiac  syndrome.  It  occurs  in  both  male  and  female  after 
sexual  excesses  and  organic  diseases. 

MALE    SEXUAL    ORGANS. 

In  men  gonorrhoea,  prostatitis,  and  especially  masturbation  are  among 
the  first  conditions  to  be  thought  of  when  a  patient  presents  himself  with 
these  symptoms.  Curschmann  and  Bachus  have  especially  called  attention 
to  the  latter  condition  and  have  found  that  masturbation  may  even  lead 
to  cardiac  hypertrophy.  Bachus  has  made  the  very  significant  observa- 
tion that  in  many  of  his  masturbators  the  thyroid  glands  were 
somewhat  enlarged,  so  that  he  believed  that  the  abnormal  sexual 
activity  might  have  led  to  a  secondary  over-activity 
of  the  thyroid.  (Perhaps  this  may  occur  through  the  action  of  a 
hormone  in  the  testicles,  seminal  vesicles,  or  prostate.)  At  all  events, 
since  this  organ  may  be  affected  reflexly,  the  secondary  activity  of  the 
thyroid  is  to  be  thought  of  in  all  cases  of  pseudocardiac  disease  of  sexual 
or  of  purely  nervous  origin.  It  is  also  possible  that  the  prostate  gland 
may  have  an  internal  secretion  of  similar  character. 

The  diagnosis  must  be  made  from  the  history,  as  well  as  from  a  careful 
physical  examination  in  which  the  mouth  of  the  urethra  is  especially  exam- 
ined, and  careful  palpation  of  the  prostate  and  prostatic  secretion. 

Treatment  is  directed  mainly  to  the  primary  condition,  but  the  bro- 
mides should  be  used  somewhat  more  freely  in  sexual  disturbances  than 
in  the  other  conditions. 

FEMALE. 

In  women  the  pseudocardiac  disturbances  are  not  only  more  common 
but  more  severe  than  is  usual  in  men.  Palpitation,  with  tachycardia  and 
weakness,  is  very  common  at  the  age  of  puberty  and  is  practically  universal 
in  chlorosis  which  is  then  so  common. 


708  DISEASES  OF  THE  HEART  AND  AORTA. 

In  young  and  healthy  married  women  Kisch  has  found  that  attacks 
of  palpitation  with  rapid  pulse  and  dyspncea  may  occur — 

1.  As  the  result  of  sexual  excesses  in  women  whose  sexual  desire  is  very  keen. 

2.  After  attempted  coitus  when  vaginismus  is  present  (cured  by  operation  upon  the 

vagina) . 
-3.  In  women  who  have  practised  coitus  interruptus  for  a  long  time  without  attaining 
sexual  satisfaction. 

Kisch  believes  that  in  general  coitus  stimulates  the  cardiac  nerves 
in  proportion  to  the  intensity  of  the  orgasm.  Masturbation,  on  the  other 
hand,  has  a  much  less  intense  effect  on  women  than  on  men  (Kelly),  and 
is  rarely  responsible  for  cardiac  disturbances. 

Veit  calls  attention  to  the  fact  that  asthmatic  attacks  from 
cardiac  insufficiency  constitute  an  early  symptom  of 
myoma.  He  believes  that  these  arise  in  the  early  stages  of  brown 
atrophy  and  cardiac  obesity,  as  these  lesions  have  been  found  by  Lehmann 
and  Strassman  and  also  by  Fleck  in  40  per  cent,  of  all  cases  of  myoma.1 
Kelly  and  Cullen,  however,  deny  that  myomata  i-n 
themselves  are  associated  with  any-cardiac  disturb- 
ances except  those  due  to  the  anaemia  which  is  pres- 
ent. In  a  very  careful  study  of  1428  cases  of  myoma  they  found  that 
"In  the  majority  of  cases  (with  cardiac  manifestations,  92)  an  apical  sys- 
tolic murmur  was  detected.  This  murmur  was  usually  very  soft  in  character. 
In  some  it  was  limited  to  the  apex,  but  in  others  it  could  be  traced  to  the 
axilla  and  in  some  patients  to  the  base  of  the  heart."  In  nearly  all  the 
cases  (92)  in  which  cardiac  lesions  were  present,  the  patient  gave  a  history 
of  menorrhagia,  often  associated  with  intermenstrual  bleeding.  These 
patients,  as  a  rule,  stood  the  anaesthetic  well  and  in 
a  comparatively  short  time  they  had  gained  much  in  strength  and  their 
cardiac  murmurs  had  disappeared.  Some  authorities  claim  that  the  myoma 
in  itself  brings  about  cardiac  changes.  If  such  were  the  case,  then  the 
larger  the  myoma  the  more  pronounced  should  be  the  cardiac  murmurs. 
This  has  not  been  our  experience.  The  largest  tremors  have  not  been 
associated  with  any  cardiac  symptoms,  but  the  heart  complications  have 
almost  invariably  been  associated  with  copious  bleeding  from  the  uterus 
(i.e.,  submucous  myomata). 

"Most  of  the  murmurs  noted  in  our  cases  were  at  the  time  considered 
to  be  functional."  (Cullen.)  That  there  is  little  danger  from  functional 
impairment  of  the  heart  is  shown  by  the  fact  that  Kelly  and  Cullen's  mor- 
tality in  their  last  240  cases  of  myoma  was  less  than  1  per  cent. 

Lenhartz  has  found  that  cardiac  symptoms  are  almost  always  more 
frequent  during  the  week  preceding  the  menstrual  flow.  They 
are  also  more  frequent  as  the  climacteric  is  approached,  an  angioneurosis 
(flushing)  with  palpitation  and  more  or  less  tachycardia  being  universal. 
Strassman  and  Lehmann  have  called  attention  to  the  similarity  between 
these  phenomena  in  ovarian  secretion  and  those  of  the  thyroid  gland, 
and^.as  has  been  stated,  the  thyroid  varies  in  size  with  the  changes  in  ova- 
rian activity.    Leo  Loeb,  Starling,  and  others  have  shown  that  this  is  due 

1  In  34.6  per  cent,  of  Fleck's  cases  there  was  no  anaemia. 


DISTURBANCES  OF  CARDIAC  FUNCTION.  709 

to  the  action  of  a  hormone  arising  in  the  ovaries  and  especially  in  the  corpus 
iuteum,  which  acts  upon  the  uterus,  mammary  glands,  and  thyroid.  No 
doubt  it  also  has  some  action  upon  the  heart,  but  this  is  still  obscure,  and  it  is 
difficult  to  determine  how  much  of  the  effect  is  due  to  the  ovarian  secretion 
itself  and  how  much  to  the  secondary  hyperthyroidism. 

R.  G.  Hoskins  and  Wheelon  (Am.  Journ.  Physiol.,  1914,  xxxv,  119)  have 
found  heightened  blood-pressure  and  heightened  irritability  of  the  sympathetic 
nervous  system  in  castrated  bitches. 

Prognosis  and  Therapy. — The  prognostic  importance  of  cardiac  disturb- 
ances arising  in  the  sexual  organs  varies  with  the  primary  lesion  and  its 
chronicity.  In  the  presence  of  gonorrhoea  or  pelvic  abscesses  the  probability 
of  a  metastatic  myo-  or  endocarditis  must  not  be  forgotten.  In  the  presence 
of  anaemia  the  development  of  fatty  degeneration  must  be  thought  of.  In 
masturbating  men  there  is  a  true  cardiac  hypertrophy  with  the  usual  accom- 
panying changes.  These  factors  must,  therefore,  be  excluded  before  the 
diagnosis  of  a  true  neurosis  is  made  and  an  unqualified  favorable  prognosis 
can  be  given. 

In  the  simple  cardioneurosis  or  pseudocardiac  sexual  disturbance  the 
cardiac  outlook  is  favorable  if  the  primary  condition  can  be  removed.  If 
not,  the  prolonged  reflex  stimulation  of  the  cardiac  nerves  leads  first  to  a 
"work  hypertrophy"  and  then  probably  to  cardiac  overstrain  and  premature 
cardiosclerotic  or  atrophic  changes. 

The  treatment  is  therefore  in  the  field  of  the  gynaecologist  or  genito- 
urinary specialist  and  not  in  that  of  the  internist.  Even  masturbation 
and  sexual  excesses  may  have  a  basis  in  organic  irritation  and  should  not 
be  regarded  as  entirely  psychogenic  without  examination.  These  may 
be  much  helped  by  psychotherapy,  cold  baths  in  the  morning  and  cold 
packs  at  night,  and  exercise  during  the  day.  The  psychic  effect  of  the 
treatment  will  be  greatly  enhanced  if  the  impression  is  clinched  at  once 
by  the  administration  of  potassium  or  sodium  bromide  (1  Gm.  =gr.  xv, 
t.i.d.  and  before  going  to  bed)  disguised  in  elixir  of  calisaya  or  in  com- 
pound tincture  of  gentian  or  of  cardamom;  for  the  patient's  confidence 
in  the  outcome  is  gained  by  finding  the  abnormal  desire  to  decrease  at 
once  with  the  onset  of  treatment. 

ADENOIDS  AND  RESPIRATORY  OBSTRUCTION. 

Adenoids. — The  presence  of  adenoid  growths  in  the  nasopharynx  is  also 
of  importance,  not  only  because  they  interfere  with  the  respiratory  intake  of 
air  and  thus  bring  about  dyspnoea  on  exertion,  which  may  simulate  a  true 
cardiac  weakness,  but  also  because  attacks  of  mild  asphyxia  may  occur 
during  sleep  and  cause  the  patient  to  awaken  suddenly  with  a  severe  palpi- 
tation and  other  cardioneurotic  symptoms.  Besides  this,  during  waking 
hours  the  lesions  may  continue  to  produce  reflex  irritation  of  the  cardiac 
nerves  and  give  rise  to  cardioneurotic  symptoms  in  the  same  way  as  do 
disturbances  in  other  organs. 

Arrhythmia  of  Nasal  Origin. — A  physiological  basis  for  these  clinical 
findings  has  been  furnished  by  Francois-Franck  (1889),  who  found  that 
an  arrhythmia  of  vagal  origin  could  be  produced  by,  stimulating  the  nasal 


710  DISEASES  OF  THE  HEART  AND  AORTA. 

mucosa.  His  studies  have  recently  been  confirmed  by  Koblanck  and 
Roeder,  who  found  that  in  8  cases  with  arrhythmia  and  nasal  disease 
there  were  alterations  in  the  mucous  membrane  of  the  nasal  septum  in 
a  spot  opposite  the  middle  turbinate  bone.  There  were  often  nose-bleeds 
as  well.  Touching  this  spot  with  a  blunt  probe  in  man  and  animals 
produced  a  similar  arrhythmia.  No  other  area  of  nasal  mucosa 
gave  this  reflex.  The  arrhythmia  was  characterized  by  series  of  beats  with 
increasing  rapidity  interrupted  by  long  pauses,  sometimes  simulating 
extrasystolic  bigemini  (Curves  1  (man)  and  3  (rabbit),  K.  and  R.),  but  it 
could  not  be  produced  after  either  vagus  was  cut.  Stimulation  of  other 
mucous  membranes  in  this  manner  did  not  give  rise  to  such  arrhythmia. 
The  authors  showed  that  these  stimuli  are  carried  by  the  septal  branch  of 
the  trigeminus  which  lies  in  this  vicinity,  for  they  could  not  be  produced 
after  cutting  the  trigemini,  and  believe  that  they  are  carried  directly  from 
the  trigeminus  nucleus  to  that  of  the  vagus  through  the  fasciculus  longi- 
tudinalis  medialis.  With  cure  of  the  nasal  condition  the  arrhythmia  and 
allied  disturbances  disappeared. 

Cardiac  Asthma  from  Disease  of  Nasal  Septum. — Francois-Franck  also 
showed  by  careful  graphic  methods  that  stimulation  of  the  nasal  reflex  can 
give  rise  to  cough,  laryngeal  spasm,  asthma,  and  even  a  reflex  bronchitis, 
reflexes  which  in  themselves  may  add  to  the  impression  of  a  primary 
cardiac  disturbance.  He  found  that  these  reflex  conditions  were  more 
pronounced  in  animals  with  aortic  insufficiency  than  in  normal  animals. 
The  condition  in  man  is  similar,  and  in  the  presence  of  an  organic  cardiac 
lesion  these  contributing  factors  may  play  a  role  which  determines  the 
security  of  the  cardiorespiratory  symptoms,  so  that  the  cause  of  the 
paroxysmal  dyspnoea  may  in  some  cases  have  to  be  looked  for  in  the  nose. 


TOXIC   CARDIONEUROSES. 

"TOBACCO  HEART." 

Persons  who  suffer  from  excessive  use  of  tobacco  may  be  divided  into 
three  classes: 

1.  Non-smokers  suffering  from  a  single  indulgence  (acute  tabagism  or  nicotinism). 

2.  Young  habitual  smokers,  especially  those  who  inhale  cigarette  smoke  (subacute 

nicotinism) . 

3.  Old  habitual  smokers,  especially  of  cigars  and  pipes,  who  suffer  from  the  patho- 

logical changes  produced  in  the  arteries  (especially  the  coronary  arteries)  and 
myocardium,  and  partly  from  the  added  effects  of  the  nicotine. 

PHYSIOLOGICAL   EFFECTS. 

The  physiological  effect  of  smoking  has  recently  been  studied  by  Lee, 
as   well   as   by   Bruce,   Miller,    and   Hooker. 

Lee  found  that  ordinary  tobacco  smoke  obtained  from  1000  Gm.  tobacco  contained 
nicotine  1.165  Gm.,  pyridine  bases  (chiefly  pyridine  and  collidine)  0.148  Gm.,  HCN  0.08 
Gm.,  NH3  0.36  Gm.,  CO  410  c.c.  The  chief  toxic  product  is  therefore  nicotine.  The 
composition  varied  considerably  with  both  the  quality  of  the  tobacco  and  the  mode  of 
smoking.    The  greater  part  of  the  nicotine  at  the  seat  of  combustion  is  destroyed,  and  that 


DISTURBANCES  OF  CARDIAC  FUNCTION.  711 

which  reaches  the  mouth  is  volatilized  by  the  hot  gases  while  passing  over  the  unburned 
area.  Accordingly  a  thick  cigar  has  the  worst  effect,  since  it  acts  as  a  chimney  leading 
the  gases  to  the  mouth,  while  in  a  thin  cigar,  "  stogie,"  or  cigarette  they  escape  into  the 
surrounding  air.  (In  cigarette  smoking  inhaling  the  smoke  more  than  compensates  for 
this  difference  in  combustion.)  In  long-stemmed  pipes  much  of  the  nicotine  condenses 
before  reaching  the  mouth. 

Lee  found  that  in  non-smokers  the  first  effect  of  smoking  a 
cigar  was  to  produce  a  rise  of  10-20  mm.  Hg  in  the  maximal  blood-pressure, 
which  was  often  associated  with  palpitation.  Within  five  minutes  after 
this  the  maximal  blood-pressure  fell  50  mm.  Hg,  and  this  fall  was  accom- 
panied by  pallor,  sweating,  weakness,  and  colicky  pains  in  the  abdomen,  as 
well  as  by  the  appearance  of  muscse  volitantes,  irregularity  and  weakness 
of  the  pulse, — or,  in  other  words,  the  symptom  complex  of  arterial  ansemia. 

In  more  habitual  smokers,  those  of  the  second  group,  a  single 
cigar  produced  only  the  rise  of  blood-pressure  and  palpitation.  The  subacute 
symptoms,  therefore,  come  on  only  as  the  result  of  excessive  indulgence. 

In  old  habitual  smokers  these  observers  found  either  no 
effect  whatever  or  only  a  slight  rise  of  pressure  resulting  from  a  strong 
cigar,  without  any  of  the  disagreeable  symptoms. 

Lee's  observations  have  been  repeated  by  Bruce,  Miller,  and  Hooker, 
who  found  that  smoking  increases  the  maximal,  minimal,  and 
pulse-pressures  in  man,  though  later  these  return  to  normal.  The 
cardiac  output,  therefore,  seems  to  be  increased  at  first,  as  Lee  had  found 
in  cats.  Bruce,  Miller,  and  Hooker  also  found  that  the  volume  of 
the  hand  always  decreased  during  smoking  (vasoconstriction) , 
whereas  Lee  found  that  the  volume  of  the  cat's  intestine  also  decreased. 
It  is  probable  that  a  little  later  there  occurs,  in  man,  a  dilatation  of  the 
abdominal  vessels,  but  it  is  not  yet  certain  that  it  does  so. 

The  chief  sufferers  from  tobacco  are  the  young  cigarette  smokers  who 
inhale  the  smoke  and  thus  soon  suffer  immediately  from  the  physiological 
effects  of  the  nicotine.  They  complain  of  weakness,  giddiness, 
intense  palpitation  and  tachycardia  (from  continued  stim- 
ulation of  the  cervical  ganglion  cells),  and  often  of  irregularity  of 
the  heart,  which  may  be  very  distressing.  It  is  most  noticeable  that  the 
intense  sensory  disturbances  occur  without  any  motor  insufficiency  of 
the  heart.  Thus,  a  young  man  of  20  years,  an  habitual  inhaler  of  cigarette 
smoke,  recently  consulted  the  writer,  complaining  of  fatigue,  giddiness, 
muscae  volitantes,  intense  palpitation,  but,  on  further  questioning,  stated 
that  he  was  in  the  habit  of  running  a  quarter  of  a  mile  every  evening  for 
exercise,  and  after  this  exercise  he  had  neither  palpitation  nor  shortness 
of  breath!    Needless  to  say,  he  improved  at  once  after  stopping  tobacco. 

On  the  other  hand,  all  sufferers  from  nicotine  are  not  free  from  motor 
symptoms  nor  do  they  recover  so  readily.  In  many  cases  the  nicotinism 
is  supplemented  by  the  use  of  alcohol,  and  secondary  myocardial  changes, 
and  in  the  older  persons  arteriosclerotic  changes,  have  been  superinduced. 

In  the  middle-aged  smokers  the  symptoms  are  chiefly  those  of  angina 
pectoris  and  precordial  pain.  Very  commonly  this  is  a  true  angina  of  coro- 
nary sclerosis,  but  there  is  a  certain  number  of  cases  in  which  the  unpleasant 
symptoms  completely  subside  upon  cessation  of  smoking. 


712  DISEASES  OF  THE  HEART  AND  AORTA. 

It  would  be  a  very  fascinating  hypothesis  to  believe  that  in  such  cases  the  effect  of 
smoking  is  to  produce  a  transitory  constriction  of  the  coronary  arteries  and  this  to  cause 
the  symptoms,  but,  on  the  contrary,  some  recent  experiments  upon  dogs,  done  under  the 
writer's  direction  by  Dr.  George  Bond,  have  shown  that  the  flow  through  the  coronary 
veins  is  actually  increased  by  smoking.1  It  is  probable,  therefore,  that  in  early  tobacco 
poisoning  at  least,  the  sensory  symptoms  are  due  to  stimulation  of  the  cardiac  nerves  and 
not  to  ischaemia  of  the  myocardium.  The  commonness  and  insidiousness  of  coronary 
sclerosis,  however,  render  it  difficult  to  decide  in  any  individual  case  whether  the  effect 
is  entirely  functional  or  has  also  a  basis  in  arterial  changes. 

COFFEE  AND  TEA. 

The  palpitation,  tachycardia,  and  tremor  which  result  from  over- 
indulgence in  coffee  and  tea  are  familiar  to  most  persons  from  personal 
experience.  They  often  manifest  themselves  in  chronic  forms  and  cause 
cardioneurotic  symptoms.  Precordial  pain  and  tenderness  are  quite  com- 
mon. Foote  and  Simpson,  under  D.  R.  Hooker's  direction,  have  found 
that  when  a  person  accustomed  to  coffee  takes  a  cup  of  it  there  is  a  transi- 
tory rise  in  maximal  and  minimal  blood-pressure  and  a 
slight  vasoconstriction  of  the  hand.  In  persons  unaccustomed  to 
coffee  these  changes  are  much  more  intense.  Indeed  this  partial  immunity 
to  coffee  is  very  transitory,  for  the  writer  has  found  that  after  discontinuing 
its  use  for  several  months  a  single  cupful  would  give  rise  to  palpitation, 
tachycardia,  and  insomnia,  while  a  few  months  before  and  a  few  months 
later  two  cups  could  be  taken  at  a  time  without  producing  symptoms. 

Coffee,  like  tobacco,  gives  rise  to  sensory  cardiac  symptoms  by 
increasing  the  irritability  of  the  nerves  without  causing  any  motor  insuf- 
ficiency, and  consequently  the  patients,  as  a  rule,  do  not  show  muscular 
or  cardiac  fatigue  on  exertion  in  spite  of  the  symptoms. 

Tea. — Owing  to  its  content  of  caffeine,  tea  causes  the  same  symptoms 
as  coffee,  but  is  less  extensively  used  in  large  quantities.  In  England, 
however,  similar  cases  are  occasionally  reported. 

ALCOHOL. 

Palpitation  and  the  other  symptoms  of  "cardioneurotic"  (pseudo- 
cardiac)  weakness  also  occur  in  persons  who  take  alcohol  in  quantities 
that  are  just  in  excess  of  their  tolerance,  and  the  possibility  of  this  cause 
must  be  borne  in  mind.  In  some  individuals,  as  in  Reissner's  case,  palpi- 
tation and  irregularity  may  follow  the  ingestion  of  a  single  glass  of  wine, 
without  any  symptoms  of  intoxication  setting  in.  That  these  conditions 
may  continue  without  the  patient's  recognizing  the  cause  is  a  common 
experience,  and  a  considerable  number  of  cardioneurotic  cases  result  from 
this  unintentional  over-indulgence  in  alcohol.  Women  and  young  persons 
are  more  sensitive  than  men.  The  functional  power  and  endurance  of  the 
heart  muscle  is,  moreover,  weakened  by  alcohol;  and  acute  dilatation  may 
set  in  from  comparatively  slight  exertion.  If  the  use  of  alcohol  is  long 
continued,  it  may  lead  to  fatty  and  fibrinous  myocardial  change,  but  this 
in  mild  cases  subsides  when  the  cause  is  removed. 

1  Bond  registered  the  outflow  from  the  coronary  veins  by  the  drop  method. 


DISTURBANCES  OF  CARDIAC  FUNCTION.  713 


SIMPLE    EMOTIONAL    CARDIONEUROSES. 

As  has  been  seen,  by  far  the  greatest  number  of  so-called  cardioneurotic 
cases  are  of  postural,  reflex,  or  toxic  origin.  However,  it  still  remains 
beyond  question  that  emotional  disturbances  alone,  or  in  conjunction  with 
other  conditions  which  in  themselves  are  not  sufficiently  intense  to  pro- 
duce symptoms,  may  give  rise  to  cardioneurotic  symptoms.  Palpitation 
and  even  precordial  pain  are  almost  universal  after  severe  emotional 
disturbances  and  shocks  and  during  periods  of  worry. 

The  motor  effects  are  usually  shown  by  tachycardia,  though  occa- 
sionally arrhythmias  may  occur.  This  the  writer  has  observed  upon  him- 
self on  an  occasion  of  intense  emotion,  during  which  the  pulse  became 
extremely  rapid  and  seemed  either  to  drop  an  occasional  beat  or  to  give 
rise  to  an  extrasystole.  When  the  cause  of  the  worry  was  removed,  within 
five  minutes  the  pulse  again  became  regular,  so  that  the  arrhythmia  could 
not  be  accurately  studied  nor  has  it  recurred  at  any  other  time  during  the 
four  years  that  have  elapsed. 

Similar  cases  are  found  in  the  literature  (Reissner).  In  rare  cases  an 
emotional  shock  may  cause  death,  even  when  the  heart  is  otherwise  healthy 
(Gibson),  but  the  nervous  mechanism  by  which  this  is  brought  about  is 
not  clearly  understood.  It  is  probably  a  condition  of  exaggerated  vaso- 
motor shock  arising  in  response  to  a  cortical  stimulus,  just  as  it  may 
result  from  over-stimulation  of  a  peripheral  nerve.  In  most  cases  of 
the  sort,  however,  the  heart  and  especially  the  coronary  arteries  are 
already  diseased  (see  page  369). 

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714  DISEASES  OF  THE  HEART  AND  AORTA. 

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INDEX 


Abdominal  aorta,  aneurism  of,  636 
pain  from  distended  liver,  227 

in  tricuspid  insufficiency,  502 
Abscess  of  heart-muscle,  316 
Absolute  arrhythmia,  effect  of  digitalis  in, 

127  (see  also  Arrhythmia) 
Acapnia,  Cheyne-Stokes  breathing  from,  221 
in  cardiac  dyspncea,  217 
in  shock  and  fevers,  48 
Accelerations,  reflex,  102 
Accessory  heart-sounds,  170 
Accidental  murmurs  in  splanchnoptosis,  701 
Acetonitrile  test  for  hyperthyroidism,  680 
Aconite,  267 

pharmacological  action  of,  267 
therapeutic  use  of,  267 
with  digitalis,  267 
Aconitin,  267 
Acrocyanosis,  372 
Acroparesthesia,  372 

Adams-Stokes    disease    (see    also    Adams- 
Stokes    syndrome ;     Heart- 
block),  565 
auricular  fibrillation  in,  581 
auricular  heart  sounds  in,  566, 

582 
blood-pressure  in,  41 
differential  diagnosis  of,  582 
effect  of  atropine  in,  580 
effect  of  iodides  in,  585 
effect  of  posture  on,  586 
electrocardiogram  in,  577 
etiological  factors,  580 
experimental,  568 
lesions  of  auriculoventricular 

bundle  in,  576 
occasional      confusion      with 
paroxysmal    tachycardia, 
583    \ 
prognosis  in,  584 
relation  of  heart-block  to,  573 
stoppage  of  ventricles  in,  576 
stoppage  of  ventricles  in  tor- 
toise, 567 
syncopal  bradycardia,  565 
treatment  of,  585 
X-ray  examination  in,  582 
Adams-Stokes     syndrome      (Adams-Stokes 
disease),  565 
from  extrasystoles  alone,  579 
without  lesion  of  auriculoven- 
tricular bundle,  578 
Adenoids  as  cause  of  Basedow's  disease,  686 
asthma  due  to,  710 
cardiac  disturbances  due  to,  709 


Adherent  pericardium,  610 

absence  of  symptoms  from  intra- 

pericardial  adhesions,  610 
anginal  attacks  in,  389 
ascites  and  hydrothorax  in,  613 
ascites  in,  613 
Broadbent's    sign     (retraction    of 

ribs)  in,  614 
cardiac  dulness  in,  614 
cardiolysis  for,  620 
diastolic  shock  in,  615 
effect  on  circulation,  611 
fixation  of  lung  borders  in,  615 
hallucinations  in,  613 
hydrothorax  in,  613 
indications  for  cardiolysis,  620 
paradoxical    respiratory    ratio    in, 

614 
physical  signs  of,  614 
polyserositis  in,  619 
pseudocirrhosis  of  liver  in,  619 
pulse  in,  614 

pulsus  paradoxus  in,  614,  617 
reduplication  of  first  heart  sound 

in,  616 
Riegel's  pulse  in,  616 
Riess'  gastric  sounds  in,  616 
sites  of  adhesions,  611 
sounds  over  stomach  in,  616 
third  heart  sound  and  shock  in, 

615 
treatment  of,  619 
X-ray  shadows  in,  617 
Adhesions,     pleural,     simulating    adherent 

pericardium,  615 
Administration  in  heart  failure,  267 
production  of  aneurism  with,  635 
test  for  hydrothyroidism,  680 
Adrenalin,  267 
Adrenals,  hypersecretion  in  arteriosclerosis, 

356 
Afferent  impulses,  17 

Air  in  pericardial  cavity   (pneumopericar- 
dium), 604 
Air-swallowing,  705 

in  angina  pectoris,  395 
treatment  of,  395 
Albuminous  expectoration,  test  for,  219 
Albuminuria,  129,  205,  224 
Alcohol  as  cause  of  arteriosclerosis,  352 
cardiac  weakness  from,  712 
in  cardiac  disease,  236 
Allorrhythmias,  98 

classification  of,  99 
neurogenic,  99 

715 


716 


INDEX 


Allorrhythmias,  occurrence  of,  101 
production  of,  101 
reflex,  98 

from  nose,  101 

from  stimulation  of  gastric  walls, 
101 
Amyl  nitrite,  action  of,  in  man,  269 

administration  in  angina  pectoris,  394 

in  oedema  of  the  lungs,  219 
aortic  insufficiency,  479 
Anacrotic  pulse,  68 
Ansemia  in  cardiac  overstrain,  201 

in  endocarditis,  416 
Anastomosis     of     blood     vessels     in     the 
treatment  of  thromboangitis  obliterans, 
377 
Anatomical  terms,  synonymous,  xxvii 
Aneurism,  631 

age  of  occurrence,  633 

angina  pectoris  in,  389 

blood-pressure  in,  644 

brassy  cough  in,  640 

characteristics  at  various  sites,  647 

classification  of,  631 

delay  of  pulse  wave  in,  644 

development  of,  637 

diagnosis  of,  656 

differentiation  from  tortuous  arteries, 

656 
dilatation  of  pupils  in,  643 
dissecting,  657 

pathology  and  pathogenesis,  657 
symptoms  and  signs,  658 
dulness  over,  642 
dysphagia  in,  641 
electrolysis  in  (Moore-Corradi  method) , 

652 
embolic,  636 
erosion  from,  637 
etiology,  632,  636 
experimental,  635 
experimental  production  of,  671 
experimental  surgery  of,  671 
frequency  of,  in  women,  633 
inequality  of  pulse  in,  644 
ligature  of,  method  of  Antyllus,  668 
method  of  Brasdor,  669 
method  of  Hunter,  668 
low  diet  (Tufnell's)  in,  661 
mesarteritis  in,  635 
multiple,  633 
murmur  in,  641 
mycotic,  636 
of  abdominal  aorta,  660 
pain  in,  660 
paralysis  in,  661 
rupture  of,  661 
tumor  in,  660 
of  the  heart,  324,  647 
of  the  pulmonary  artery,  659 

signs  of,  659 
pain  in,  641 
pulsations  in,  642,  643 
role  of  syphilis  in,  632 
rupture  of,  637,  639 
shock  in,  641 
sites  of,  632 


Aneurism,  spontaneous  clotting  in,  639 
suffocation  in,  640,  641 
symptoms  of,  640 
tracheal  percussion  shock  in,  643 
tracheal  tug  in,  643 
treatment  by  compression,  668 

by  obliteration  of  sac  (Matas),  670 
by  occlusion  with  metal  bands,  669 
use  of  calcium  chloride  in,  662 
use  of  gelatin  in,  662 
use  of  potassium  iodide  for,  662 
venesection  in,  661 
wiring  of  (Moore's),  662 
X-ray  examination  in,  646 
Angeioneuroses,  372 

treatment  of,  376 
Angina  pectoris,  382 

and  palpitation,  384 

diagnosis  of,  392 

diet  in,  395 

differentiation     from     abdominal 

disease,  393 
due  to  coronary  sclerosis,  386 
from  tobacco,  391,  711 
Heberden's  description  of,  382 
hysterical,  390 
importance  of  diet  in,  395 
in  acute  dilatation,  388 
in  aneurism,  389,  641 
in  children,  389 
in  hyperthyroidism,  391 
in  valvular  diseases,  388 
referred  pains  in,  385 
sudden  death  in,  386 
symptoms  of,  382 
theobromine  in  treatment  of,  266, 

394 
treatment  of,  266,  393 
varieties  of,  386,  390 
vasomotor,  389 
Anginal  pain,  theories  as  to  causation  of,  387 
Antagonistic  muscles,  contraction  of,  201 
Aorta,  dextroversion  (Rechtslage)  of,  537 
hypoplasia  of,  559 
stenosis  of  isthmus,  557 

adult  type,  558 
signs  of,  559 
treatment  of,  559 
type  of  new-born,  557 
Aortae,  primitive,  526 
Aortic  area,  168 

disease  in  pregnancy,  521 
facies,  469 
insufficiency,  462 

amount  of  blood  regurgitating,  465 
and  mitral  stenosis,  differentiation 

between,  452 
asthma  from  lesion  of  nasal  septum 

in,  710 
blood-pressure  in,  40,  467,  474 
cardiac  impulse  in,  469 
cardiac  outline  in,  470 
Cheyne-Stokes  respiration  in,  468 
diagnosis  of,  478 
diastolic  murmur  in,  471 
double  murmur  (Duroziez's)  over 
the  arteries  in,  472 


INDEX 


717 


Aortic     insufficiency,     Flint's     presystolic 
rumble,  473 

functional,  462,  464 

hallucinations  in,  468 

historical,  462 

mitral  insufficiency  in,  479 

organic,  462 

pathological  physiology  of,  464 

precordial  pain  in,  468 

presystolic  thrill  in,  469 

prognosis,  478 

propagation  of  murmurs  in,  472 

pulmonary  circulation  in,  467 

pulse  in,  474 

pulse-rate  in,  467,  476 

relation  of  collapsing  pulse  to 
blood-pressure,  regurgitation, 
and  resistance,  475 

rupture  of  valves,  463 

sclerosis  of  aortic  valves,  463 

symptoms,  468 

treatment,  478 

of  anginal  attacks  in,  481 

use  of  digitalis  and  strophanthus, 
479 

venesection  in,  480 

X-ray  shadow  in,  470 
sclerosis,  461 
stenosis,  483 

anacrotic  pulse  in,  488 

arrhythmia  in,  489 

atheromatous,  483 

auscultation,  486 

blood-pressure  in,  489 

cardiac  outline  in,  486 

congenital,  556 

endocarditic,  483 

etiology  of,  484 

extrasystoles  in,  489 

failing  compensation  in,  485 

intraventricular  pressure  in,  485 

occurrence  of,  484 

palpation,  486 

pathological  anatomy,  483 

percussion,  486 

pulsus  tardus  in,  484,  487 

symptoms  of,  485 

thrill  and  murmur  in,  486 

treatment  of,  490 

with  aortic  insufficiency,  484 

X-ray  examination  in,  486 
Aortitis,  361 
acute,  345 
tuberculous,  352 
Apex  beat,  mechanics  of,  153 

method  of  recording,  153 

"mixed  type,"  155 

time  of,  153 
in  aortic  insufficiency,  469 

mitral  insufficiency,  428 
Apnoea,  derivation  of,  in  cardiac  and  pul- 
monary diseases,  219 
Apoplexy,  blood-pressure  in,  40 
Arches,  visceral  (branchial),  527 
Arrhythmia,  98 
absolute,  118 
differential  diagnosis  of,  120,  134 


Arrhythmia,  effect  of  digitalis  in,  123 

effect  of,  on  circulation,  127 

extrasystolic,  126 

from  emotional  excitement,  713 

from  lesions  of  nasal  septum,  709 

in  increased  intracranial  tension,  102 

in  myocarditis,  327 

in  tricuspid  insufficiency,  504 

of  psychic  origin,  102 

permanent,  electrocardiogram  in,  121 

respiratory,  102 

sinus,  98,  134 

vicious  circle  of,  123 

youthful  type,  101 
Arterial  pulse,  63 
tension,  25 
Arteries,    changes   in,    in   congenital   heart 
disease,  538 

normal  changes  in,  339 

sounds  in,  182 

strength  of  walls  of,  633 

tortuous,  resembling  aneurism,  656 
Arterionecrosis,  experimental,  from  adrena- 
lin, 355 
from  tobacco,  354 
from  toxins,  354    • 
in  animals,  354 
Arteriosclerosis,  339 

and  hypertension,  45 

blood  count  in,  361 

blood-pressure  in,  40,  359,  360 

clinical  manifestation  of,  357 

diet  in,  362,  363 

etiology  of,  352 

experimental,  355 

following  infectious  diseases,  352 

hypercholesterinsemia,  355 

in  children,  356 

in  hypothyroidism,  675 

intermittent  claudication  from,  357 

nervous  symptoms  from,  357 

nitrites  in,  364 

of  abdominal  aorta,  358 

of  abdominal  vessels,  356 

of  retinal  vessels,  358 

potassium  iodide  in,  364 

pulse  in,  359 

role  of  salt  in,  356 

salvarsan  in,  364 

second  heart  sound  in,  361 

syphilitic,  353 

theories  of,  339,  355 

treatment,  362 

use  of  warm  water  in,  363 

venesection  in,  364 

X-ray  examination,  358 
Arteriosclerotic  changes  in  vasa  vasorum, 
340 

lesions,  classifications  of,  342 
distribution  of,  356 
Arteritis,  acute,  345 

tuberculous,  352 
Artery,  compression  of,  sources  of  error  in,  28 
Ascites,  223 

in  adherent  pericardium,  613 
Asphyxia,  effects  of,  38 


718 


INDEX 


Aspiration  of  hydrothorax,  dangers  in,  224 
technic  of,  224  (see  also  Para- 
centesis) 
Astasia  abasia  in  Basedow's  disease,  685 
Asthma,  cardiac,  217 

from  lesions  of  nasal  septum,  710 
Atrioventricular  bundle    (see  Auriculoven- 

tricular  bundle) 
Atrophy  of  the  heart,  301 

and  cardiosclerosis,  306 
Atropin,  264 

Atropine,  effect  of,  in  heart-block,  571 
effect  of,  on  changes  in  tonus,  17 
effect  of,  on  extrasystoles,  114 
test  in  heart-block,  580 
use  of,  in  pulmonary  oedema,  219 
Auricles,  fibrillation  of  in  mitral  stenosis,  457 

mitral  stenosis  in  paralysis  of,  444 
Auricular  fibrillation,  118 

arrhythmia  in,  123,208 
cardiac  overstrain  in,  208 
venous  pulse  in,  79 
flutter,  124,  127 

clinical  picture,  131 
diagnosis  of,  101 
paralysis,  venous  pulse  in,  79 
in  mitral  stenosis,  444 
Auriculo ventricular  bundle,  anatomy  of,  568 
clamping  of,  569 
lesions  of,  in  Adams-Stokes  disease, 

576 
physiology  of,  568 
valves,  transmission  of  murmurs  from, 
177 
Auscultation,  162 

in  suprasternal  notch,  168 
methods  of,  166 
of  the  veins,  72 
through  the  stomach  tube,  170 
Azygos  vein,  role  in  hydrothorax,  224 

Bacterial   vaccines   in  treatment  of  endo- 
carditis, 410 
Basedow's  disease,  674,  676 
acute,  688 

anginal  attacks  in,  687 
arrhythmia  in,  684 
astasia  abasia  in,  685 
blood  count  in,  683 
blood -pressure  in,  41,  684 
calcium  salts  in,  689 
diagnosis  of,  686 

in  "formes  frustes,"  687 
etiological  factors,  680 
eye  signs,  684 

Dalrymple,  684 

Mobius,  684 

v.  Graefe,  684 

v.  Stellwag,  684 
force  of  heart  in,  683 
galvanization    of   cervical  sympa- 
thetic, 689 
Joffroy's  sign  of,  682 
loss  of  weight  in,  685 
metabolism,  682 
mortality  in,  688 
psychic  symptoms,  683 
psychotherapy  in,  689 


Basedow's  disease,  relation  to  hysteria,  680 
secondary  to  adenoids,  686 
specific  sera  in,  689 
spontaneous  recovery  in,  688 
sympathectomy  for  (Jonnesco),  691 
sympathicotonic  in,  680 
symptoms  and  signs  of,  681 
tachycardia  in,  683 
thyroidectomy  for,  690 

indications  for,  690 
results  of,  690 
treatment  of,  688 
tremor  in,  685 

triad  and  tetrad  of  symptoms,  681 
wet  packs  in,  689 
X-ray  treatment  of,  689 
Bath  treatment,  advisability  of,  289 
Baths,  electric,  288 
mud,  288 
Nauheim,  artificial,  286 

natural,  286 
peat,  288 

physiological  action  of,  286 
precautions  of,  286,  287 
Bathycardia,  704 
Beer  in  cardiac  disease,  236 
Belts,  effect  of,  in  producing  cardiac  over- 
strain, 203 
Bicycle  riding,  effect  of,  on  heart,  201 
Bigeminal  pulse,  114 

causes  of,  117 
Bigeminus,  112 
full,  112 
shortened,  112 
Bleedings  in  congenital  heart  disease,  541 
Blood  count  in  congenital  heart  disease,  545 
flowthrough  muscles  during  exercise,  197 
inarm,  determination  of  velocity,  36 
plasma,  volume,  determination,  61 
residual,  15 
viscosity  of,  59 

apparatus  clinical  determination,  59 
factors  influencing,  60 
Blood-pressure,  25,  209 

apparatus,  Erlanger's  with  Hirsch- 
f  elder's  polygraph  attachment,  74 
apparatus,  forms  of,  30 
changes  in  anginal  attack,  386 
in  exercises  of  speed,  198 
determination       of,       auscultator 
method  for,  33 
of  maximal,  28 
of  minimal,  28 
Erlanger,  28 
Janeway,  33 
Masing,  29 
Sahli,  30 
Strasburger,  32 
oscillatory  method,  33 
palpatory  method,  32 
effect  of  digitalis  on,  251 
effect  of  exercises  of  strain  on,  200 
end  pressure,  25 
in  aortic  insufficiency,  467 
in  Basedow's  disease,  41,  68-- 
in  chronic  nephritis,  42 
in  different  parts  of  the  vascular 
system,  34 


INDEX 


719 


Blood-pressure  in  normal  individuals,  33 

in  paroxysmal  tachycardia,  125, 129 

in  various  diseases,  39 

lateral  pressure,  25 

maximal,  26 

minimal,  26 

normal,  33 

physiological  factors  influencing,  35 

variations   in,    under   pathological 
conditions,  38 

variations  in,  under  physiological 
conditions,  37 

venous,  50 
Blowing  diastolic  murmur  in  mitral  stenosis, 

450 
Blue  babies,  541 
Bradycardia,  69 

in  Adams-Stokes  disease,  565,  581 
Brain  tumors,  blood-pressure  in,  40 
Brandy  in  cardiac  disease,  236 
Brauer  chamber  in  operations  on  heart,  627 
Breath-holding  test,  218 
Breathing,  Cheyne-Stokes,  220 
Broken  compensation  as  indication  for  in- 
ducing labor,  519 

blood-pressure  in,  42 

functional  valvular  insufficiencies 
in,  207 

pseudo-elephantiasis  in,  222 

pulmonary,  207 

systemic,  206 

venous  pressure  in,  209 
Broken  pulmonary  compensation  in  mitral 

insufficiency,  426 
Bronchitis  in  mitral  insufficiency,  433,  436 

Cachexia,  blood-pressure  in,  50 
Caffeine,  265 

in  angina  pectoris,  394 
in  cup  of  coffee,  237 
Calcification  in  arteriosclerosis,  341 
of  the  intima,  344 
pathogenesis  of,  341 
Calcium  chloride  for  aneurism,  662 
salts  as  cardiac  tonics,  265 

effect  of,  on  cardiac  contraction,  2 
in  Basedow's  disease,  689 
Calomel,  238 
Camphor,  264 
Canalis  auricularis,  527 
Capillaries,  changes  in,  in  congenital  heart 
disease,  538 
determination  of  the  pressure  in,  51 
malformation   of,    in   congenital   heart 
disease;  539 
Capillary  pulse  in  aortic  insufficiency,  469 
Carbon  dioxide,  effects  of,  38 
use  of,  for  anginal  pain,  241 
use  of,  in  cardiac  dyspnoea,  241 
Cardiac  and  adrenal  hypertrophy,  296 
area,  diameter  of,  159 
asthma,  217 

from  coronary  sclerosis,  381 
from  nasal  disease,  218 
in  aortic  insufficiency,  468 
chambers,  coordination  of,  9 


Cardiac  cicatrices,  324 

dilatation,  mountain  sickness  as  cause 
of,  194 
recovery  from,  195 
transitory,  194 

fright  as  cause  of,  194 
disease,  accumulation  of  fluid  in,  222 
renal  changes  in,  224 
symptoms  cf,  215 
diseases,  acute,  blood-pressure  in,  50 
disturbances  due  to  myoma,  708 
due  to  sexual  disorders,  707 
in  females,  707 
in  males,  707 
from  lesions  of  nasal  septum,  709 
from  masturbation,  707 
reflex,  705 

air-swallowing  in,  705 
associated  symptoms,  705 
gastro-intestinal,  705 
relation  to  menstrual  flow,  708 
sexual,  treatment  of,  709 
dulness  area  in  children,  160 

relative,  157 
dyspnoea,  morphine  and  strychnine  in, 

217 
efficiency,  functional  tests  of,  209 
facies,  228 

failure  with  a  small  heart,  209 
flatness,  160 

absence  of,  160 

fixation   of   area    of,    in    adherent 

pericardium,  615 
pear-shaped,    in   pericarditis   with 

effusion,  600 
variations  in,  160 
impulse,  153 
course  of,  5 

in  aortic  insufficiency,  469 
mechanics  of,  153 
movements  in,  154 
origin  of,  5 

protodiastolic  wavelet  on,  154 
muscle,  tonicity  of,  13 
nerves,  action  of,  17 

effect  of  exercise  on,  20 
excision  of,  20 
tonic  action  of,  17 
neurasthenia,  694 
neuroses,  694 

arrhythmia  in,  694 
classification  of,  696 
sexual,  707 
symptoms  of,  694 
venous  pressure,  694 
overstrain,  anaemia  in,  192 

as  cause  of  Adams-Stokes  disease, 

581 
auricular  fibrillation  and  arrhyth- 
mia in,  208 
cases  of,  189 
chlorosis  in,  192 
diagnosis  of,  195 
dilatation  of  heart  in,  193 
extrasystoles  in,  194 
mountain  climbing  as  cause  of,  194 
precordial  pain  in,  192 


720 


INDEX 


Cardiac  overstrain,  primary,  189 
etiology  of,  192 
sexual  excess  as  cause  of,  192 
tight  belts  as  cause  of,  192 
plexus,  20 

rhythm,  alterations  in,  98 
shadow,  145 

as  an  index  of  cardiac  volume,  17 
tonicity,    effect    of,  on  regurgitation, 

465 
tonus  in  functional    insufficiency,  423 
volume,  cardiac  shadow  as  an  index  of, 
17 
Cardiohepatic  angle  (Ebstein's)  in  pericar- 
dial effusion,  599 
Cardiolysis  for  relief  of  adherent  pericar- 
dium, 620 
Cardiometer,  11 
Cardiopathia  thyreoprica  (hypothyroidism), 

675 
Cardioptosis,  697 
Cardiosclerosis,  325 

and  atrophy,  306 
Cardiosphygmograph,  74 
Cerebral  thrombosis,  blood-pressure  in,  40 
Chest,    flat,  in    congenital  heart  disease, 

544 
Cheyne-Stokes  breathing,  220 
from  acapnia,  221 
treatment  of,  221 
types  of,  221 
Chlorosis  in  cardiac  overstrain,  192 
Choc  en  dome,  469 
Cholera,  blood-pressure  in,  50 
Chronic  hypertension,  42 

hypertrophy  of  the  heart,  blood- press- 
ure in,  40 
Circulation  in  foetus,  mechanics  of,  531 
mechanism  of,  34 
pulmonary,  51 
Claudication,  intermittent,  371 
Clubbed  fingers  in  congenital  heart  disease, 

543 
Coffee,  effect  of,  712 

prohibition  of,  237 
Coitus,  avoidance  of,  in  cardiac  disease,  521 
Cold  applications  over  the  heart,  232 
Collapse,  blood-pressure  in,  50 

hypotension  in,  50 
Collapsing  pulse,  68 

in  aortic  insufficiency,  475 
in  arteriosclerosis,  360 
Compensation,  broken,  hydraemia  in,  60 
broken  pulmonic,  206 
broken  systemic,  206 
symptoms  of  broken,  206 
Compression  of  the  artery,  sources  of  error 

in,  28 
Concato's  arch  in  pericarditis  with  effusion, 

600 
Concretio  pericardii  cum  corde,  610 
Connective-tissue     proliferation,      interfas- 
cicular, 324 
Constipation,  effect  on  heart,  706 
Constricting   the   femoral   arteries,    rise   of 
blood-pressure  on,  210 


Constriction,  effect  of,  in  producing  cardiac 

overstrain,  202 
Contractility,  diminished,  in  pulsus  alter- 

nans,  106 
Contractions  of  heart,  maximal,  5 
Conus  arteriosus,  dilated,  in  mitral  stenosis, 

446 
Convulsions  in  congenital  heart  disease,  541 
Coordination  of  the  cardiac  chambers,  9 
Cor  biatriatum  triloculare,  518 
Coronary  arteries,  distribution  of,  378 
ligation  of,  378 
sclerosis  of,  379 
vasomotor  nerves  in,  379 
circulation,  physiology  of,  378 
sclerosis  in   patients  with  paroxysmal 
tachycardia,  381 
symptoms  of,  380 
"Corset  heart,"  701 

Corsets,  effect  of,  in  producing  cardiac  over- 
strain, 202 
Cough,  221 

(brassy,  stenotic,  paretic)  in  aneurism, 
640 
Cyanosis,  blood-pressure  in,  42 

in  congenital  heart  disease,  theories  of, 

542 
in  pulmonary  stenosis,  541 
in  tricuspid  stenosis,  510 

Dalrymple's  sign  in  Basedow's  disease,  684 
Death  from  labor,  cause  end  frequency  of, 
516 

from  sudden  emotion,  713 
Degeneration,  calcareous,  314 

hyaline,  314 

parenchymatous,  314 

waxy,  314 
Delusions,  228 

from  digitalis  poisoning,  229 

typical,  228 
Determination  of  the  blood-pressure,  aus- 
cultatory method  for,  33 
Dextrocardia    (dexiocardia),    electrocardio- 
gram in,  561 

relation  to  transpositions  in  embryo,  560 
Dextroversion  of  the  aorta,  537 
Diaphragm,  high,  704 

high,  in  fat  persons,  704 
Diarrhoea,  blood-pressure  in,  50 
Diastasis  and  diastole,  11 
Diastole  and  diastasis,  11 

position  of  the  valves  in,  12 
Diastolic     closure     of     auriculoventricular 

valves,  12,  79  _ 
Dicrotic  notch,  time  of,  in  cardiac  cycle,  78 

pulse,  69 

wave,  66 

of  pulse,  66 
Diet,  235 

effect  of,  on  viscosity,  60 

in  cardiac  disease,  235 

Karen's,  236  _ 

lacto- vegetarian,  236 

limited  milk,  236 

restricted  liquids  (Karell),  236 

restriction  of  salts,  236 


INDEX 


721 


Digalen,  246 

Digestive  distuibances,  227 

Digipuratum,  259 

toxic  affects,  259 
Digitalis,  245.  2G2 
action  of,  248 

on  coronary  arteries,  249 
stage  of  incoordination,  250 
stage  of  iriegularity,  249 
therapeutic  closes,  248 
administration   in   fresh   mitral   endo- 
carditis, 436 
and  nitrites,  260,  479 
and    strophanthus    in    aortic    insuffi- 
ciency, 479 
arrhythmia  and  heart-block  caused  by, 

249 
contraindication  to,  261 
derivatives  of,  259 
drugs  of  series,  246,  247 
on  normal  heart,  248 
on  the  blood-pressure,  251 
on  tonicity,  252 
electrocardiogram,  effect  on,  251 
flavoring  of,  257 
hallucinations  from,  262 
in  arrhythmia,  123,  255 
in  auricular  fibrillation,  123,  332 
in  heart-block,  585 
in  second  stage  of  mitral  insufficiency, 

437 
intramuscular  administration,  258 
intravenous  administration,  258 
in  weakened  hearts,  255 
methods  of  administration,  257 
period  of  administration,  258 
poisoning,  delusions  from,  229 
preparations  of,  246 

choice  of,  257 
rectal  administration  of,  258 
standardization  of,  246 
weakness  of  ventricle  due  to,  123 
Digitoxin,  246 

Dilatation  of  the  heart,  acute,  angina  pec- 
toris in,  388 
acute,  pain  due  to,  387 
from  constriction,  202 
in  cardiac  overstrain,  193 
in  myocarditis,  317 
physiological  factors  bringing 

about,  203 
transitory,  194 
Diphtheria  as  cause  of  endocarditis.  402 

blood-pressure  in,  48 
Diplococcus  rheumaticus,  400 
Displacement  of  the  heart,  696 
Drugs,  mode  of  action  on  circulation,  245 
Duct  of  Cuvier,  526 

Ductus  arteriosus  (Botalli),  closure  of,  553 
factors  causing  persistence  of, 

553 
open,  538 
patent,  552 

diagnosis  of,  556 
murmur  in,  554 
pathogenesis  of,  552 


Ductus  arteriosus  (Botalli),  patent,  pulsus 
paradoxus  in,  555 
respiratory      interchange 

in,  556 
signs  of,  554 
symptoms  of,  554 
treatment  of,  556 
X-ray  shadow  in,  554 
role  in  fatus,  532 
venosus,  atrophy  of,  532 
Duroziez's  double  murmur  over  the  arteries 

in  aortic  insufficiency,  472 
Dysentery,  blood-pressure  in,  50 
Dyspnoea,  216 

in  congenital  heart  disease,  541 
mechanical  changes  in  circulation,  216 

Ebstein's  cardiohepatic  angle  in  pericardial 

effusion,  599 
Ectopia  cordis,  533 
Ectopic  impulses,  112 
Efferent  impulses,  17 
Effusion  in  pericarditis,  597 
Electricity,  239 

in  treatment  of  angina  pectoris,  295 
Electrocardiogram,  81 

cause  of  waves  upon,  90 

form  of,  89 

in  auricular  fibrillation,  121 

in  extrasystoles,  113 

in  heart-block,  577 

in  hypertrophy  of  left  ventricle,  94 

in  hypertrophy  of  right  ventricle,  94 

in  paroxysmal  tachycardia,  126 

in  situs  transversus,  562 
Electrocardiograph,  81,  138 

installation  of,  84 
Embolism  in  mitral  stenosis,  455 

in  patent  foramen  ovale,  552 

pulmonary,  220 
Embryocardia,  170 

in  paroxysmal  tachycardia,  130 
Emotion,  arrhythmia  from,  713 

effect  of,  on  the  heart,  713 
Emptying  of  the  heart,  10 
Endarteritis,  345,  352 

Endocarditic  vegetations,  bacterial  origin, 
398 
development  of,  3C8 
Endocarditis,  398 

anaemia  in,  416 

cerebral  embolism  in,  407 
type,  407 

choked  disk  in,  407 

chronic,  399,  405 
infective,  408 

cocci  (streptococcus  viridens)  in,  408 

complications  of,  414 

differential  diagnosis  of,  408 

digitalis  in,  415 

due  to  pyogenic  cocci,  401 

effect  on  circulation,  403 

from  miscellaneous  infections,  402 

gonorrhceal,  402 

influenzal,  402 

involvement  of  valves,  411 


722 


INDEX 


Endocarditis,  jaundice  in,  406 
malignant,  404,  405 
complications,  405 

brain  symptoms,  405 
embolic  aneurisms,  405 
enlarged  spleen,  405 
hsematuria,  405 
heart  failure,  405 
petechias,  405 
retinal  hemorrhages,  405 
treatment,  409 
frequency  of,  405 
valves  involved  in,  405 
microbes  producing,  400 
mural,  399 

palliative  treatment  of  tonsils  in,  417 
pathological  physiology  of,  403 
pathology  of,  399 
pneumococcic,  402 
prophylaxis,  416 
reinfection,  414 
retinal  hemorrhages,  407 
rheumatic,  400,  410 
septicsemic,  406 
simple  acute,  404,  410 

compensation  in,  414 
course  of,  412 
pathology  of,  412 
signs,  413 
symptoms  of,  412 
statistics  of,  410 
subacute,  410 
syphilis  in,  403 
treatment  of,  415 
typhoidal  type,  407 
ulcerative,  399 
Endocardium,  atheroma  of,  403 

pockets  of,  in  aortic  insufficiency,  537 
Endothelial  cells  in  sputum,  222 
Endurance,  exercises  of,  199 
Energy,  waste  of,  in  fatigue,  199 
Enteroptosis  (see  Splanchnoptosis) 
Epilepsy,  blood-pressure  in,  40 
Epinephrin,  267 
Ergot,  268 

Ergotism,   resemblance  to   Raynaud's  dis- 
ease, 373 
Erosion  of  bone  by  aneurism,  637 
Erythromelalgia,  372 
Erythromelia,  375 
Exercise,  choice  of,  284 

effect  of,  on  blood-pressure.  38 
Schott,  281 

systems  of,  in  therapeutics,  279 
test  of  cardiac  function,  210 
Exercises,  effect  of,  on  size  of  heart,  201 
of  endurance,  199 

circulation  in,  199 
mechanics  of,  197 
of  speed,  mechanics  of,  197 
of  strain,  200 

effect  on  blood-pressure,  200 
mechanics  of,  279 
Exophthalmic  goitre  (see  Basedow's  disease) 
Exophthalmos  from  stimulation  of  sympa- 
thetic, 684 


Extrasystoles,  107,  130,  135 
auricular,  Hz,  lbo 
auriculo  (atiioj  ventricular,  114,  136 
auriculoventiicular,  lesions  in,  116 
diagnosis  of,  123 
effect  of  at:  opine  on,  114 
electrocardiogram  in,  112 
experimental  production  of,  113 
heart  sounds  in,  114 
in  cardiac  ovei strain,  194 
in  myocarditis,  328 
ineffectual,  114 
neurogenic,  108 
palpitation  with,  113 
prognosis,  116 
treatment,  116 
stimuli  causing,  113 
venous  pulse  in,  112 
ventricular,  109,  136 

Face,  cedema  of,  222 
Facies,  aortic,  152 
abdominal,  228 
cardiac,  152,  228 
mitral,  152 
Fatigue,  effect  of,  on  energy  used  up,  199 
Fats,  diminished  absorption  of,  227 
Fatty  degeneration  of  the  heart,  304,  309 
etiology,  311 
nature  of,  310 

pathological  anatomy  of,  309 
prognosis,  312 
rupture  of  the  heart  in,  311 
strength  of  heart  with,  311 
symptoms  and  signs  of,  312 
treatment,  312 
of  the  intima,  344 
infiltration  of  the  heart,  304,  305 

cardiac   conditions  associated 

with,  306 
etiology,  307 

nature  of  the  fatty  deposit,  305 
physical  signs  of,  307 
treatment  of,  307 
Fetal  heart  sounds,  graphic  record  of,  170 
Fevers,  acapnia  in,  49 
Filling  of  the  heart,  10 

of  the  ventricles,  11 
First  sound  at  aorta,  165 
cause  of,  165 
character  of,  165 
duration  of,  166 
in  suprasternal  notch,  166 
reduplicated,  170,  171 
Fluid  in  cardiac  diseases,  accumulation  of, 

222 
Fluoroscope,  144 

diagnosis  by,  147 
Foetus,  circulation  in,  531 
Football  playing,  effect  of,  on  heart,  201 
Foramen  ovale,  development  of,  529 

effect  of  patency  on  circulation,  551 
open   538 
patent,  550 

crossed  embolism  in,  552 
occurrence  and  pathogenesis, 
550 


INDEX 


723 


Foramen  ovale,  patent,  paroxysmal  cyanosis 
in,  552 
signs  of  patency,  552 
symptoms  of  patency,  551 
treatment  of,  552 
vicious  circle  in,  540 
Formative  stimulus  in  arteriosclerosis,  339, 

342 
Fragmentation  of  muscle  fibres,  315 
Friction  in  pericarditis,  594 

pleuropericardial,  594 
Functional  mitral  insufficiency,  421 
tests  of  cardiac  efficiency,  209 

of  cardiac  insufficiency,  valueof, 211 
relation  of,  to  mode  of  life,  211 

Gallop  rhythm,  presystolic,  171,  172 

protodiastolic,  171,  173 
Galvanometer,  string,  85 

thread,  85 
Gastric  ferment  action,  705 
Gonococcus  as  cause  of  endocarditis,  402 
Graefe's  sign  in  Basedow's  disease,  684 
Graves's  disease  (see  Basedow's  disease) 
Gymnastics,  279 

fundamental  principles  of,  27t 

Hsematuria,  205 
Haemopericardium,  603 

from  cardiac  tumors,  336 
Haemoptysis  from  pulmonary  stasis,  220 

in  pulmonary  insufficiency,  494 
Hallucinations,  229 

in  adherent  pericardium,  613 
Headaches  in  congenital  heart  disease,  541 
Heart,  changes  in  position  of,  161 
changes  in  size  of,  161 
development  of,  early  stages,  525 
dilatation  of,  from  constriction,  202 
diminution  in  size  of,  in  exercise,  201 
disease  and  matrimony,  523 
congenital,  525 

blood  count  in,  545 
etiological  groupings,  534 
flat  chest  in,  544 
groups  of  lesions  in,  533 
syndrome  of,  534 
effects  of  labor  pains  in,  516 
displacement  of,  696 

effect  on  circulation,  697 
emptying  of,  10 

endothelial  tube  in  embryo,  526 
failure,  mechanism  of,  205 
urine  in  chronic,  225 
filling  of,  10 
high,  705 

effect  on  circulation,  705 
treatment  of,  705 
xiphisternal  line  with,  705 
insensibility  of,  384,  625 
lesions,  congenital,  classification  of,  533 
low,  697,  704 

signs  of,  704 
metastatic  involvement  of,  336 
mobility  of,  in  cardioptosis,  697 
muscle,  properties  of,  1 

structure  of,  1 
muscular  tube  in  embryo,  526 


Heart,  non-perforating  injuries  of,  628 
normal  mobility,  t>97 
nouiishment  ol,  379 
relaxation  of,  13 
sensory  symptoms  about,  225 
small,  in  cardiac  failure,  209 
sound,  first,  reduplication  of,  in  adhe- 
rent pericardium,  616 
second   aortic,    in   arteriosclerosis, 

361 
second,    in    mitral     insufficiency, 

432 
third,  causation  of,  173 

in  adherent   pericardium,  614 
sounds,  accessory,  170 
causes  of,  165 
clinical  diagram  for,  165 
digital  imitation  of,  182 
graphic  record  of,  162 
reduplicated,  170,  171 
reproduction  of,  164 
split,  171 
three-chambered,  538 
tuberculosis  of,  334 
tumors  of,  335 
work  of,  36 
wounds  of,  623 

cause  of  death  from,  624 
experimental  surgery  of,  623 
hemorrhage  in,  627 
murmurs  in,  625 
operative  treatment  of,  625 
spontaneous  recovery  in,  623 
suture  of,  626 
symptoms  of,  625 
X-ray  examination  of,  625 
Heart-beat,  origin  of,  2 
role  of  salts  in,  2 
theories  of,  4 
Heart-block    (see    also    Adams-Stokes    dis- 
ease), 104,  565,  567 
asphyxial,  572 
auriculo  ventricular,  104 
complete,  105,  571 
effect  of  atropine  on,  571,  580 
effect  of  vagus  on,  571 
extrasystoles  simulating,  584 
factors  affecting  degree  of,  569 
stoppage  of  ventricles,  570 
from    cutting    interauricular    sep- 
tum, 566 
functional,  104 
in  infectious  diseases,  580 
interventricular,  105 
in  tortoise,  567 
irregular  rhythm  in,  573 
organic,  104 
partial,  105,  571 

effect  of  heart  rate  in,  571 
from  digitalis,  585 
relation     to     Adams-Stokes     syn- 
drome, 573 
role  of  vagus  in,  566 
sino-auricular,  105 
treatment  of,  585 
with  auricular  fibrillation,  581 
with  rapid  ventricular  rate,  582 


724 


INDEX 


Hemisystole,  105 

Hemorrhage,  blood-pressure  in,  50 

control  of,  627 

fall  of  blood-pressure  in,  50 

from  the  lungs,  219 

in  congenital  heart  disease,  220 

in  mitral  disease,  220 

in  pulmonary  insufficiency,  220 

in  wounds  of  heart,  627 

intracranial,  blood-pressure  in,  40 
Heredity  in  arteriosclerosis,  354 
Herzfehlerzellen,  129,  222 
Heterogenetic  auricular  tachycardia,  126 

impulses  (see  Ectopic) 
in  extrasystoles,  110 
in  paroxysmal  tachycardia,  126 
Hiccough  in  pericarditis,  593 
High  diaphragm,  704 

heart,  705 
Hippocratic  fingers,  543 
His  bundle,  anatomy  of,  568 
Hoarseness  in  pericarditis,  593 
Hormone     action     in    cardiac    symptoms, 

709 
Hydropericardium,  603 
Hydrotherapy,  286 

in  arteriosclerosis,  363 
Hydrothorax,  224 

in  adherent  pericardium,  613 

production  of,  224 
Hyperdicrotic  pulse,  68 
Hypermyotrophy,  arterial,  346 
Hypertension   as   factor   in   production   cf 
arteriosclerosis,  355 

and  arteriosclerosis,  45 

chronic,  42 

and  cerebral  circulation,  46 
effects  upon  circulation,  45 
prognosis,  48 
treatment  of,  46 

diseases  with,  39 
Hyperthyroidism,  676 

acetonitrile  test  for,  680 

accidental,  676 

adrenalin  test  for,  680 

angina  pectoris  in,  391 

effect  on  heart  muscle,  680 

effect  on  nervous  system,  679 

vicious  circle  of,  680 
Hypertrophied  heart,  reserve  force  of,  300 
Hypertrophy,  291 

adrenal,  196 

and  abdominal  arteriosclerosis,  276 

and  arteriosclerosis,  295 

cardiac,  296 

concentric,  293 

electrocardiogram  in,  297 

excentric,  293 

from  overdrinking,  295 

from  work,  294 

in  chronic  nephritis,  295 

of  the  auricles,  300 

of  the  heart  in  Basedow's  disease,  684 

of  the  left  ventricle,  297 

of  the  right  ventricle,  297 

pathological  anatomy  of,  291 

prognosis,  300 


Hypertrophy,  reserve  force,  300 

sites  of,  293 

types  of,  293 

work,  294 
Hypotension,  48 

disease  with,  48 

failure  of  vasomotor  centre  in,  48 
Hypothyroidism,  effect  on  circulation,  675 
Hysterical  angina,  390 

Ice-bag  over  heart,  233 

contraindications  to,  233 
effect  on  pulse  rate,  233 
Impulses,  afferent,  17 

efferent,  17 
Increased  intracranial  pressure,  blood-pres- 
sure in,  40 
Infectious  diseases  as  causes  of  arteriosclero- 
sis, 352 
as  causes  of  Basedow's  disease,  681 
hypotension  in  48 
Influenza  as  cause  of  Basedow's    disease, 
681 
as  cause  of  endocarditis,  402 
Influenzal  myocarditis,  210 
Inhalation  of  carbon  dioxide,  241 
oxygen,  240 
rarefied  air,  242 

as  cause  of  myocarditis,  320 
Injuries  of  heart,  628 
Insufficiency,  mitral,  420 

of  valves  in  broken  compensation,  207 
Intermittent  claudication,  371 
Interventricular  septum,  defects  in,  546 
patent,  546 

murmur  in,  548 
with  pulmonary  stenosis,  537, 
541 
Intima,  calcification  of,  344 

fatty  degeneration  of,  344 
Intranasal  tracings,  81 
Intravenous  injections  in  treatment  of  endo- 
carditis, 410 
of  strophanthin,  259 
Intraventricular  pressure,  25 
Iodothyrin,  676 
Irregularity  (see  Arrhythmia) 

permanent,  120 
Irritability  in  cardiac  disease,  228 

Jaundice,   catarrhal,   in  broken  compensa- 
tion, 227 
in  endocarditis,  406 
Jellinek's  sign  of  Basedow's  disease,  680 
Joffroy's  sign  of  Basedow's  disease,  682 

Karell's  milk  diet,  236 
Kinematographs,  149 

Labor  (see  Pregnancy) 

and  pregnancy  in  persons  with  heart 
disease,  prognosis,  517 

cardiac  overstrain  during,  516 

cause  of  death  during,  516 
Langendorff's  perfusion  apparatus,  4 
Laryngeal  paralysis  in  aneurism,  640 


INDEX 


725 


Lead  poisoning,  blood-pressure  in,  40 
Left  auricle,  pressure  in  fetal  life,  532 
Liquids,  restriction  of,  236 

in  arteriosclerosis,  363 
Liver,  abdominal  pain  from  distended,  227 
presystolic  pulsation  in  tricuspid  steno- 
sis, 510 
pulsation  of,  in  tricuspid  insufficiency, 
504 
in  tricuspid  stenosis,  509 
signs  simulating  cirrhosis  of,  in  adherent 
pericardium,  619 
Low  heart,  704 
Lungs,  hemorrhage  from,  219 

Magnesium  sulphate,  238 
Manometers,  30 
aneroid,  32 
compressed  air,  32 
spring,  32 
Marching,  effect  of,  on  heart,  201 
Massage,  239 

Masturbation,  effect  of,  on  heart,  707 
Matrimony  and  heart  disease,  521,  522 
Meals,  effect  of,  on  blood-pressure,  38 
Measles,  blood-pressure  in,  48 
Mechanical  factors  in  the  production  of  mur- 
murs, 175 
Mechanism  of  the  circulation,  34 
Mechanogymnastics,  283 
Media,  calcification  of,  349 
degeneration  of,  349 
hypertrophy  of,  346 
Medial  changes  in  aneurism,  635 
Mediastinopericarditis,  610 
Meningitis,  blood-pressure  in,  40 
Menstruation,  relation  of,  to  cardiac  symp- 
toms, 708 
Mental  distraction,  231 

exertion,  effect  of,  on  blood-pressure,  38 
Mesaortitis,  syphilitic,  346 
Mesarteritis,  346 
Metabolism,  increase  from  thyroid  secretion, 

679 
Micrococcus  rheumaticus,  400 
Micrograph,  76 

Mid-diastolic  rumble  stenosis,  449 
in  aortic  insufficiency,  471 
in  mitral  stenosis,  449 
Mill-wheel  murmur  in  pneumopericardium, 

604 
Mitral  area,  168 

disease,   pulmonary  complications   of, 

426 
facies  in  mitral  insufficiency,  428 
insufficiency,  420 

and  tuberculosis,  435 
arrhythmia  in,  433 
blood-pressure  in,  432 
broken  compensation  in,  438 
broken    pulmonary    compensation 

in,  426 
broken  systemic  compensation  in, 

427 
cardiac  area  in,  429 
complications,  435 


Mitral  insufficiency,  digitalis  in,  437 

early  administration  of  digitalis  in, 
436 

functional,  421,  422,  423 

lungs  in,  433 

mechanics  of  circulation,  423 

murmur  and  sounds  in,  430 

oesophageal  tracing  in,  81 

organic,  420 

outward  displacement  of  apex  in, 
428 

papillary,  421,  422 

pathology  of,  420 

physical  examination  in,  428 

prognosis  in,  438 

propagation  of  murmur,  431 

pulmonary  stasis  in,  424,  435 

pulse  in,  432 

purgation  in,  437 

re-education  of  heart  muscle  in,  436 

relative,  422 

second  heart  sound  in,  432 

second  stage  of,  426 

stages  of,  425 

stasis  in  left  auricle,  423 

statistics  of,  420 

systolic  murmur  in,  430 

third  stage  of,  427 

tonicity  of  the  heart  in,  427 

treatment,  435 

treatment  of  second  stage  of,  437 

treatment  of  third  stage,  438 

with  mitral  stenosis,  448 

without  symptoms,  425 

X-ray  shadow  in,  429 
stenosis,  440 

anaemia  in,  456 

and  aortic  insufficiency,   differen- 
tiation between,  452 

and  tricuspid  stenosis,  454 

arrhythmia  in,  457 

auricular  fibrillation  in,  457 

blood-pressure  in,  50 

blowing  diastolic  murmur  in,  450 

bronchitis  in,  456 

cardiac  outline  in,  446 

complications,  454 

congenital  form,  441 

diagnosis,  451 

diastolic  murmur  in,  450 

digital  and  phonetic  imitation  of 
the  heart  sounds  in,  448 

dilated  conus  arteriosus  in,  446 

disappearance  and  reappearance  of 
presystolic  rumble  in,  444 

effect  of  auricular  contraction  on 
filling  of  ventricles,  443 

embolism  in,  455 

endocarditic  form,  441 

etiology,  441 

historical,  440 

laryngeal  paresis  in,  444 

mid-diastolic  rumble  in,  449 

operations  on  mitral  valve,  459 

paralysis  of  auricles  in,  444 

pathological  physiology  of,  442 

pathology  of,  440 


'26 


INDEX 


Mitral  stenosis,  presystolic  rumble  in,  446 
thrill  and  systolic  tap  in,  445 
prognosis,  459 
pulmonary  oedema  in,  458 

tuberculosis,  456 
pulse  in,  451 
quality    and    production    of    the 

sounds,  447 
role  of  oedema  and  anaemia  in.  441 
sclerotic  form,  441     • 
snapping  first  sound  in,  447 
stages  of,  450 
symptoms  and  signs,  444 
third  heart  sound  in,  449 
thrombosis  in  left  auricle  in,  455 
treatment  of,  455,  456 
tuberculosis  in.  441 
volume  of  ventricles  in,  442 
with  mitral  insufficiency,  441,  448 
X-ray  shadow  in,  447 
valve,  atheroma  of,  422 

demonstration  of  action  of,  12 
hemorrhage  in,  422 
malformation  of,  563 
tests  for  sufficiency,  421 
Mitralized  pulse,  433 
Mobility  of  heart,  162 
Mobius'  sign  in  Basedow's  disease,  684 
Monckeberg's  arteriosclerosis,  349 
Moore-Corradi    method    in    treatment    of 

aneurisms,  662 
Morbus  cceruleus,  540 
Morphine,  dangers  from,  in  myocarditis,  333 

in  cardiac  dyspnoea,  217 
Mountain  climbing,  Oertel's,  284 
Movements,  passive,  280 
resisted.  280 
Schott,  280 
Murmur  at  back  in  patent  ductus  Botalli, 
544 
attack  in  mitral  insufficiency,  431 
diastolic,    in    pulmonarv    insufficiencv, 

494 
mitral,  differentiation  from  accidental 
and  tricuspid,  431 
digital  imitation  of,  430 
phonographic  tracing  of,  430 
propagation  of,  431 
Roger's  systolic  in  open  septum  ventric- 

ulorum,  548 
systolic,  in  aortic  stenosis,  486 
in  mitral  insufficiency,  430 
in  tricuspid  insufficiency,  502 
Murmurs,  175 

accidental,  178 

causation  of.  180 
differential  diagnosis  of,  179 
nature  of.  180 
time  of.  178 
arterial,  185 

cardiopulmonary,  178,  181 
character  of,  176 
combined,  184 

differentiation  between  cardiopulmo- 
nary and  other  accidental  murmurs, 
182" 


Murmurs,  functional,  178 

hsemic,  178,  180 

mechanical  factors  in  the  production  of, 
175 

phonetics  of,  175 

single,  184 

tabulation  of,  184 

transmission  of,  to  chest  wall,  177,  431 

venous,  185 
Muscle  fibres  in  the  ventricle,  arrangement 

of,  9 
Mvocardial  changes,  distribution  of,  315 
Myocarditis,  314 

acute,  arrhythmia  in,  318 

alcoholic,  321 

and  nephritis,  330 

arrhythmia  in,  327,  328 

bronchitis  in,  328 

catalase  in,  330 

chronic,  324 

blood-pressure  in,  327 

diagnosis  of,  322 

differential  diagnosis  in,  331 

dilatation  in,  317 

diphtheritic,  320 

extrasj-stoles  in,  328 

hypersensibilitv  to  digit alis,  323 

influenzal,  210,"  320 

morphine  in,  333 

murmurs  in,  328 

pathological  physiology  of,  326 

rheumatic,  316,  319 

signs  and  symptoms  of,  319 

strychnine  in,  324 

svmptoms  and  signs  of,  328 

treatment  of,  322,  332 

weakness  of  heart  in,  318 
Myocardium,  affections  of,  314 

syphilis  of,  334 
Myoma  as  cause  of  cardiac  weakness,  708 

Xasal  disease,  cardiac  asthma  from,  218 

septum,    arrhvthmia    from    lesion    of, 
709 
asthma  from  lesion  of,  710 
Xauheim  treatment,  232 
Xephritis  and  myocarditis,  330 

blood-pressure  in,  40,  42 
Xerve- fibres  producing  changes  in  tonus,  17 
Xerves,  accelerator,  19 

sympathetic,  19 
Xeurasthenia,  cardiac,  694 
Xitrites,  269 

action  of,  269 

and  digitalis,  260 

effect  of,  in  hypertension  of  intracranial 
origin,  40 

effect  of  on  the  circulation,  269 

use  of,  in  angina  pectoris,  393 

in  aortic  insufficiency,  479 
in  arteriosclerosis,  364 
Xitroglycerin,  269,  270 

mode  of  administration,  270 

tolerance  to,  270 
Xodal  rhythm,  118 
Xode,  auriculoventricular,  of  Tawara,  568 

sino-auricular,  of  Keith  and  Flack,  8 


INDEX 


727 


Oarsmen,  longevity  of,  205 
Obesity,  diet  in,  308 

high  diaphragm  in,  306,  704 

of  the  heart,  304 

physical  signs  of,  307 

treatment  of,  307 

with  cardiac  atrophy  and  cardiosclero- 
sis, 306 

with  coronary  sclerosis,  306 
(Edema,  219 

effect  of  drugs  and  diet  on,  223 

fluid,  salt  content  of,  223 

lymphagogue  substance  in  the  blood  in, 
222 

of  face,  222 

of  heart  muscle,  206 

pulmonary,  219 

treatment  bv  drainage,  223 

types  of,  221 
Oertel's  mountain  climbing,  284 
(Esophageal  auscultation,  170 
of  mitral  murmur,  431 

tracings,  80 

in  mitral  insufficiency,  81 
Orthodiagraph,  147 
Orthopercussion,  157 
Orthoplessimeter,  158 
Orthopncea,  216 

mechanical     changes     in     circulation, 
217 
Ossification  in  arteriosclerosis,  341 
Outflow  during  systole,  11 
Oxygen    inhalations    of,    in    treatment    of 
cardiac  diseases,  240 


"Pace-maker"  of  the  heart,  5 
Pain  down  the  arms,  227 

on  swallowing  in  pericarditis,  593 
precordial,  226 

referred  from  cervical  ganglia,  227 
sensations,  paths  traversed  by,  384 
Palpation  of  heart,  156 
Palpitation,  225 

and  angina,  384 
cardiac  sensations  in,  225 
with  extrasystoles,  113 
Papillary  insufficiency,  422 
muscles,  fatiguing  of,  77 

in  propagation  of  mitral  murmur, 
431 
Paracentesis  abdominis,  223 

pericardii,  605 
Paradoxical  respiration  in  enteroptosis,  700 
Pararrhythmias,  98 
Paroxysmal  irregularity,  118 
tachycardia,  124 

associated  lesions,  124 
auricular  fibrillation  in,  124 
belching  in,  132 

cardiac  dulness  during  attacks,  129 
cerebral  anaemia  in,  129 
coronary-  sclerosis  in,  125 
diagnosis  of,  131 

differentiation  from  simple  tachy- 
cardia, 124 


Paroxysmal   tachycardia,  doubling  of  rate 
in,  124 
drugs  in,  132 
dyspnoea  in,  129 
effect  on  circulation,  124 
embryocardia  in,  130 
exercise  for  stopping  attacks  of ,  132 
fall  of  blood-pressure  in,  125 
fulness  of  neck  in,  12S 
heterogenetic  impulses  in,  126 
idiopathic,  124 
in  coronary  sclerosis,  381 
in  mitral  stenosis,  124 
inactivity  of  cardiac  nerves  in,  9 
inception  of  rhythm  by  auriculo- 

ventricular  bundle,  135 
interpolated  extrasystoles,  132 
irregularity,  127 

lesions  in  auriculoventricular  bun- 
dle in,  127 
mechanism  of,  125 
myogenic  origin  of,  125 
neurogenic  origin  of,  125 
occasional  contusion  with  Adams- 
Stokes  disease,  583 
occurrence  of,  124 
palpitation,  128 
pathological  physiology  of,  128 
physical  signs,  129 
precordial  pain  in,  128 
rise  of  venous  pressure  in,  125 
sino-auricular  block,  569 
stimulation  of  vagi  in,  132 
sudden  exercise  in,  132 
swallowing  in,  132 
symptoms  of,  128 
theories  as  to  origin,  132 
treatment  of,  132 
tricuspid  insufficienev  in,  130 
types  of,  126 
venous  pulse  in,  125 
vomiting  in,  133 
Parry's  disease  (see  Basedow's  disease) 
Passive  movements,  280 
Patent  foramen  ovale,  550 

pathogenesis  of,  550 
Pathological  conditions,  variations  in  blood- 
pressure  under,  38 
Percussion,  156 
errors  in,  158 
methods  of,  157 
Perfusion  of  excised  mammalian  heart,  4 
Periarteritis,  diffuse,  352 

nodosa,  349 
Pericarditis,  590 

adhesive    (see  Adherent  pericardium), 

610,  614 
blood-pressure  in,  50,  595 
etiology-  of,  590 
exudation,  forms  of,  591 
friction  at  back  in,  595 

sound  in,  594 
hiccough  in,  593 
hoarseness  in,  593 
pain  on  swallowing  in,  593 
precordial  pain  in,  593 
purulent,  603 


728 


INDEX 


Pericarditis,  simple  fibrinous,  593 
diagnosis  of,  595 
prognosis  in,  597 
treatment  of,  596 
signs  of,  593 
symptoms  of,  593 
tuberculous,  604 
fluid  in,  604 
with  effusion,  597 

amount  of  fluid,  597 
blood-pressure  in,  601 
cardiac  outline,  599 
drainage  in,  607 
Ebstein's  cardiohepatic  angle 

in,  599 
effect  on  circulation,  597 
enlargement  of  liver  from,  600 
fulness  of  interspaces  in,  599 
irrigation   of   pericardium   in, 

608 
paracentesis  of,  605 
position  of  heart  in,  600 
Rotch's  sign  in,  599 
signs  at  back  in,  600 
signs  of,  599 
symptoms  of,  598 
treatment  of,  605 
X-ray  examination  of,  601 
Pericardium,  adherent,  389,  610 

development  of,  530 
Peripheral  resistance,  66 
Peritonitis,  blood-pressure  in,  48 
Petechias  in  endocarditis,  406 
Phenolsulphonphthalein  test  for  renal  in- 
sufficiency, 225 
in  chronic  hypertension,  42 
in  myocardial  weakness,  330 
Phosphorus  poisoning,  effect  of,  on  heart  in 

fatigue,  202 
Photographic  record  of  the  venous  pulse,  75 
Phthisis,  blood-pressure  in,  48 
Physiological  conditions,  variations  in  blood- 
pressure  under,  37 
Physical  examination,  152 
Physico-chemical  phenomena,   rhythmicity 

in,  1 
Pigmentation  in  hyperthyroidism  (Jellinek's 

sign),  680 
Pituitary  extract,  268 
Placenta,  vessels  to,  526 
Pleurisy,  blood-pressure  in,  50 
Pleuropericardial  friction,  594 
Pneumococci    as    causes    of     endocarditis, 

402 
Pneumonia  as  cause  of  pericarditis,  590 
blood-pressure  in,  48 
interstitial,  222 
Pneumopericardium,  604 
Polycythemia,  blood-pressure  in,  41 
Polygraph,  Gibson,  74 
Mackenzie,  73,  74 
Marev,  73 
Uskoff,  30 
Position,  changes  in,  161 

effect  of  change  of,  on  blood-pressure,  37 
on  electrocardiogram,  93 
Posture,  effect  of,  on  pulse-rate,  210 


Potassium  iodide,  272 

effect  of,  on  viscosity  of  blood,  60 
for  aneurisms,  662 
in  angina  pectoris,  393 
in  arteriosclerosis,  364 
mode  of  administration,  272 
supposed    effect    on    viscosity    of 
blood,  272 
salts,  effect  of,  on  cardiac  contraction,  2 
thiocyanate,  274 

therapeutic  use  of,  274 
Precordial  pain,  226 

in  angina  pectoris,  383 
in  cardiac  overstrain,  192 
in  hyperthyroidism,  687 
in  pericarditis,  593 
Pregnancy  and  labor,  pulmonary  oedema  in, 
515 
aortic  disease  in,  521 
as  cause  of  Basedow's  disease,  680 
blood-pressure  in,  41 
broken  compensation  in,  518 
effect    on    pulse    and    blood-pressure, 

515 
hypertrophy  during,  515 
termination  of,  520 

in  broken  compensation,  519 
treatment  of  heart  lesions  during,  518 
tricuspid  insufficiency  during,  516 
Presphygmic  period,  10 
Pressure  pulse,  68 
Presystolic  gallop  rhythm,   172 

resemblance  to  mitral  stenosis, 
452 
rumble,    disappearance   and  reappear- 
ance of,  in  mitral  stenosis,  444 
(Flint's)  in  aortic  insufficiency,  473 
in  mitral  stenosis,  446 
in  tricuspid  stenosis,  511 
Protodiastolic  gallop  rhythm,  173 
Pseudo-anginal  pain,  387 
Pseudo-aortic  insufficiency,  469 
Pseudo-cardiac  disturbances,  696 
Psychic  disturbances,  228 
Psychotherapy  in  Basedow's  disease,  689 
Puerperal  infection  as  cause  of  Basedow's 

disease,  681 
Pulmonary  area,  168 

artery,  aneurism  of,  659 
blood-pressure  in,  168 
blood-pressure  in,  before  birth,  51 
development  and  maldevelopment 

of,  536 
sclerosis  of,  362 
vasomotor  nerves  in,  52 
circulation,  51 

action  of  drugs  on,  52 
embolism,  219 
hemorrhage,  219 
insufficiency,  diagnosis  of,  496 
diastolic  murmur  in,  395 
etiological  factors,  493 
forms  of,  492 
functional,  492 
haemoptysis  in,  492 
pathological  physiology,  493 
prognosis  in,  496 


INDEX 


729 


Pulmonary  insufficiency,  pulse  in,  495 
signs  of,  494 
symptoms  of,  494 
treatment  of,  496 
with  pulmonary  stenosis,  544 
oedema,  219 

artificial  respiration  in,  219 
in  mitral  stenosis,  458 
in  pregnancy  and  labor,  516 
signs  of,  219 
treatment  of,  219 
pressure,  52 

conditions  affecting,  52 
stenosis  and  atresia,  causes  of,  534 
diagnosis,  545 
due  to  endocarditis,  534 
due    to    maldevelopment    of 

branchial  arches,  535 
duration  of  life  in,  545 
statistics  of,  534,  545 
in   cpen   interventricular  septum, 

537 
pathological  physiology  of,  539 
systolic  murmur,  543 
treatment  of,  545 
with  patent   interventricular   sep- 
tum, 537,  541 
Pulsations,  inspection  of,  642 
over  chest,  156 
over  veins,  71 
Pulse,  anacrotic,  in  aortic  stenosis,  488 
arterial,  63 
characteristics  of,  26 
curve,  significance  of,  66 
dicrotic,  63 

discrepancies  in  examining,  65 
examination  of  the,  63 
form,  66 

in  aortic  insufficiency  (Corrigan,  water- 
hammer,  collapsing),  474 
pressure,  68 
qualities  of  the,  63 
rate,  69 

effect  of  ice-bag  on,  233 
effect  of  posture  on,  210 
relation  to  temperature,  69 
in  soldier's  heart,  210 
Riegel's,  103,  135 
types  of,  68 

anacrotic,  68 
bisferiens,  68 
collapsing,  68 
dicrotic,  68 
hyperdicrotic,  68 
normal,  68 
tardus,  68 
venous,  71 
volume,  68 

wave,  inequality  and  delay  of,  in  aneu- 
risms, 644 
Pulse-pressure,  26 
Pulsus  alternans,  135 

contractility   diminished  in,  106 
bisferiens,  69 
irregularis  perpetuus,  118 
paradoxus,  103 
tardus  in  aortic  stenosis,  484,  487 


Pupils,  inequality  of,  in  aneurism,  643 

Purgation,  237 

in  broken  compensation,  237 

rise  of  venous  pressure  during,  237 

Purgatives,  237 

Quiet  in  treatment,  231 

Radiographs,  stereoscopic,  149 

technique  of,  149 
Rarefied  air,  inhalation  of,  242 
Raynaud's  disease,  372 

pathology  of,  373 
Rectal  administration  of  digitalis,  258 
Reduplicated  heart  sounds,  170 
Re-education  of  heart  muscle  in  mitral  in- 
sufficiency, 436 
Referred  pains  in  angina  pectoris,  385 
Reflex  cardiac  disturbances,  705 

air-swallowing  in,  705 
associated  symptoms,  705 
gastro-intestinal,  705 
Relative  insufficiency,  422 
Renal  complications  of  cardiac  diseases,  224 
Residual  blood,  15 
Respiration,  method  of  recording,  73 

paradoxical  type,  700 
Respiratory  ratio,  218 

in  adherent  pericardium,  614 
Rest  in  bed,  232 
Retina,  arteriosclerosis  of,  358 

dilatation  of  veins  of,  in  tricuspid  insuf- 
ficiency, 502 
Retinal  changes  in  congenital  heart  disease, 

542 
Rheumatic  fever  as  cause  of  pericarditis,  590 

foci  of  myocarditis  in,  316 
Rheumatism,  blood-pressure  in,  48 

cocci  causing,  400 
Rhythmicity,  physico-chemical  phenomena 

in,  1 
Riess'  sign  of  adherent  pericardium,  616 
Right  ventricle,  tonicity  of,  53 

work  of  the,  51 
Rise  of  blood-pressure  on  constricting  the 

femoral  arteries,  210 
Rotch's  sign  of  pericardial  effusion,  599 
Rupture  of  aneurism,  637 

"Safety-valve"  action  of  tricuspid  valve, 

499 
Sajodin,  use  of  in  cardiac  disease,  272 
Salts,  restriction  of,  236 

r61e  of,  in  origin  of  heart  beat,  2 
Salvarsan,  use  of  in  cardiac  disease,  273 
Sauerbruch  chamber  in  operations  on  heart, 

627 
Scarlatina  as  cause  of  endocarditis,  402 
blood-pressure  in,  48 
pericarditis  from,  591 
Schott  movements,  280 

effect  of,  in  reducing  cardiac  dila- 
tation, 283 
precautions  in,  281 
Second  sound,  166 
wind,  198 


730 


INDEX 


Sensory   stimulation,   effect  of,   on   blood- 
pressure,  38 
Septum  auriculorum,  528 
interpositum,  529 
ventriculorum,  529,  546 

patent,  effect  on  circulation,  548 
prognosis  in,  549 
signs  of,  547 
symptoms  of,  547 
systolic  murmur  in,  548 
trauma  as  cause  of,  546 
treatment  of,  549 
tuberculosis  in,  546 
Sexual  cardiac  disorders,  707,  709 

excess  as  cause  of  Basedow's  disease, 
681 
Shock,  acapnia  in,  49 

blood-pressure  in,  48 
diastolic,  over  aneurism,  656 
Sino-auricular  block  from  cooling  sinus,  5 
in  mammals,  105 
in    paroxysmal    tachycardia, 
127 
node  of  Keith  and  Flack,  6 
Sinus  allorrhythmias,  characteristics  of,  103 
as  "pace-maker"  of  the  heart,  5 
region  in  mammals,  anatomy  of,  5 
reuniens,  528 
role  of,  in  mammals,  7 
wave  on  venous  pulse,  79 
Situs  transversus,  560 

Skull,  fracture  of  the,  blood-pressure  in,  40 
Sleep,  effect  of,  on  blood-pressure,  38 

importance  of,  231 
Smallpox  as  cause  of  endocarditis,  402 
Smoke,  tobacco,  composition  of,  710 
Smoking,  effect  of,  on  circulation,  711 

precordial  pain  from,  711 
Snapping  first  sound  in  aortic  insufficiency, 
473 
in  mitral  stenosis,  447 
Sounds,  alteration  of,  by  pressure,  167 
in  arteries,  184 
over  veins,  184 
Southey's  tubes,  223 
Spa  treatment,  232 
Sphygmobolometer,  Sahli,  30 
Sphygmogram,  the  absolute,  65 
Sphygmograph,  clinical,  63 
Dudgeon,  64 
v.  Jaquet,  64 
Marey,  64 
Roy  and  Adami.  65 
Sphygmography,  errors  in,  64 
Sphygmomanometer,  v.  Basch,  26 
Erlanger,  28 
Gibson,  30 
Hill  and  Barnard,  27 
Lauder  Brunton,  32 
Marey,  26 
Pachon,  32 
Potain,  27 

v.  Recklinghausen,  26 
Riva-Rocci,  27 
Tycos,  32 
Sphygmoscope,  Pal,  30 


Sphygmotonometer,  v.  Recklinghausen,  32 

Uskoff,  30 
Splanchnoptosis,  699 

abdominal  binder  in,  701 

air-cushion  for,  702 

blood-pressure  in,  700 

corset  in  producing,  701 

effect  on  circulation,  700 

effect  of,  on  respiration,  699 

level  of  diaphragm,  699 

overfeeding  in,  702 

pulsus  paradoxus  in,  701 

syncope  from,  700 

tracheal  tug  in,  700 

treatment  of,  701 
Split  sounds,  171 

albuminous  in  pulmonary  oedema,  219 
Sputum,  prune-juice,  220 
Squills,  248,  253 
Stair  climbing,  beneficial  effects  of  graded 

pauses,  283 
Stasis,    effect    of,    on    producing    cardiac 

oedema,  206 
Stellwag's  sign  in  Basedow's  disease,  684 
Stenosis  of  isthmus  of  aorta,  557 
Sterilization  of  patients  with  broken  com- 
pensation, 521 
Stethoscope,  binaural,  essentials  of,  167 

differential,  167 

monaural,  166 

telephone,  162 
Stomach,  sounds  over,  in  adherent  pericar- 
dium (Riess),  616 
Stoppage  of  ventricles,  570 

in  Adams- Stokes  disease,  576 
Strain,  effect  of,  on  the  heart,  204 

exercises  of,  200 
Streptococcus,  in  endocarditis,  401 

in  myocarditis,  316 

viridans  (endocarditis  cocci)  in  chronic 
endocarditis,  409 
Strophanthin,  248,  259 
Strophanthus,  247,  253 
Strychnine,  262 

and  digitalis,  415 

clinical  effects,  262 

effect  on  blood-pressure,  262 

effect  on  cardiac  tonicity,  262 

in  cardiac  dyspnoea,  217 

indications  for,  262 

pharmacological  action  of,  262 

preparations  of,  262 
Sudden  death  in  angina  pectoris,  386 

from  emotion,  713 
Suture  of  blood-vessels  for  thromboangitis 
obliterans,  377 

of  wounds  in  heart,  626 
Swimming,  effect  of,  on  heart,  201 
Sympathectomy  in  Basedow's  disease,  691 
Sympathetic  nerves,  relation  to  exophthal- 
mos, 684 
stimulation  by  thyroid  secretion, 
679 
Sympathicotonic,  19,  368 

in  Basedow's  disease,  680 
Symptoms  of  adherent  pericardium,  613 

of  cardiac  disease,  215 


INDEX 


731 


Syncope  in  paroxysmal  tachycardia,  131 
in  Adams-Stokes  disease,  505 
from  extrasystolic  arrhythmia,  584 

Synechia;  pericardii,  (510 

Syphilis  as  cause  of  arteriosclerosis,  340,  353 
as  cause  of  endocarditis,  403 
in  etiology  of  aneurism,  032,  030 
of  the  myocardium,  334 

with  precordial  pain,  334 

Systole,  outflow  during,  11 

treatment  of,  in  cardiacdiseases,  272, 273 
Wassermann  reaction  in,  335,  403 

Systolic  murmur  in  mitral  insufficiency,  430 
retraction  along  left  cardiac  border,  428 
retractions  over  heart,  155 

Tabagism,  710 

Tachycardia,  paroxysmal,  124 

heterogenetic  auricular,  120 
Tea,  effect  of,  712 

prohibition  of,  237 
Teleroentgenography,  148 
Tests,  functional,  of  cardiac  efficiency,  209 
Theobromine,  200 

in  angina  pectoris,  200,  394 
Theocin,  200 

Theophylline  in  angina  pectoris,  394 
Theories  of  heart-beat,  4 
myogenic,  4 
neurogenic,  4 
Third  heart  sound,  frequency  of,  in  normal 
individuals,  175 
in  adherent  pericardium,  010 
in  aortic  insufficiency,  473 
in  mitral  stenosis,  449 
mechanism  producing,  174 
Thread  galvanometer,  82 
Threshold  percussion,  157 
Thrill,  systolic,  in  aortic  stenosis,  480 

in  congenital  heart  disease,  543 
in  mitral  insufficiency,  429 
Thrills,  mechanics  of,  150 
Thrombi  in  cardiac  chambers,  333 

in  mitral  stenosis,  333 
Thromboangitis  obliterans,  374 

differentiation   from   angeioneuro- 
ses,  374 
Thyroglobulin,  070 

Thyroid  gland  changes  in  Basedow's  disease, 
080 
size  of  normal,  080 
heart,  074 

formes  frustes,  074 
from  pressure,  074 
(hypothyroidism),  075 
in  simple  goitre,  074 
secretion  (see Hyperthyroidism),  079 
of   thvroglobulin   and   iodothyrin, 

070' 
physiological  effects  of,  077 
relation  to  histological  structure, 
070 
Thyroidectin,  089 
Thyroidectomy,  690 
Tobacco  angina,  391 

effect  of,  on  circulation,  711 

on  coronary  circulation,  712 


"Tobacco  heart,"  710 

precordial  pain  from,  711 
prohibition  of,  237 
smoke,  composition  of,  710 
Tonicity,  effect  of  digitalis  on,  252 

effect  of,  on  cardiac  overstrain,  203 

on  residual  blood,  203 
factors  producing  changes  in,  10 
of  the  cardiac  muscle,  13 
of  the  heart  in  mitral  insufficiency,  427 
of  the  right  ventricle,  53 
Tonograph,  30 
Tonsillectomy  in  endocarditis,  417 

in  mitral  insufficiency,  430 
Tonsillitis  as  cause  of  Basedow's  disease,  681 

as  cause  of  endocarditis,  410 
Tonus  (see  Tonicity) 
Tortuous  arteries,  358 
Tracheal   percussion    shock    in   aneurism, 
043 
tug  in  aneurism,  043 
Training  at  end  of  treatment,  285 

effect  of,  198 
Trauma  as  cause  of  thoracic  aneurism,  636 
cardiac,  623 
lesions  due  to,  629 
of  heart,  628 
Treatment  of  heart  failure,  general  princi- 
ples, 231 
relation  of,  to  occupation,  285 
Tricuspid  area,  168 

Tricuspid  insufficiency,  arrhythmia  in  cases 
of,  504 
blood-pressure  in,  504 
diagnosis  of,  506 
effect  on  circulation,  499 
functional,  498 

in  paroxysmal  tachycardia,  130 
organic,  498 

pathological  physiology,  499 
pulse  in,  504 
symptoms  of,  501 
systolic  murmur  in,  502 
treatment  of,  500 
variations  in  murmur,  503 
venous  pulse  in,  500 
stenosis,  5C8 

cyanosis  in,  510 
diagnosis  of,  511 
effect  on  the'  circulation,  509 
etiology  of,  508 
occurrence  of,  5G8 
pathology  of,  509 
presystolic  rumble  in,  511 
pulmonary  infarction  in,  511 
treatment  of,  513 
valve,  demonstration  of  action  of,  12 
malformation  of,  563 
opening  of,  78 
Trigeminal  pulse,  114 
Truncus  arteriosus,  526 
division  of,  529 
Tuberculosis  as  cause  of  arteritis,  352 
as  cause  of  endocarditis,  402 
in  persons  with  mitral  stenosis,  441 
in  pulmonarv  stenosis,  544 
of  the  heart,* 344 


732 


INDEX 


Tuberculous  pericarditis,  604 
Tumors  of  the  heart,  335 

hsemopericardium  from,  336 
Typhoid  fever  as  cause  of  Basedow's  disease, 
681 
blood-pressure  in,  48 


Uraemia,  blood-pressure  in,  40 
Urine,  albumin  and  casts  in,  224 

amount  of  in  cardiac  disease,  224 
chloride  metabolism  in,  224 


Vagotonic  and  sympathicotonie,  19 
Vagus  currents,  with  heart-beat,  225 
with  respiration,  225 
effect  in  producing  heart-block,  566 
Valve,    Eustachian    (of    the    inferior   vena 

cava),  528 
Valves,  abnormality  of,  563 

auriculoventricular,  diastolic  closure  of, 

76 
in  veins,  movements  of,  10 
position  of,  in  diastole,  12 
Valvular  areas  in  auscultation,  168 
Vasa  vasorum,  changes  in,  in  arteriosclero- 
sis, 340 
Vascular  crises,  blood-pressure  in,  40 

sounds,  185 
Vasomotor  angina,  389 
crises,  368 

hypotensive,  372 
use  of  nitrites  in,  368 
Vasotonin,  271 
Veins,  cardinal,  526 
sounds  over,  185 

umbilical  (omphalomesaraic),  526 
visible  pulsations  in,  71 
vitelline,  526 
Venesection,  233 

contraindications  to,  234 

effect  of,  in  hypertension  of  intracranial 

origin,  40 
effect  of,  on  the  circulation,  234 
in  aortic  insufficiency,  480 
in  arteriosclerosis,  364 
in  pulmonary  oedema,  219 
technique  of,  233 
Veno-auricular  junction,  anatomy  of,  7 
Venous  auscultation,  72 
pressure,  209 

determination  of,  50 
effect  of,  on  filling  of  the  heart,  14 
in  broken  compensation,  209 
in  neurasthenics,  694 
in  paroxysmal  tachycardia,  130 
pulsations,  134 
pulse,  71 

abnormal  types  of,  79 

diastolic,  79 

double,  134 

in  auricular  fibrillation,  79 

paralysis,  79 
in  extrasystolic  arrhythmias,  109 


Venous  pulse,  in  heart-block,  581 

information  furnished  by,  80 
in  paroxysmal  tachycardia,  125 
inspection,  134 
photographic  record  of,  75 
positive,  80 
presystolic,  79 
technique  of  tracings,  72 
visual  examination  of,  79 
visual  examination  of,  differential 
diagnosis     of     arrhythmia     by 
means  of,  79 
tracing,  interpretation  of,  76 
Ventricle,  left,  pressure  within,  25 
right,  tonicity  of,  53 
third,  536 
Ventricles,  filling  of,  11 
Ventricular  muscle,  anatomy  of,  9 
tachycardia,  127 
weakness,  due  to  digitalis,  123 
Viscosity  of  the  blood,  59 

apparatus  for   clinical  determina- 
tion of,  59 
factors  influencing,  60 
diet,  60 
hydraemia,  60 
number  of  red  blood-cells, 
60 
Volume  curve,  method  of  recording,  11 
Vomiting,  blood-pressure  in,  50 
Von  Graefe's  sign  in  Basedow's  disease,  684 


Walking  in  treatment  of  heart  lesions,  283 
regulation  of  speed  and  respiration,  284 
Water-hammer  pulse,  68 
Weather,  effect  of,  on  cardiac  symptoms,  215 
Whiskey  in  cardiac  disease,  236 
Wiring  treatment  of  aneurism,  662 
Work  hypertrophy,  294 
of  the  heart,  36 

right  heart,  51 
Worry,  effect  of,  on  circulation,  713 
Wounds  of  the  heart,  623 

control   of  hemorrhage  from, 
627 

results  of  operation,  628 

suture  of,  626 
Wrestling,  effect  of,  on  the  heart,  201 


Xiphisternal  line  as  sign  of  level  of  dia- 
phragm, 699 
X-ray,  cardiac  shadow,  133 

examination  in  oblique  axes,  134 
of  adherent  pericardium,  617 
of  sclerotic  arteries,  358 
magnification  of  shadow,  132 
methods  of  examination,  132 
oblique  illuminations,  133 
pulmonary  shadows,  133 
shadow  in  aneurism,  646 


Zander  exercises,  283 


4/ft 


0 


R0681  H61 

1918 
Hirschfelder  Copy  1 

Diseases  of  the  heart  and  aorta. 


[ 


Hani 


